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477 Cards in this Set
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what produce by lungs
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CO2.. carbonic acid produced and blow off from lungs
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what produce by kdney
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noirmal production of H
metabolism of protein for production of sulfuric and phosphoric acid reabsorbtion of filtered HCO3 secreting of 1 H+ mg/kg/day titrable acid phosphate , sulphate generation of ammonia |
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1 acidemic or alkalemic
is this primary metabolic or repsiratory is this simple or mixed |
look for pH
< 7.40- acidemia > look at HCO3 and pCO2 low Hco3 and low Pco2 primary metabolic in simple -- physiolog responce is predicted from normogram if HCO3 drops by 10, pco2 falls by 12.. or pCO2= 1.5x HCO3+8 |
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causes of metabolic acidosis
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causes of metabolic acidosis
overproduction of lactic or ketoacids underexcretion of endogen produced acids ingestion that will metabolized to other acids renal or GI loss of bicarbonate |
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metabolic acidosis.. classic approach
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anion-/ NA gap
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cations
anions anion gap |
cations- na ka ca mg
anions HCO3, Cl, PH organic acid, albumi anion gap= NA- ( Cl+HCO3) = 12+_2 |
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elevate AG
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ketones (DKA AKA starvation)
AKA ( alcoholic keto acidosis) : present with low Phosphor and glucose, low Phosphor may cause rhabdomyolysis lactic acidosis( decreased perfusion, drugs) renal failure ingestions: salycilates methanol ethylen glycol prophylen glycol |
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when d lactic acidosis can occur
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if P with short bowel syndrome( after operation on bowel)
who have current episodes of encephalopathy will have normal lactic level by standard test TX NPO and i/ V dextrose look for history of bowel disease and maybe in some past point P could get tx with glucose and get better |
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metabolic acidosis: ingections
osmolar gap- what is normal and how to calculate when could be elevated if it is elevate and it is history of alcohol ingestion in vignette, you may think to eliminate the answer- methanol or glycol |
metabolic acidosis: ingections
osmolar gap useful in alcoholics. OG=2( NA)+ BUN/2.8+ glucose/18 normal osmolar gap is < 10 elevated in ingesters |
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isopropyl alcohol
metabolized to ... cause .... |
metabolized to acetone
cause osmolar gap and ketosis , but NO AG!!!! |
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ethylene glycol
tx |
ingested as antifreeze
can cause profound shock metabolized to Ca oxalate in urine tx folic acid fomepozole( ethon dehydrogenase inhibitor) dialysis high AG |
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methanol
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methanol
converted to formic acid cause blindness tx ethon fomepizole dialysis |
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propylene glycole-
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propylene glycole- solvent in IV lorazepam
diazepam could lead to lactic acid was sees in propophol |
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mechnism of non anion gap metabolic acidosis
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loss of HCo3-
diarrhea ureteroentero stomy(ileal loop) inability to excrete H- in RTA exogenous acid - TPN ( total parenteral nutrition) on boards will be diarrhea or RTA but will not show diarrhea but will show UAG- urine anion gap additon of lysin ,argynin |
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non anion gap metabolic acidosis-- when and what to check
what will show by UAG |
diarrhea, RTA check urine NAG
UAG-- ( uNA+UK)-UC)l kidney ability to produse ammonius negative UAG- diarrhea-- kidney generate NH4 and Cl in urine increased positive UAG- RTA- no production of NH4 |
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what type of RTA
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distal-4,1 proximal 2
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what type of RTA is hyperkalemic
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distal 4 (много калия( 4) в конце( дистал)
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what type of RTA is HYpokalemic
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distal 1 type
proximal 2 type |
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1 type RTA mechanism
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cant excrete H from tubule across the concent gradient
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1 type RTA urni pH
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despite acidemia- urine pH will be never less 5,5
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proximal type 2 RTA mechanism
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bicarbon wasting
urine ph is high and decrease when serum pH falls |
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proximal type 2 RTA etiology
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drugs CA inhibitors
amphotericine heavy metals myel;oma shogren syndrome |
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proximal type 2 RTA what could be find
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fanconi syndrome
AA uria Fanconi syndrome (also known as Fanconi's syndrome) is a disease of the proximal renal tubules[1] of the kidney in which glucose, amino acids, uric acid, phosphate and bicarbonate are passed into the urine, instead of being reabsorbed. The clinical features of proximal renal tubular acidosis are: Polyuria, polydipsia and dehydration Hypophosphatemic rickets (in children) and osteomalacia (in adults) Growth failure Acidosis Hypokalemia Hyperchloremia Other features of the generalized proximal tubular dysfunction of the Fanconi syndrome are: Hypophosphatemia/phosphaturia Glycosuria Proteinuria/aminoaciduria Hyperuricosuria |
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proximal type 2 RTA tx
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lots of HCO3
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type 4 RTA other name and mechanism
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hyperchoric
hyperkalemic metab acidosis mechanism-- hypoaldo, hyporenin Type 4 RTA is not actually a tubular disorder at all and nor does it have a clinical syndrome similar to the other types of RTA described above. It was included in the classification of renal tubular acidoses as it is associated with a mild (normal anion gap) metabolic acidosis due to a physiological reduction in proximal tubular ammonium excretion, which is secondary to hypoaldosteronism, and results in a decrease in urine buffering capacity. Its cardinal feature is hyperkalemia, and measured urinary acidification is normal Causes Aldosterone deficiency-Primary (rare) Primary adrenal insufficiency Congenital adrenal hyperplasia Aldosterone synthase deficiency Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction)[36] Renal dysfunction-most commonly diabetic nephropathy ACE inhibitors NSAIDs Cyclosporine Aldosterone resistance Drugs (Amiloride, Spironolactone, Trimethoprim, Pentamidine) Pseudohypoaldosteronism |
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type 4 RTA mcc and when can be seen
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diabetic mellitus maybe with mild renal disease
interstitial renal disease obstructive uropathy sikle cell disease drugs cyclosporine |
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type 4 RTA tx
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furosemide , HCo3
florinef( mineralocarticoids |
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barttler syndrome
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hypokalemia
metabolic alcalosis normal BP low mg high renin and aldo hypercalciuria abnormal Na Ch transport in thick ascend loop and resemble furosemide intake tx- NSAiD and K appear in infanc/childhood |
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gittelman syndrome
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normal blood pressure
metabolic alkalosis looks like somebody is taking the thiaside early adult problem in distal convoluted tubule with NA- ch transport low K, Mg hypocalciuria tx amiloride , spirono lactone and Mg and K chondrocalcinosis |
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water status of your body what system
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ADH system- serum
reflect Na cant be measured) think! serum NA-water= ADH |
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total body sodium reflect what
and what system |
ECF volume status , and it is clinical assement possible
total body Na= volume status RAA system |
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approach the NA disorder
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remember that it is the water problem
need to know U Na and Uosmolarity need Volume status |
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hyponatremia types and association
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hypertonic hyponatremia- increased of hyperosmolar substances: glucose
mannitol .... water shifts out of cells Isotonic hyponatremia- no change in cell size-- excess of lipid and protein Hypotonic: most common causes- intracellular swelling |
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hypotonic hyponatremia
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will have 3 type of ECF volume( low, high and normal)
low ECF volume ---decrease NA and Water If renal losses-: diuretics, addison diseses, salt wasting If non renal losses: GI, 3rd spaces RX- 9N/S high ECF---- increase NA increase Water edema status-- RF CHF- ARF Cirrhosis CRF Nephrotic CRF those patients have extra total NA and greater excees of total body water they are hyponatremic but total body Na is elevated RX: restict water and diuretics Normal ECF volume Norm- Na and increased Water SIDH Psychogenic polydipsia Hypothyroidism Glucocorticoid deficiency RX: restict water,, N/S?? rarely3% ( if patient is syptomatic-- seizures , coma) |
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SIADH
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uOSMO WILL BE VERY HIGH for the present Serum osmolarity
clue-- very low uric acid level. rule out Addison Dises always! etiology: pulm,CNS, Neoplasm drugs- phenothiazine NSAIDS cyclophosphamide RX- Demeclocycline and litium vasopressin RP antagonist- CONIVAPTAN ( V2 and V1a blockers) correct slowly- < 1-2 mm / hour if cell shrink- will be Central pontine myelinolysis explanation-- patients cant excrete the water- too much ADH This largely depends upon the rate of fall in serum sodium: Slow fall in serum sodium - asymptomatic or non-specific features e.g. impaired memory, difficulty concentrating and possibly even falls.1 Rapid fall in serum sodium (i.e. rate of fall greater than 0.5 mmol/l/h) - this is potentially fatal. Features may include: Confusion Hallucinations Drowsiness Convulsions Coma Respiratory arrest leading to death Symptoms are uncommon until the serum sodium falls below 120 mol/l, or the plasma osmolality drops below 268 mOsmol/kg. |
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High uric acid levels in the urine
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High uric acid levels in the urine are seen with gout, multiple myeloma, metastatic cancer, leukemia and a diet high in purines. Those at risk of kidney stones who have high uric acid levels in their urine may be given medication to prevent stone formation.Low urine uric acid levels may be seen with kidney disease and chronic alcohol us
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Low urine uric acid levels
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Low urine uric acid levels may be seen with kidney disease and chronic alcohol us
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Normal Uric acid levels
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Normal Uric acid levels are 2.4-6.0 mg/dL (female) and 3.4-7.0 mg/dL (male). Normal values will vary from laboratory to laborator
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hypernatremia
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hypernatremia: 3 types
1. low ECF ( decrease Na! water!! lost more water than salt, a) renal loss -- osmotic(old patients hyperosmotic coma diuresis b) non renal loss -- sweating Rx: Water and .9N/S 2 High ECF volume ( increased Na !!, increased Water!) Salt water drowning Resuscitation- ACLS,,, patiens were given lots of salt Rx- diuretucs 3 Normal ECF volume Na- normal decrease Water !!! diabetis insipidus a) central- RX- ADH b) nephrogenic- Rx- Thasides |
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primary polydispsia / DI
both present with Polyuria and polydipsia and cause the wash out of the medullary gradient and suppress ADH level |
case- patint drinks alots of water
ds- in PP - Na<137 DI Na>142 DS- water restiction testing ADH administration |
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central D insipidus pathogenesis
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inadequate ADH production
>>> water loss and polyuria Na is >>> up and P gets polydipsia |
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central D insipidus causes
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granulomatous dieases- ( infiltration)sarcoid histocytosis CVA
infections-- TBC syphillis, encephalitis trauma, familial idiopatic |
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central D insipidus tests
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with water restriction
no increase in U osm if complete central DI will respond to ADH administration |
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central D insipidus RX
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RX- desmopressin- DDAVP is primay therapy
in partial DI may use these drugs , they will stimulate of some ADH production chlorpropamide carbamazepine clofibrate NSAIdS |
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Nephrogenic DI pathogenesis
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collection tubiles donot response to ADH-- dumping the water >>>polydipsia
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Nephrogenic DI etiology
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etiology
herediatary- X linked defect in V2 receptor gene drugs - lithium. demeclocycline amphotericin hypercalce,mia hypokalemia shogren |
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Nephrogenic DI RX
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thiaside diuretics
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water restriction test and ADH
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water restriction test and ADH
follow--- U vol, U osm. S osm ( norma. when U psm rises above 600 mosm/kg if U osm doesnot rise or S osm increase above 295-- give ADH and follow... in cDI-- Uosm- rises , urine output falls in nDI- u osm may rise slightly, but remaine dilute in PP Uoasm rises. max is 5-600 mosm/kg, but no responce to ADH |
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litium toxicity
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nDI-- polyuria polydispsia
nocturia prevention- Tx- amiloride thiaside NSAIDs |
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hypokalemia
mechanisms |
hypokalemia
increased mineralocortocoids increased the delivery of Na to the distal tubules increased urine flow alkalosis increased excretion of non reabsopbable solutes |
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what move the K into the cells and maybe responsible for hypokalemia
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insulin Beta adrenergis
aldosterone alkalosis |
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where K go
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into cells--- insulin catecholamines
familial periodic paralysis ( case- sudden hypokalemia and family history of sudden paralysis everything in unremarkable, BP is normal) thyrotoxic hypokalemic periodic paralysis (clinical scenario,,, thyreo toxicosis, low potassium with episodes of weakness.. more common in Asian than other races Extrarrenal losses: diarrhea laxatives.. maybe history of fistulas associated with acidosis Renal losses with normal blood pressure type 1 distal RTA type 2 proximal RTa low magnesium ( ciplatin( chemo in the past, assoc with tubule defect) ETON diuretics barttler and gitelman syndromes |
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renal potassium loses
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with HTN and high Renin\
-primary hyperaldesteronism -congenital adrenal hyperplasia -11-oh dehydrogenase deficiency -Liddle syndrome with HTN and high renin( first renin ig going UP and then HTN occurs) - renovascular HTN - malignant HTN -renin- secreting tumor - essencial HTN with excess diuretics |
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hyperkalemia when?
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shift out of cells
insulin deficiency periodic paralysis beta blockers rhabdomyolysis Impaired renal excretion: RTA type 4 renal failure addison drugs: NSADIs CYa tacrolimus pentamidin heparin ( both) trimetaprim |
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what is on ECG in hyperkalemia
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wide QRS
absent of P tall T bradyarrhyrtmia look for P after dialysis with high K- start Tx |
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Rx for hyperkalemis
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Rx- K shift
Ca glucose insulin beta agonists ( albuterol 20 mg) Na bicarbonate if P has acidosis tx_ K removal sodium polystryene sulfonate dialysis |
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.ADDISON DISEASE
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LOSS OF ADREANAL FUNCTIONS WIL >>> lead to hyponatremia. because of lost of aldosterone
aldosterone cause the sodium re absorption if the body lost aldo, it lost nA |
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what tip for looking for PP
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bipolar disorder- tx by Li
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why volume overload could be in hypotyroidism
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because thyroid hormone need to excrete the water
id not enough TH H-free water excretion will be decrease |
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SIADH WHAT COULD CAUSE IT
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any lung or brain disease
SSRIs sulfonurea vincristine cyclophpspchamide TCA small Cr of lungs pain |
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which symptoms are characterize the hyponatremia
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confusiaon
lethargy disoreintation seizures coma |
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MAT in SIADH
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high ADH level
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what is U_Na , BUN uric acide in SIDH
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u na- very high
BUN and Uric acid are .ow |
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what could happen in SIADH if will be given only saline
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will be worse
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tx for severe symptomatic SIADH
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tolvapatan
conivaptan -- they are antogonists for ADH only for urgent help in the hospital- no oral version is available |
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tx for chronic SIADH
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depend on underlined disease and sometime will not be corrected ( like CR)
demeclocycline- is tx for chronic SIADH( it blocks the action of ADH at the collecting duct of the kidney |
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tx of hyponatermia by severety
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mild= no sympt= restict fluids
moderate= minimal conmfusion= saline and loops diuretics( furasemide) severe= lethargy, seixures . coma- hypertonc saline conivaptan, tolvaptan |
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what us the first clue of presenting DI
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high volume nocturis
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symptoms of hyper -Na -tremia
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neurologic symptoms- confusion
disorientation lethargy and seizures id not corrected- severe hypernatremia causes coma and irreversible brain damage |
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what is the best IT for DI
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wate deprivation test ( observe volume and osmolarity of urine)
with DI - volume stay highand urine osmolaritry stay low depite vigorous urine productiun and despite developing dehydration 2- give ADH--= CDI-- sharp decrese in ukrine volume, increse th eosmolairty NDI- no chnge in urine colume nor osmolairy after ADH administration single most accurate test CDI/NDI---- ADH level ADH level will be low in CDI and markedly elevated in NDI |
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single most accurate test CDI/NDI----
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single most accurate test CDI/NDI---- ADH level
ADH level will be low in CDI and markedly elevated in NDI |
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positive water deprivation test means
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urine volume stays high despite with holding water
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comparasin of CDI/NDI
1 polyuria and nocturia 2 urine osmolarity and Na 3 + water depr test 4 response to ADH 5 ADH level |
1- both
2 both low 3both - yes 4. CDI- response to ADH, NDI- no 5 ADH level is???? in CDI and ??? in NDI |
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Rx for DI
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CDI_ replace ADH- vasopressin( DDAVD)
NDI_ 1correct K and CA 2 stop LI or demeclocycline gIve hydrochlorthiaside or NSIDS for these who still having NDI despite these interventions |
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distal tubule is responsible for what
what drugs or IMMUNOL Dises could damage the distal tubule |
1. generating bicarbonate under the influence of aldosterone
2 shogren, SLE, amphotericin if ne bicarb cant be generated in the distal tubule, then acid cant be secreted into the tubule and will raise the pH of the urine in alkaline urine is increase the formation of kidney stones from Ca oxalate |
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best initial test for distal RTA ( type 1)
the most accurate test |
UA- look fro abnormal pH,,,>5.5
infuse acid into the blood with ammonium chloride and healthy patient will be able to excrete the acid and will decrees the urine pH those with distal RTA cannot excrete the acid and the urine pH will remain basic( over 5.5) despite an increasingly acidic serum |
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Rx of distal RTA
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replace bicarbonate THAT WILL BE ABSORB IN THE PROXIMAL TUBULE, SINCE THE MAJORITY OF BICARB IS ABSORBED AT PROXIMAL TUBULE, DISTAL rta IS RELATIVELY EASY TO CORRECT, JUST GIVE MORE BICARBONATE PROXIMAL TUBULE WILL ABSORB IT AND CORRECT THE ACIDOSIS
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the most accurate test for proximal RTA
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evaluate the bicarb reabsorbtion in the kidney by giving bicarb and test in urine pH. because kidney cant absorb bicarb, urine pH will raise
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Rx for proximal RTA
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necessary massive doses of bicarbonate.
thiazide will give volume depletion and enhance the bicarb reabsorbtion |
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type 4 RTA when it could occurs
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diabetes.. there is a decreased amount or effect of aldosterone at
kidney tubule.. ( hyporeninema, hypoaldesteronism) this>>> to Na loss and retention of K and H test for IV type RTA-- finding the high urine Na despite of sodium depleted diet hyperkalemia is the clue for Most likely diagnosis... fludcortiosone is the steroid with hiest mineralocorticoid or aldosteronlike |
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what steroid has the highest mineralocorticoid effect( or aldosteronlike effct)?
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fludrovortisone
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RTA types
1 urine PH 2 blood K level 3. nephrolithiasis 4 diagnostic tests 5 RX |
type 1 type2 type4
1 variable high. 5.5 <5.5 2 low low high\ 3 no yes no\ 4 bicarb acid urine salt loss 5 thaz bicarb fludrocortison |
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metabolic alkalosis
compesation for metab alkalosis |
elevate serum bicarb level
resp acidosis will be relative hyperventilation that will increasing the Pco2 to compensate the metab alkalosis |
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metab alkalosis etology
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gi loss- vomiting or nasoga suction
increased aldosterone-- primary hyperaldesterosism cushing syndrome ectopic ACDH volumecontraction, licorice |
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etiol of met alkal
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GI loos- vomit or NG suction
increased aldosterone- primary hyperaldoster crushing s ectopic ACTH volume vontraction licorice diuretics milk alkali syndrome- high volume of liquid antacids hypokalemia- hydrogen move into cells and K can be release |
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aterial blood in met alkalosis
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pH>7.4
increased pco2 ( respirat acidosis as compenstion) increased bicarb both are increased you cant determ the etiology as met alkalosis from blood gases |
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respiratory acidosis
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increased pco2
decreased Min ventilation metabolic alkalosis as compes |
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respiratory acidosis caused by
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COPD /EMP
DROWNING OPIATE OVERDOSE ALFA1 ANTITRYPSIN DEF kyphoscoliosis sleep apnea/ morbid obecity |
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respiratory alkalosis
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decreased pco2
increased the minute ventilation metabolic cidosis as compensation |
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respiratory alkalosis causedby
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anemia
anxiety pain fever interstitial lung disease pulmonary emboli |
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MCC of nephrolithiasis
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calcium oxalate ( in alkalina urine)
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MCC RF of nephrolithiasis
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over excretion of ca in urine
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what is the next step in man if p is present with pain in flank and blood in urine
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ketoralac- NSID- give analgesia like opiate
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why crohn cause the kidney stones
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increaesd oxalate absorption
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what i s the most accurate test f nephrolithiasis
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CT scan
IVP is never right answer |
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how can we see uric acid stones
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on Ct(not visible on Xray)
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how to manage cystine stones
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surgical removal
alkalinizing the urine |
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will fat malabsorb increase stone formation
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yep
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best initial therapy for renal colic is
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analgetics
hydration image to control the location of stone |
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howto determ the etiology of stone
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stone analysis
serum CA, uric acid PTH Mg. Ph level 24 hours urine for volume, CA oxalate citrate cystine pH uric acid phosphate Mg |
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when to order litotripsy
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1 stone-0.5-2-3 cm
2 fever 3 infections 4 severe nausea and vomiting 5 complete obstruction or anuria ,Extracorporeal shock-wave lithotripsy would be warranted in these settings or in a patient with a stone that is less than 1 cm in diameter located within the kidney or higher than mid ureter, if stone is in the mid ureter - do flexible ureteroscopy Percutaneous nephrostomy --- in a staghorn calculus, to relieve an obstructed urinary collecting system if retrograde nephrostomy cannot be performed, or to obtain anatomic access in conjunction with extracorporeal shock-wave lithotripsy. small stones will pass larger stones- manage surgically |
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what for stentin nephrolitiasis
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stent placement relieve hydronephrosisfrom ctones in distal ureters
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if stone is on halfway in ureter- rx?
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litotripsy
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how to reat struvite stones
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they are after inf( protey) - RX- surgery
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lomg term of management of nephrolithiasis
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50 % - recccurec
HTZ removes ca from urine by increasing distal reabsorb of ca by distal tubules |
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ca diet?
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wont help and more likely to form th estone
because Ca bind to oxalate in the bowel when Ca ingestion is ow, there is increased oxalate absorb in gut because no ca to bind in the gut. |
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stent placement is done when
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when it is obstruction especially at the ureteropelvic junction
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when is the risk of stone formation
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when dietary decrease of CA
increase in oxalate decrease in citrate |
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why met acidosis increase stones formation
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met acidosis removed Ca from bones and increased stone formation
it also decrease the citrate level citrate bind the ca, making it unavailable for stone formation |
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stress incontinence
who test RX |
woman with painless leak with cough, lauh lifting heavy objects
have a P stand and cough and observe the leakage kegel local estrogen cream surgical tightening the urethra |
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urge incontinence
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sudden pain in the bladder
folowwing immediately by the owerwelming urge to urinate pressure measurement in half full bladder manometry bladder training exercise local antycholinergic therapy oxybuturin tolterodine solifenacin dariferancin surgical tightening of urethra |
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HTN DEFINITIONJ
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systolok.140
diast.90 diabetic P or someone with chronic renal disease---HTN is above 130-80 |
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HTN etiology
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95% essen
renal artery stenosis GN coarct of aorta acro megaly PHeochromocytoma hyperaldesteronism cushing syndrome or any cause of hypercorticolism , including therapeutic use of glucocorticoids congenital adreanal hyperplasia |
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HTN Presentation
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if HTN has symptoms--- they are from aterosclerosis ( end organ damage)
CAD CV disease CHF visual disturb renal insuff PAD |
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presentation of secondary HTN
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renal artery stenosis
bruit!!- continues throughout systole and diatole GN Coarc of A- upper extr BP is . then in low extr pheochromoc- episodic HTN with flushing hyperaldesteronism weakness from hypokalemia |
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HTN- Diag
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repeat measure of BP in office
if they have HTN- do: ecg UA glucose measurement to exclude concomitant diabetes cholesterol screening |
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HTN RX
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best initial therapy---- life style manag ( weight loss- more effective)
sodium restriction diet ( less fat and red meat- more fish and veget) exres tobacco cessation doesn't stop HTP but prevent cardio vascular disease |
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HTN drug therapy
best initial step |
thaside
if BP is very hight on presentaion-- 160/100-- add the second drug 90 % will be controlled by 2 medication if diuretuics wont control- next step-- ACE ing ARB BB CCB |
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what medication are not first line therapy for htn
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central acting A agonists-:
methyldopa, clonidin perif acting alfa antagonists: prazosin, terazosin doxazosin direct actin vasodilators: (hydralasin. minoxidil) |
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compelling indications
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if is another significant disease in history, you should add a specific drug to lifestyle modific
in this case dont start with thazide |
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BIT if history of
CAD |
BB, ACE, ARB
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BIT if history of
DM |
ACE, ARB
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BIT if history of BPH
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alfa blockers
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BIT if history of depression and asthma
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avoid BB
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BIT in HTN if history of osteoporosis
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thasides
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HTN crisis
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confusiaon
blurry vision dyspnea chest pain |
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BIN for HNT crisis
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labetalol or nitroprussid ( not fist choice- need to be monitored)
also CCb- verapamil diltiazem enalapril esmolol |
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why dont lower the BP in the crisis to normal?
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will provoke the stroke
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hyperkalemis etiology...
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1 pseudo:
-hemolysis -repeated fist clenching with tourniquet in place - thrombocytosis or leukocytosis will leak out of cell in the lab specimen no treatment!! or testing 2 decreased excretion: renal failure aldosterone decrease: ACE inhibitors/ ARBs type 4 tubular acidosis( hyporeniemic, hypoaldeosteronism) spironolacton and eplerenone ( aldosteron inhibitors) triamterene and amiloride ( potassium sparing diuretics) addison disease 3 release of K from tissue: any tissue distruction- hemolys rhabdomyolys tumor lysis decresed insulin( it normally drives K into cells) Acidosis- cells will pick up the H( acid) and release K in exchange betablokers and digoxin-- they inhibit Na/K atpase than normally bring the potassium into the cells heparin increased K level, presumably through increased tissue release |
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hyperkalemia- presentation
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interact with musle contr and cardia conductance
weakness paralysis when severe ileus card rhythm dist |
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does hyperkalemia cause seizures
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no
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hyperkalemia
diag tests |
most urgent tst- ECG( PEAKED t WAVES
WIDE QRS PR interval- prolonged |
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hyperkalemia Rx lifethreat
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CaCl or Ca gluconate
insulin and glucose( to drive K into cells) bicarbonate- drives K into the cells but should be used most when acidosis caused hypekalemia |
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hyperkalemia- remov K from body
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sodium polystrene sulfonate-- kayexalate
it binf K ingut and remove insuin and bicarb lower K level through redistr into the cell other methods to lower K - inhale albuterol loop diuretics dialysis |
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does CA decrease K level
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we use CA only to protect he heart, it does not lower K level
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does insulin remove K from the body
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no- it shift it inside the cell
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when hyperkalemia and abnormal aecg what to do
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most appropriate next step is CACl or CA glucnate
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NA_ CNS symptoms K??
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musc and cardiac symptoms
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primary aldesteronism cause by what
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Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction of the mineralocorticoid hormone aldosterone by the adrenal glands.,[1] when not a result of excessive renin secretion. Aldosterone causes increase in sodium and water retention and potassium excretion in the kidneys, leading to arterial hypertension (high blood pressure). An increase in the production of mineralocorticoid from the adrenal gland is evident. It is among the most common causes of secondary hypertension,[2] renal disease being the most common.
Primary hyperaldosteronism has many causes, including adrenal hyperplasia and adrenal carcinoma.[3] When it occurs due to a solitary aldosterone-secreting adrenal adenoma (a type of benign tumor), it is known as Conn's syndrome |
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etiology of primary hyperadesteronism
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bilateral idiopathic adrenal hyperplasia 70 %
unilateral idiopathic adrenal hyperplasia 20 % aldosterone-secreting adrenal adenoma (benign tumor, < 5%) rare forms, including disorders of the renin-angiotensin system |
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for what pump will aldosteron work
what will be K H NA as result of hyperaldestronis why hydrogen-/ Na pump is more acitive what exnzyme generatehydrogen ions and what it couse what acid base will be in hyperaldesteronism what will be with CA |
Aldosterone enhances exchange of sodium for potassium in the kidney so increased aldosteronism will lead to hypernatremia and hypokalemia. Once the potassium has been significantly reduced by aldosterone, a sodium/hydrogen pump in the nephron becomes more active leading to increased excretion of hydrogen ions and further exacerbating the hypernatremia. The hydrogen ions that are exchanged for sodium are generated by carbonic anhydrase in the renal tubule epithelium causing increased production of bicarbonate. The increased bicarbonate and the excreted hydrogen combine to generate a metabolic alkalosis. The high pH of the blood makes calcium less available to the tissues and causes symptoms of hypocalcemia (low calcium levels)
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what will be with Na in hyperaldesteronism , where this will lead to
what happen with GFR and renin why musle cramps why musle weakness |
The sodium retention leads to plasma volume expansion and elevated blood pressure. The increased blood pressure will lead to increased glomerular filtration rate and cause a decrease in renin release from the granular cells of the juxtaglomerular apparatus in the kidney. If there is a primary hyperaldosteronism the decreased renin (and subsequent decreased angiotensin II) will not lead to a decrease in aldosterone levels (a very helpful clinical tool in diagnosis of primary hyperaldosteronism).
Aside from high blood pressure manifestations of muscle cramps (due to hyperexcitability of neurons secondary to hypocalcemia), muscle weakness (due to hypoexcitability of skeletal muscles secondary to hypokalemia), and headaches (due to hypokalemia or high blood pressure) may be seen. |
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primnary aldesteronism-- DS
if plasma level and of renin and aldosterone suggest hyperaldest, what to do next |
Measuring aldosterone alone is not considered adequate to diagnose primary hyperaldosteronism. Rather, both renin and aldosterone are measured, and a resultant aldosterone-to-renin ratio is used for diagnosis.[5][6] A high aldosterone-to-renin ratio indicates presence of primary hyperaldosteronism.
If plasma levels of renin and aldosterone suggest hyperaldosteronism, CT scanning can confirm the presence of an adrenal adenoma. If the clinical presentation primarily involves hypertension and elevated levels of catecholamines, CT or MRI scanning can confirm a tumor on the adrenal medulla, typically an aldosteronoma. cortison->>> cushong Hyperaldosteronism can be mimicked by Liddle syndrome, and by ingestion of licorice and other foods containing glycyrrhizin. In one case report, hypertension and quadriparesis resulted from intoxication with a non-alcoholic pastis (an anise-flavored aperitif containing glycyrrhizinic acid).[7] |
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acute renal failure name then
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pre- renal, renal post renal
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acute renal failure pathphys
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elevation of BUN over several hours to days with or without uremia
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uremia .. what does it indicate
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a need for urgent dialysis
metab acidosis hyperkalemia hyperphosphatemia HYPOCALCEMIA PLEURITIS OR PERICARDITIS PL EFFUSION AND/ OR MENTAL STATUS CHANGE |
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what is the best measure of renal function
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cretinine clearance
if age > 65 and Cr < 1.0mg/dl you masu round creatinine up to 1.0mg/Dl |
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prerenal renal failure
cause |
most common is dehydration and shock due to decrease renal perfusion from any cause: CHF, diuretucs, vomiting, diarrhea
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how to establish the ds of prerenal failure
|
BUN/CR ration of =>20:1
decreased Fena (<1%) high urine osmolarity ( high specific gravity, > 1.010, usually 1.030) |
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what prerenal syndromes
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bilateral renal artery stenosis
hepatorenal syndrome ACE inhibitor- induced renal insufficiency or failure |
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bilateral renal stenosis clinica
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clinical finding
multidrug resistant HTN and signs of prerenal azotemia |
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bilateral renal stenosis
ds |
rapid rise in BUN/Cr after starting therapy
2. suspect in young people with fibromuscular dysplasia 3 suspect in elderly with history of atherosclerotic disease |
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bilateral renal stenosis
tx |
first line- stenting
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hepato renal syndrome clinica
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prerenal azotemia and history of liver diases
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hepato renal syndrome ds
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failure of BUN/CR ration to improove after > 1.5 L of IV normal saline
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hepato renal syndrome tx
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treat liver disease and dialysis if evidence of uremia
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ACE inhibitopr- induced renal insufficiency
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rise in BUN/Cr ration after initiating the therapy, seen in those with baseline renal insufficiency or bilateral RAS( renal artery stenosis)
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intrarenal renal failure
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MCC based upon age and RF
due to intrinsic renal defects, GN and ATN |
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intrarenal renal failure ds
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look for BUN/Cr ration of 10:1, other finding dependent on case
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intrarenal causes of RF
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acute papillary necrosis
cholesterol embolisation syndrome allergic interstitial nephritis contrast induced renal failure ethylen glycol poisoning rhabdomyolysis tumor lysis syndrome |
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acute papillary necrosis
important history |
use of NSAIDs in elderly or baselinerenal disease
sickle cell crisis sudden fever and flank pain |
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acute papillary necrosis studies and tx
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BIT-UA with microscopy and culture WBC, negative urine culture, and granular necrotic sediment
tx- stop NSADIs and tret underlined cause |
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cholesterol embolization syndrome
import history |
recent catheterization ( cause embolization from vessels walls- followed by ARF and bluish discoloration of fingers/ toes (vascular occlusion from emboli)
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cholesterol embolization syndrome
BIT |
BIT Ua with microscopy(increased eosinophills on Whrigh- hansel stain
MAT skin biopsy, shown cholesterol cristals |
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cholesterol embolization syndrome tx
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supportive
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allergic interstitial nephritis important history
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new medication causing allergic drug reaction,or infection, fevr
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allergic interstitial nephritis ds
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BIT UA with microscopy(increased eosinophills on Whrigh- hansel stain)
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allergic interstitial nephritis tx
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first line- stop the drug or treat the infection
second line: if failure to improve- start steroids |
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contract-induced RF h/o
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h/o recent IV contract usually in person with baseline renal disease or Diabetes on oral hypoglycemic
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contract-induced RF ds
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BIT UA
disease usually cause he acute tubular necrosis look for muddy brown cats on UA |
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contract-induced RF tx
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first line- vigorous Iv hydration
prevention: stop all oral hypoglycemic at least 24 hours before IV contrast study and provide hydration with or w/o N-acetylcycteine |
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ethylene Glycol poisoning h/o
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suicidal ideation ( anti freeze ingestion)
look for drank P with high anion gap metabolic acidosis |
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ethylene Glycol poisoning ds
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BIT Ua will show oxalate in urine
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ethylene Glycol poisoning tx
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first line- fomepizole, then dialysis
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rhandomyolysis h/o
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severe trauma
crashing recent strenuous exers Hypokalemia ( hypokalemia may cause the rhabdomyolysis, but hypokalemia is the result of muscle break down ABO incompatibility with ARF |
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rhandomyolysis ds
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BIT
urine A will show + urine dipstick for hemoglobin microscopy will show absence of RBC also check CPK if muscular damage is suspected |
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rhandomyolysis h tx
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first line- check ECG to rule out hyperkalemc changes and treat if needed
hen: IV normal Saline + sodium bicarbonate add mannitol if severe |
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tumor lyssis syndrome h.o
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recent hemo therapy with SARF shortly thereafter
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tumor lyssis syndrome ds
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BIT---UA ( microscopy with urate crystall)
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tumor lyssis syndrome tx
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first line- vigorous hydration with sodium bicarb
2. prevent with prechemotherapy ---IV hydration = allpurinol |
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post renal RF h\o
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look for oligouria in history
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post renal RF different pathog in young and old
|
young-obstructng calculi on the level of bladder neck
elderly- BPH |
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post renal RF ds
|
BUN/Cr ratio of >20:1
decreae FeNA ( 1 %) distended bladder on examination or bilateral hydronephrosis on renal sonogram or CT scan or post void residual volume of > 50 ml use foley to measure |
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post renal RF tx
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relive obstruction
start prazosin or terazosin if elderly man with newly diagnosed BPH |
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chroni renal failure indica for dialysis
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fluid overload with oliguria or anuria
pericaditis pleuritis uremia signif platelet dysfunction signif electrolytes abnormalities altered mental status |
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what type of dyalisis are available
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1 hemodyalysis
2 perit dialysis-- increased evidence of infc- peritonitis |
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why to put on transplant list
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less mortality compared to long term dyalisis
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what almost all Patients with dialysis are requir
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EPO to prevent normoc anemia ( kydney no longer produce EPO)
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what will be in CA and PH in with CRF
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hypocalcemia
hyperphosphatemia- secondary to inability to proue 1.25 dyhydro vit D need vit D replacement and Ca acetate or Ca carbonate-- ( phosphate binders) |
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end stage renal disease is equivalent of what
and how P should be treated |
= CAD
tx betta blokers, statin ACE inhibitors( monitor K level keep BP< 130/80 |
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what diet in hemodyalisis patients
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protein and elemetn restricted diet( Na K Mg Ph)
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berger diseas pathphsy
most comon in who |
dpst of IGa aft recenbt vral infect
most comon in young asian |
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berger dis clin
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hematurian , HTN in young asian patient
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berger dis ds
what is gold stnrt |
BIT- SERUM igA but notr always elevated
gold standart is renal biopsy |
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berger d tx
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fish oil may improove, other vise- supportive
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hemolytic uremic syndrome and TTP
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HUS
triad of microangiopatic hemolytic anemia9 shistocytes on per blood, increase serum LDH with normal GGT, indicating hemolysis, thromobocytopenia and renal insuff |
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what kind of patints could be in HUS
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childern 9 ususally0 and assoc with E coli 0157:h7
kid ate under cooked hamburg-- typical scenario |
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TTP
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pentad
microangiopatic hemolytic anemia thromobocytopenia fever neurologic finding( head ache, neurolog deficit renal insuff |
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what kind of patints could be in TTP
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adult, may be assoc with HIV/AIDS or ticlopidine( antiplatelet)
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TTP tx
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don't transfuse regardless of platelets counts( will be worsening of thrombosis)
dipiridamol to inhbit the platelet aggregation plasmapheresis if severe |
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rapidly progressive GN assoc with
tx |
hiv/ aids
clnical - rapid onset of ARFG look for creshent formation tx steroid +cyclophosphamide , but usually progress to ESRD and requiring hemodyalisis |
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what is the most accur test for all GN
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renal biop
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criteria of nephrotic syndrome
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1.protein loss . 3mg in 24 hours
2. hypoalbuminemia( from protein loss) --------> ---->3.edema T 3th spacing fom decreased oncotic pressure) and hyperelipidemia ( loss of chylomicrons protein substrates and hyperlipiduria( seen as cross in the urine |
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nephrotic syndrom - types of GN
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fical segmental
lipoid nephrosis( minimal change) membranous membrano proliferative |
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focal segmental
microscopy/ association |
assoc with HIV and heroin abuse
light microscopy--- focal segmental sclerosis with hyalinization electron microc-- show loss of foot processes usually progress to ESRD despite the treatment tx-- ace inh or ARB+ steroids add or switch to cyclosporine or cyclophosphamide id disease not controlled |
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lipoid nephrosis ( minimal change disease
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mcc case of nephrotic syndrome in kids
light microscopy is normal electron microscopy shows _ fusion of foot processes add or switch to cyclosporine or cyclophosphamide id disease not controlled |
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membranous
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MCC of nephrotic syndrom ein adults
assoc with maligmacy. hepatitus and NSAIDs light micro shows--- thickened capillary walls electron microscopy-- subepithelial spikes tx add or switch to cyclosporine or cyclophosphamide id disease not controlled |
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membrano -proliferative
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assoc with hepatitis and cryoglobulinemia
light microscopy--- thikened split basement membrane with mesangial proliferation elect micros-- either subendothelial deposits( type1) or dense deposits( type 2) tx add or switch to cyclosporine or cyclophosphamide id disease not controlled serum C# nephritic factor is specific but widely availabe treat underl disease |
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type 1 distal type RTA pathphys
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multip etopl
sporadic cases reumatic dis drug induced infect familial cases hep B or C |
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type 1 distal type RTA clinical
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clinical urineph.5.4 ( alcalotic) cannot ectreete H= ions
HYPOKALEMIA 9 loss of k , secondary tpo inability to ecrete H secondary hyperaldesteronis nephrocalcinosis nephro lithiasis |
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type 1 distal type RTA ds
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acid load test - oral ammon chloride fails to decrease urinary pH below , 5.0
increase urine AN |
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type 1 distal type RTA tx
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oral sodim bicarb tablats + oral K choride replacement
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type 2 proximal RTA pathphys
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multiple etiology
includin any cause of hypocalcemia reum dies MM amiloidosis heavy metal toxicity |
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type 2 proximal RTA clinical
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urine pH IS ALCALINE UNTIL DEPELETIONOD TOTAL BOSY BICARB ( CANNT REABS BICARB)
THEN Ph , 5.4 hypokalemia osteomalacia rickets |
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type 2 proximal RTA ds
|
IV sodium bicarb load test
urine pH remains acidic |
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type 2 proximal RTA tx
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high doses of bicarb + thazide = K
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type 4 hyporeninemic hypoaldestreronism pathphys
|
etiology diabetes
addison renal failure aldoste defici |
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type 4 hyporeninemic clinicalhypoaldestreronism ds
|
oral sodium restrict test--- high urinar sodium conct
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type 4 hyporeninemic clinicalhypoaldestreronism tx
|
fludrocortisone
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ca oxalate stones
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malabs synrome
vit D def mts MM oXalate envelope.... |
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cystein
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hereditary
Cystine c- octogonal cristalls |
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struvite
|
urease prod bacteria causing cystitis and pyelonephritis ( Proteus, klebsiella, pseudom) Cristal as coffin lids-- ammonium , mg, triphosphate or struvite
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uric acid
|
gout malignancy
chron diases tip:Uric acid ... look to fisrt letter- UU on micro of urine... shape of cristal./.. |
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manag of stones
same for all type |
<4 mm- will pass spontaneously
agress hydration andpain ontrol 5-10 mm-- shock wave litotripsy is the best Imanag >10 mm- flexible urereteroscopy combined with laser lithotripsy is the best man |
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good pasture
|
hematuria
hemoptisis dyspnea ds BIT- anti basement membrane antibody confirmation test-- hemosiderin laden microphages or renal biopsy tc plasmaferesis and iv methyl prendisonelone |
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hyponatremia general
|
MCC fluid overload ( CHF ARF
SAIDH PP excessive Na loss |
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hyponatremia import points
|
always correct for hyperglycemia ( false low NA) , BUN hyperlipidemia
serum osmol-- 2xserum Na+ bun/2.8+glycose /18 hyperglycemia--for every 100 g/dl of glucose over normal Na decreases by 1.6 mg/dl |
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hypo Na clinical
|
sympomps may be neurologic and range from altered mental status to coma
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hypo na - tx
|
no change in mental statuys-- restict fluids and correct underl disease
altered mental status-- IV saline = loop diaretics( furasem or acetazolamide) stupot ot coma iv hypertonic saline.. correct at rate 0.5 mEg hour to prevent central pontine myelinosis |
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hypernatremia
|
MCC is exs fluid loss -- diarr, vomiting, sweat. cellular shift
DI |
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hypernatremia
|
clinicalneurolog proble
tx- no chqnge in altered ment status- free water relacemet altered MS- D5W or 1/2normal saline with max dorrections of 12 meg/ day seisures stupor or coma-- iv D5W with nmax correction rate of 1 meg/ hour |
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hypo kalemia mcc
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mcc insendible loss ( mainly GI, vomiting and diarrhea, transcellular shift
hypo,agmesia hypelaldesteronemia loop or thiaside diuretics |
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hypo kalemia clinical
|
skeletal muscle weakness may progress to paralyses, ileus
cardiac arrhtmia ECG will show flat T waves or U waves |
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hypo kalemia tx
|
fisrt always check the MG level
if low- give it by iv- mg sulphat otr orally- mg oxide , decrease dose if diarrhea occurs |
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asymptomatic hypokalemia tx
|
oral K replacement if adequate
if diuretic induced, switch to K sparing- spironolacton or add supplemental K to daily meds( usually 10-40 meg . dl |
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symptomatic hypokalemia tx
|
symptomatic hypokalemia- mean ileus , arrhythmia --- give IV potassium chloride or potassium phosphate in normal or 50 %normal saline at max rate of 20 meg/ hour, avoid any dextrose containing fluid( cause cellular shift and worsen hypokalemia)
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hyperkalemia clinical
|
most feared complication is fatal arrhythmia . first check ECG
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hyperkalemia ECG IN ORDER OF PROGRESSION
|
in order of progression- prolong PR interval> short Qt interval> diffuse peaked T waves> whide QRS COMPLEX> TORSADES DE POINTES> VTACH> v fIB> DEATH
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hyperkalemia TX
|
potassium <5.8 and asymp--->review n=medication ( especially ACE or ARB) and stop them, limit oral K intake
K>5.8 or synptomatic( musc weakness) oral kayexalate( first line) or kayexalate retention enema ( second lne) if ecg changes present- first lin etx- Iv ca chloride( stabilizes myocard membrane), folow with IV sodium bicarb drip, dextrose ( 50 mg.. prevent hypoglycemia) folowed by Iv insulin( 10 U) to drive potassium intracellularly arrange hemodialisis emergently after above measures if needed |
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acid base disorders basics metab alkalosis
|
increased serum HCO3
exes oral or Iv bicarb, mil;k alkali syndrome, trancell shift, diuretics, vomiting, Conn and or Cushing syndromes |
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acid base disorders basics respir alkalosis
|
decreased PCO2
hyperventilation from any cause- acute anxiety, increased progesterone( pregn and chronic liver disease) pain |
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acid base disorders basics metab acidosis
|
decreased serum HCO3
increased AG : DKA AKA ethyl glycol, lactic acido, methanol uremia normal AG diarrhea, RTA decreased AG: MM, hypoalbuminemia lithium |
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acid base disorders basics respir acidosis
|
increased PCO2
hyperventilation from any cause,, copd. astma exacerbation. chest wall disorders , opiate over dose |
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acid base primary disorders with compensation
|
arrows move in thew SAME directions ( respir acidosis .. increased PCO2 compensate with metabol alcalosis---> increased HCO3
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acide base mixed disorders
|
arrows move in the OPPOSItE directions (respir acidosis-- increased PCO2 compensate with metabolic acidosis --> decrease HCO3
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|
1 Stage of Chronic Kidney Disease
|
1 Kidney damage with normal GFR ≥90
Treatment of comorbid condition, interventions to slow disease progression, reduction of risk factors for cardiovascular disease |
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2 Stage of Chronic Kidney Disease
|
2 Kidney damage with mildly decreased GFR 60-89 Estimate disease progression
|
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3 Stage of Chronic Kidney Disease
|
3 Moderately decreased GFR 30-59 Evaluation and treatment of disease complications (such as anemia, renal osteodystrophy)
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4 Stage of Chronic Kidney Disease
|
4 Severely decreased GFR 15-29 Preparation for kidney replacement (dialysis, transplantation)
5 Kidney failure <15 (or dialysis) Kidney replacement therapy if uremia is present |
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5 Stage of Chronic Kidney Disease
|
5 Kidney failure <15 (or dialysis) Kidney replacement therapy if uremia is present
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|
Chronic kidney disease is characterized by
|
Chronic kidney disease is characterized by either kidney damage or a glomerular filtration rate less than 60 mL/min/1.73 m2 that persists for 3 months or more
|
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|
Major risk factors for chronic kidney disease include
|
Major risk factors for chronic kidney disease include diabetes mellitus, hypertension, obesity, and the metabolic syndrome
|
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|
Clinical features predictive of accelerated disease progression in patients with chronic kidney disease include degree of
|
Clinical features predictive of accelerated disease progression in patients with chronic kidney disease include degree of proteinuria, hypertension, and black race.
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|
what carries the highest risk for developing chronic kidney d
|
A personal history of diabetes, hypertension, or cardiovascular disease carries the highest risk for developing chronic kidney d
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|
what is indicated In patients with risk factors for chronic kidney disease,
|
In patients with risk factors for chronic kidney disease, screening with urinalysis, a urine protein- or albumin-creatinine ratio from a first morning voided specimen, serum creatinine level measurement, and estimation of the glomerular filtration rate is indicated
|
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|
Evaluation of all patients with chronic kidney disease should include
|
Evaluation of all patients with chronic kidney disease should include urinalysis, evaluation of urine sediment, kidney ultrasonography, and measurement of the serum electrolytes and a random urine protein-creatinine ratio.
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|
Biopsy should be considered in patients with chronic kidney disease who have
|
Biopsy should be considered in patients with chronic kidney disease who have evidence of glomerular disease in the absence of diabetes or in patients with diabetes with atypical features, such as the absence of retinopathy or the development of sudden-onset nephrotic syndrome or glomerular hematuria.
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|
Complications associated with chronic kidney disease include
|
Complications associated with chronic kidney disease include cardiovascular disease, anemia, and chronic kidney disease-mineral and bone disorder
|
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|
Treatment of hypertension in patients with chronic kidney disease protects against both
|
Treatment of hypertension in patients with chronic kidney disease protects against both progressive chronic kidney disease and cardiovascular disease.
|
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|
Anemia of chronic kidney disease is a diagnosis of
|
Anemia of chronic kidney disease is a diagnosis of exclusion, and the presence of other causes of anemia such as gastrointestinal bleeding, vitamin B12 deficiency, or hemolysis should be investigated.
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|
what can correct erythropoietin deficiency and should be considered for patients with chronic kidney disease who have hemoglobin levels below 10 g/dL (100 g/L).
|
Use of erythropoietin-stimulating agents such as epoetin and darbepoietin alfa can correct erythropoietin deficiency and should be considered for patients with chronic kidney disease who have hemoglobin levels below 10 g/dL (100 g/L).
|
|
|
Patients with chronic kidney disease and anemia should be treated to a target hemoglobin level from
|
Patients with chronic kidney disease and anemia should be treated to a target hemoglobin level from 11 to 12 g/dL (110 to 120 g/L), and hemoglobin levels should not exceed 13 g/dL (130 g/L).
|
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|
Management of chronic kidney disease-mineral and bone disorders involves controlling the serum
|
Management of chronic kidney disease-mineral and bone disorders involves controlling the serum parathyroid hormone and phosphorus levels, restriction of phosphorus-rich foods, and the use of phosphate binders.
|
|
|
Patients with chronic kidney disease may develop renal osteodystrophy t tat manifests as
|
hPatients with chronic kidney disease may develop renal osteodystrophy tat manifests as osteitis fibrosa cystica, osteomalacia, adynamic bone disease, mixed uremic osteodystrophy, osteoporosis, and amyloidosis.
|
|
|
General management of patients with chronic kidney disease should attempt to
|
General management of patients with chronic kidney disease should attempt to delay disease progression, treat symptoms, and reduce risk factors for disorders that have an increased prevalence in patients with this disease.
|
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|
Ideally, the hemoglobin A1c level in patients with chronic kidney disease who have diabetes should be maintained between
|
Ideally, the hemoglobin A1c level in patients with chronic kidney disease who have diabetes should be maintained between 7% and 7.9%.
|
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|
Nephrotoxic agents
|
Nephrotoxic agents such as magnesium- and phosphate-containing cathartics, NSAIDs, selective cyclooxygenase-2 inhibitors, and iodinated contrast are not recommended for patients with chronic kidney disease, and metformin and bisphosphonates should be used with caution
|
|
|
Experts recommend blood pressure targets
|
Experts recommend blood pressure targets of less than 130/80 mm Hg for patients with chronic kidney disease and less than 125/75 mm Hg for patients with proteinuria greater than 1 g/24 h.
|
|
|
the preferred antihypertensive agents in patients with chronic kidney disease.
|
Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers are the preferred antihypertensive agents in patients with chronic kidney disease.
|
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|
Most patients with advanced chronic kidney disease require what medicine
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Most patients with advanced chronic kidney disease require at least two antihypertensive agents to achieve blood pressure goals, and restriction of sodium to less than 2.4 g/d and adding furosemide can enhance the effects of antihypertensive agents.
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Discussions regarding the need for kidney replacement therapy should begin when
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Discussions regarding the need for kidney replacement therapy should begin at least 1 year before the anticipated start of dialysis or when the glomerular filtration rate decreases below 30 mL/min/1.73 m2.
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treatment of choice for most patients with end-stage kidney disease.
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Kidney transplantation is the treatment of choice for most patients with end-stage kidney disease.
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To preserve veins for dialysis access,
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To preserve veins for dialysis access, venipuncture and intravenous cannulation above the level of the hands ideally should be avoided once the GFR decreases below 60 mL/min/1.73 m2.
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what are discouraged in patients with chronic kidney disease who are considering dialysis.
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Peripherally inserted central venous catheters are discouraged in patients with chronic kidney disease who are considering dialysis.
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Dialysis should be initiated when
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Dialysis should be initiated before symptoms of advanced uremia develop.
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End-stage kidney disease is associated with an increased risk for
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End-stage kidney disease is associated with an increased risk for cardiovascular disease, acquired cystic disease, and cancer of the kidneys.
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are associated with both patient and allograft survival advantages
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Preemptive kidney transplantation before initiation of dialysis and transplantation performed after shorter periods of dialysis are associated with both patient and allograft survival advantages
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Common contraindications to kidney transplantation include
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Common contraindications to kidney transplantation include recent or metastatic malignancy, current untreated infection, severe irreversible extrarenal disease, a history of nonadherence, inability to give informed consent, active use of illicit drugs, and primary oxalosis without plans for liver transplantation
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graft survival with living donor kidney transplantation /deceased donor transplantation.
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One- and 5-year graft survival with living donor kidney transplantation is significantly higher than with deceased donor transplantation.
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n the absence of kidney donation from an identical twin,
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In the absence of kidney donation from an identical twin, immunosuppression with both induction and maintenance therapy is needed in kidney transplant recipients to prevent the immune system from rejecting the transplanted organ.
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Kidney transplant recipients have an increased risk for
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Kidney transplant recipients have an increased risk for cardiovascular disease, infection, and malignancy; in addition, focal segmental glomerulosclerosis commonly recurs early in the posttransplantation period.
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Kidney transplant recipients may have an increased risk of fractures caused by
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Kidney transplant recipients may have an increased risk of fractures caused by corticosteroid use, bone quality abnormalities, and vitamin D deficiency.
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Pregnancy in a transplant recipient is possible but is considered
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Pregnancy in a transplant recipient is possible but is considered high risk.
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Risk Factors for Chronic Kidney Disease
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Diabetes mellitus
Hypertension Hyperlipidemia Cardiovascular disease Obesity Metabolic syndrome Age >60 years Malignancy Family history of chronic kidney disease Smoking HIV infection Hepatitis C virus infection Kidney stones Autoimmune disease Recurrent urinary tract infection Recovery from acute kidney injury Exposure to nephrotoxic drugs, such as NSAIDs and cyclooxygenase-2 inhibitors |
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underlying cause and stage of CKD determine the clinical manifestations of this condition.
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he underlying cause and stage of CKD determine the clinical manifestations of this condition. Patients with stages 1 and 2 CKD are often asymptomatic; for example, patients with incipient diabetic nephropathy may present with asymptomatic microalbuminuria. However, those with advanced diabetic nephropathy associated with nephrotic-range proteinuria often have evidence of retinopathy and neuropathy. Patients with stages 3 and 4 CKD usually have progressive cardiovascular disease, abnormalities in bone and mineral metabolism, and anemia.
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Manage chronic kidney disease.
Key Point |
Manage chronic kidney disease.
Key Point * Patients with risk factors for chronic kidney disease should undergo screening with urinalysis, serum creatinine measurement, first morning void random urine protein- or albumin-creatinine ratio, and estimation of the glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) study equation when the estimated GFR is below 60 mL/ min/1.73 m2. The most appropriate study for this patient |
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albumin/creatinine ratio
significance |
albumin/creatinine ratio (ACR)[3] and microalbuminuria is defined as ACR ≥3.5 mg/mmol (female) or ≥2.5 mg/mmol(male),[4
norma< 30 mg/g Significance • an indicator of subclinical cardiovascular disease • marker of vascular endothelial dysfunction • an important prognostic marker for kidney disease ○ in diabetes mellitus ○ in hypertension • increasing microalbuminuria during the first 48 hours after admission to an intensive care unit predicts elevated risk for acute respiratory failure, multiple organ failure, and overall mortality • a risk factor for venous thromboembolism |
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Protein-creatinine ratio
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Protein-creatinine ratio — less than or equal to 0.2 mg/mg
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Diabetic nephropathy
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Diabetic nephropathy is characterized by proteinuria, hypertension, and a decline in the glomerular filtration rate in patients with a long-standing history of type 1 diabetes or a 5- to 10-year history of type 2 diabetes. This condition usually progresses from microalbuminuria to macroalbuminuria to an elevated serum creatinine level over a number of years.
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Cystoscopy
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Cystoscopy would be considered in an adult with hematuria of uncertain origin in order to exclude bladder cancer. Similarly, imaging studies may help to evaluate urinary tract obstruction, kidney stones, kidney cysts or masses, renal vascular diseases, and vesicoureteral reflux. However, cystoscopy or a spiral CT would not be warranted in a patient with erythrocyte casts seen on urinalysis, which suggests glomerular hematuria.
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* An osmolal gap higher than 10 mosm/kg H2O (10 mmol/kg H2O) indicates
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* An osmolal gap higher than 10 mosm/kg H2O (10 mmol/kg H2O) indicates the accumulation of an additional solute in the plasma.
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* Manifestations of hyponatremia include
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* Manifestations of hyponatremia include nausea, malaise, headache, lethargy, muscle cramps, restlessness, disorientation, and obtundation.
* |
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* Low effective arterial blood volume is associated with
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* Low effective arterial blood volume is associated with hypovolemic and hypervolemic hyponatremia.
* |
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* The syndrome of inappropriate antidiuretic hormone secretion is characterized by
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* The syndrome of inappropriate antidiuretic hormone secretion is characterized by euvolemia or a slightly volume-expanded state and is treated with fluid restriction.
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* Cerebral salt wasting is associated with
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* Cerebral salt wasting is associated with a decrease in intravascular volume and should be treated with intravenous normal saline.
* |
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* In the treatment of chronic hyponatremia what would helps to prevent osmotic demyelination.
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* In the treatment of chronic hyponatremia, limiting serum sodium correction to less than 10 to 12 meq/L (10 to 12 mmol/L) within 24 hours and less than 18 meq/L (18 mmol/L) within 48 hours helps to prevent osmotic demyelination. * |
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Hypervolemic hypernatremia results from administration of
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* Hypervolemic hypernatremia results from administration of hypertonic saline or hypertonic sodium bicarbonate or a mineralocorticoid excess.
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what is imdicated In patients with acute hyponatremia,
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* In patients with acute hyponatremia, rapid normalization of the extracellular fluid osmolality is indicated.
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what should not be used to treat hypovolemic hyponatremia.
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* Conivaptan and tolvaptan are approved to treat euvolemic and hypervolemic hyponatremia, but vaptan agents should not be used to treat hypovolemic hyponatremia.
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Hypovolemic hypernatremia results from fluid losses in which
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* Hypovolemic hypernatremia results from fluid losses in which the sodium concentration is less than the plasma concentration.
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* Isovolemic hypernatremia is caused by
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* Isovolemic hypernatremia is caused by pure water loss via a mucocutaneous route or the kidneys.
* |
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suggestive of osmotic diuresis.
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A urine osmolality greater than 300 mosm/kg H2O (300 mmol/kg H2O) in a patient with polyuria is suggestive of osmotic diuresis.
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Water diuresis occurs in
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* Water diuresis occurs in primary polydipsia and central or nephrogenic diabetes insipidus.
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* Hypernatremia generally should be corrected slowly
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* Hypernatremia generally should be corrected slowly by water administration at a rate that leads to half-correction in 24 hours.
* |
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Use of β-agonists or excessive insulin can cause
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Use of β-agonists or excessive insulin can cause hypokalemia.
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* In the absence of a cellular shift, a low serum potassium concentration can be caused by
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* In the absence of a cellular shift, a low serum potassium concentration can be caused by losses via the gastrointestinal tract or skin, kidney potassium losses, or inadequate dietary intake of potassium.
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* In patients with hypokalemia caused by a primary increase in distal sodium delivery, the presence of metabolic acidosis is suggestive
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* In patients with hypokalemia caused by a primary increase in distal sodium delivery, the presence of metabolic acidosis is suggestive of renal tubular acidosis; the presence of metabolic alkalosis is suggestive of vomiting or diuretic use.
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* Manifestations of hypokalemia may include\
Electrocardiographic findings in patients with hypokalemia The maximum recommended rate of intravenous potassium chloride administration is |
* Manifestations of hypokalemia may include a flaccid paralysis, rhabdomyolysis, smooth muscle dysfunction, polyuria, polydipsia, kidney failure, and glucose intolerance.
* Electrocardiographic findings in patients with hypokalemia may include ST-segment depression, T-wave flattening, and an increased U-wave amplitude. * Oral administration of potassium chloride is safer than other routes and can be given in divided dosages of 100 to 150 meq/d. * The maximum recommended rate of intravenous potassium chloride administration is 20 meq/h at a maximum concentration of 40 meq/L. * |
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Electrocardiographic hyperkalemia Hyperkalemia that occurs in patients with a glomerular filtration rate higher than 10 mL/min/1.73 m2
i f p take the drug that could cause hyperkalemia |
Hyperkalemia that occurs in patients with a glomerular filtration rate higher than 10 mL/min/1.73 m2 suggests a decreased aldosterone level or a lesion of the cortical collecting duct.
* An increase in serum potassium greater than 5.5 meq/L (5.5 mmol/L) in patients taking a drug known to cause hyperkalemia warrants a decrease in the dosage or elimination of the offending drug or, in patients treated with concomitant therapy with an angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, or aldosterone receptor blocker, discontinuation of one of these agents. * Electrocardiographic findings of hyperkalemia include peaking of T waves, lengthening of the PR and QRS intervals, development of a sine wave pattern, ventricular fibrillation, and asystole. * |
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tx 0- acute and chronic hyperkalemia
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* Immediate treatment with calcium gluconate or calcium chloride is indicated for patients with life-threatening hyperkalemia or electrocardiographic changes.
* Treatment of chronic hyperkalemia may include discontinuation of drugs that can impair kidney potassium excretion, a low-potassium diet, and use of diuretics. * |
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Severe symptomatic hypophosphatemia most often develops in patients with
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Severe symptomatic hypophosphatemia most often develops in patients with chronic alcoholism.
* |
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Hypophosphatemia may manifest as
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Hypophosphatemia may manifest as severe weakness, rhabdomyolysis, hemolysis, and a leftward shift of the oxygen dissociation curve.
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* Hypophosphatemia may be caused by
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* Hypophosphatemia may be caused by decreased dietary intake of phosphate, a cellular shift, decreased gastrointestinal absorption, increased kidney excretion, or a combination of these factors.
* Hypophosphatemia in patients with diabetic ketoacidosis may only become apparent after the ketoacidosis is corrected. * Intravenous phosphate replacement therapy should be reserved for patients with a serum phosphate concentration below 1.5 mg/dL (0.5 mmol/L). |
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osmolality/tonicity.
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All particles determine the plasma osmolality, but only effective osmoles determine the plasma tonicity. Effective osmoles cannot penetrate cell membranes and therefore may affect cell volume. Conversely, ineffective osmoles such as urea and alcohols pass freely into and out of cells and do not affect cell volume. An excess of an ineffective osmole therefore would not cause a cellular shift and would be associated with a high plasma osmolality but normal plasma tonicity.
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Disorders of Serum Sodium
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The osmolal gap is the difference between the measured and calculated osmolality and is normally less than 10 mosm/kg H2O (10 mmol/kg H2O). An osmolal gap higher than 10 mosm/kg H2O (10 mmol/kg H2O) indicates the accumulation of an additional solute in the plasma
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Diagnose cerebral salt wasting.
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Diagnose cerebral salt wasting.
Key Point * Cerebral salt wasting may affect patients undergoing neurosurgery, particularly those with subarachnoid hemorrhage, and manifests as hyponatremia, increased urine sodium excretion, concentrated urine, and evidence of hypovolemia. Cerebral salt wasting (CSW) is a rare |
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CSW is distinguished from the syndrome of inappropriate antidiuretic hormone secretion (SIADH)
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CSW is distinguished from the syndrome of inappropriate antidiuretic hormone secretion (SIADH) by the presence of hypotension, which reflects the decreased intravascular volume associated with kidney salt wasting. The treatment of CSW is intravenous normal saline.
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thyroid hormone deficiency leads to increased central release of antidiuretic hormone, and
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Hypothyroidism can lead to hyponatremia but would not explain this patient’s volume-depleted state. Furthermore, thyroid hormone deficiency leads to increased central release of antidiuretic hormone, and hypothyroidism-associated hyponatremia usually resembles SIADH and not CSW.
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patients with SIADH usually have extremely decreased serum uric acid levels, because
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patients with SIADH usually have extremely decreased serum uric acid levels, because volume expansion in this setting causes decreased uric acid absorption in the proximal nephron.
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adrenal insufficiency
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patient’s kidney salt wasting and volume depletion are consistent with adrenal insufficiency. However, this patient has no predisposing factors for hypoadrenalism, such as discontinuation of long-term corticosteroid therapy, sepsis, or autoimmune disease. Furthermore, hyperkalemia and a mild, non–anion gap metabolic acidosis are found in over 60% of patients with adrenal insufficiency but are absent in this patient.
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patient has exercise-induced hyponatremia,and the most appropriate next step is
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patient has exercise-induced hyponatremia, and the most appropriate next step is an infusion of 3% saline, 100 mL over 10 minutes. Intense exercise, particularly during an endurance event such as a marathon, predisposes patients to hyponatremia.
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acute exercise-induced hyponatremia,
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Administration of hypotonic or isotonic fluids should be avoided in patients with acute exercise-induced hyponatremia, because these fluids can exacerbate the hyponatremia. Isotonic saline may be helpful in patients with mild hyponatremia and evidence of volume depletion but would not help a patient with significant hyponatremia without evidence of hypovolemia.
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This patient has exercise-induced hyponatremia, and the most appropriate next step is
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This patient has exercise-induced hyponatremia, and the most appropriate next step is an infusion of 3% saline, 100 mL over 10 minutes. Intense exercise, particularly during an endurance event such as a marathon, predisposes patients to hyponatremia.
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risk factor for exercise-induced hyponatremia,
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An increase in fluid consumption is the primary risk factor for exercise-induced hyponatremia, and patients with this condition typically either have no weight loss or experience a weight gain despite excessive exercise. In this setting, delayed absorption of ingested water may lead to a further decrease in the patient’s serum sodium concentration. Additional risk factors for exercise-induced hyponatremia include female sex, a low BMI, and lack of athletic training.
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hyponatremic athletes
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Most hyponatremic athletes are asymptomatic or have mild symptoms including nausea, dizziness, weakness, and headache. More severe manifestations may include confusion, seizures, coma, and collapse. This patient’s disorientation and seizure are consistent with acute, severe hyponatremia.
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patient has acute hyponatremia induced by use of the illicit drug 3,4-methylenedioxymethamphetamine (ecstasy), which is associated with an increased risk for
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patient has acute hyponatremia induced by use of the illicit drug 3,4-methylenedioxymethamphetamine (ecstasy), which is associated with an increased risk for developing potentially fatal hyponatremia. The most appropriate next step in her management is administration of hypertonic saline.
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manage acute hyponatremia induced by by 3,4-methylenedioxymethamphetamine (ecstasy).
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anage acute hyponatremia induced by 3,4-methylenedioxymethamphetamine (ecstasy).
Key Point * In patients with symptomatic, acute hyponatremia, rapid normalization of the extracellular fluid osmolality with hypertonic saline is indicated. This patient has acute hyponatremia |
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3,4-Methylenedioxymethamphetamine stimulates
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3,4-Methylenedioxymethamphetamine stimulates thirst and induces antidiuretic hormone secretion. Furthermore, this drug may decrease gastrointestinal motility, which can lead to retention of several liters of water in the lumen of the stomach and small intestine. This water can be absorbed abruptly once intestinal motility is restored, which causes sudden-onset severe hyponatremia that can be fatal. This condition may cause seizures and cerebral and neurogenic pulmonary edema. Rapid normalization of the extracellular fluid osmolality with hypertonic saline is indicated in patients with hyperacute symptomatic forms of hyponatremia to reduce brain edema and prevent cerebral herniation and death.
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Radionuclide kidney clearance scanning, also known as GFR scanning, is now considered the gold standard
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Radionuclide kidney clearance scanning, also known as GFR scanning, is now considered the gold standard for the estimation of the GFR in healthy persons and in those with acute kidney injury. However, use of these studies is limited because of cost, lack of widespread availability, and operator technical difficulties.
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Hyponatremia is defined as
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Hyponatremia is defined as a serum sodium concentration less than 136 meq/L (136 mmol/L). Initial manifestations of hyponatremia include nausea and malaise; as this condition progresses, headache, lethargy, muscle cramps, restlessness, disorientation, and obtundation may develop.
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Chronic hyponatremia refers
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Chronic hyponatremia refers to hyponatremia that is present for more than 48 hours and is characterized by a slowly decreasing serum sodium concentration. In patients with chronic hyponatremia, neurologic manifestations are generally minimal and the brain size remains normal. Chronic hyponatremia usually occurs in the outpatient setting.
Acute hyponatremia refers to hyponatremia that develops in less than 48 hours. Patients with acute hyponatremia frequently do have neurologic manifestations and cerebral edema. Acute hyponatremia is more common than chronic hyponatremia in hospitalized patients. |
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Acute hyponatremia
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Acute hyponatremia refers to hyponatremia that develops in less than 48 hours. Patients with acute hyponatremia frequently do have neurologic manifestations and cerebral edema. Acute hyponatremia is more common than chronic hyponatremia in hospitalized patients.
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Risk Factors hyponatremia,
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Risk Factors
Postoperative administration of hypotonic fluids is a risk factor for acute hyponatremia, because antidiuretic hormone levels remain increased for several days after a surgical procedure. Severe hyponatremia also may develop in patients undergoing bowel preparation for procedures such as colonoscopy. |
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Common causes of hyponatremia in the outpatient setting include
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Common causes of hyponatremia in the outpatient setting include overhydration, diarrhea, vomiting, central nervous system infection, extreme exercise, advanced age, liver failure, kidney failure, heart failure, and use of certain medications (Table 5 ). Hypotonic fluid intake in the setting of intense exercise, particularly during an endurance event, also frequently causes this condition. Patients with severe exercise-induced hyponatremia may collapse, and this condition can be fatal.
T |
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most common cause of drug-induced hyponatremia. T
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hiazide diuretics are the most common cause of drug-induced hyponatremia. Thiazide-induced hyponatremia typically develops within 2 weeks of drug initiation and is most likely to occur in elderly women and when consumption of hypotonic fluids usually increases. Concomitant use of NSAIDs and selective serotonin reuptake inhibitors can further increase the risk of thiazide-induced hyponatremia. Experts recommend routine monitoring of the serum sodium concentration 2 to 4 weeks after initiating a thiazide-containing agent.
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The illicit drug ecstas
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The illicit drug 3,4-methylenedioxymethamphetamine (also known as ecstasy) also can cause acute, severe hyponatremia
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can help to determine the cause of hyponatremia
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Assessment of the plasma osmolality, urine osmolality, and effective arterial blood volume (EABV) can help to determine the cause of hyponatremia
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Hyponatremia is most commonly a marker of
....(pseudohyponatremia) .... |
Hyponatremia is most commonly a marker of hypo-osmolality. Hyponatremia that occurs in the absence of a hypo-osmolar state (pseudohyponatremia) is generally caused by an increased serum concentration of an effective osmole or the addition of an isosmotic or near-isosmotic non–sodium-containing fluid to the extracellular space.
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Common causes of pseudohyponatremia
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Common causes of pseudohyponatremia include hyperglobulinemia and hypertriglyceridemia. Because these conditions are associated with a decrease of plasma water relative to plasma solids in the blood, the amount of sodium in a given volume of blood also decreases.
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True hyponatremia
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True hyponatremia may be associated with an elevation in the plasma concentration of an effective osmole. This elevation results in an increase in plasma osmolality (hyperosmolar hyponatremia), which causes water to leave the cells and results in a diluted serum sodium concentration. Hyponatremia caused by these circumstances occurs in patients with hyperglycemia or, rarely, after infusion of hypertonic mannitol.
In these settings, the serum sodium concentration quickly decreases by 1.6 meq/L (1.6 mmol/L) for every 100 mg/dL (5.5 mmol/L) increase in glucose or mannitol. The increased tonicity also stimulates thirst and antidiuretic hormone secretion, which contribute to further water retention. Finally, as the plasma osmolality normalizes, the serum sodium concentration decreases by 2.8 meq/L (2.8 mmol/L) for every 100 mg/dL (5.55 mmol/L) increase in glucose, resulting in a normal plasma osmolality but a low serum sodium concentration. |
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Isosmotic or near-isosmotic non–sodium-containing irrigating solutions
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Isosmotic or near-isosmotic non–sodium-containing irrigating solutions may enter the extracellular space during transurethral resection of the prostate or laparoscopic surgery. The systemic reabsorption of large amounts of these solutions, which usually contain glycine or sorbitol, can induce hyponatremia in the setting of a normal plasma osmolality.
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Urine Osmolality
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The presence of hyponatremia in a patient with normal kidney water excretion is suggestive of polydipsia, which is characterized by intake of water that exceeds the normal excreting capacity of the kidneys (20 to 30 L daily). These patients typically have a urine osmolality less than 100 mosm/kg H2O (100 mmol/kg H2O).
Hyponatremia that occurs in the absence of primary polydipsia is associated with decreased kidney water excretion and an inappropriately concentrated urine, which is characterized by a urine osmolality greater than 200 mosm/kg H2O (200 mmol/kg H2O). |
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Effective Arterial Blood Volume
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The EABV refers to the part of the extracellular fluid in the arterial system that perfuses the tissues and stimulates the volume receptors. Hyponatremia can be caused by a decrease in EABV, which results in baroreceptor stimulation of antidiuretic hormone secretion and increased proximal tubular reabsorption of sodium. Consequently, distal delivery of filtrate to the tip of the loop of Henle decreases.
Hyponatremia may be associated with low extracellular fluid volume (hypovolemic hyponatremia) or high extracellular fluid volume in edematous patients (hypervolemic hyponatremia). Hyponatremia associated with a normal EABV is known as isovolemic hyponatremia. |
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Syndrome of Inappropriate Antidiuretic Hormone Secretion and Cerebral Salt Wasting
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The syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt wasting (CSW) are two potential causes of hypo-osmolar hyponatremia that may develop several days after a neurosurgical procedure is performed. Manifestations of both SIADH and CSW include a decreased serum sodium concentration, low or low-normal plasma osmolality, and elevated urine osmolality. Because the treatment of SIADH and CSW differs, distinguishing between these conditions is imperative and is based largely on the EABV. SIADH is associated with antidiuretic hormone–mediated kidney water retention and is therefore characterized by euvolemia or a slightly volume-expanded state. Conversely, CSW is associated with kidney salt wasting, which leads to a decrease in intravascular volume.
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Syndrome of Inappropriate Antidiuretic Hormone Secretion and Cerebral Salt Wasting dd
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SIADH is more common than CSW. Patients with SIADH also usually have an extremely decreased serum uric acid concentration, because volume expansion in this condition causes decreased uric acid absorption in the proximal nephron. CSW, on the other hand, is suggested by the presence of hypotension and often affects patients with subarachnoid hemorrhage. Fluid restriction is the treatment of choice in patients with SIADH, whereas intravenous normal saline is indicated for CSW.
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Treatment of Hyponatremia
Acute and Slow Hyponatremia ECF normal Volume Status |
Fluid restriction
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tx of Hyponatremia
Acute rapid Hyponatremia ECF normal Volume Status |
Hypertonic saline + furosemide
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tx hyponatremia
Acute Slow Hyponatremia ECF Volume Status Low |
Normal saline
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tx hyponatremia
Acute rapid Hyponatremia ECF Volume Status Low |
Hypertonic saline
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tx hyponatremia
Acute slow Hyponatremia ECF Volume Status high |
fluid restr
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tx hyponatremia
Acute rapid Hyponatremia ECF Volume Status high |
Hypertonic saline + furosemide
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Chronic Hyponatremia
ECF Volume Status normal |
Remove cause
Discontinue drug Begin corticosteroid or thyroid hormone replacement Treat cause of SIADH |
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Chronic Hyponatremia
ECF Volume Status low |
Remove cause
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Chronic Hyponatremia
ECF Volume Status high |
Remove cause
Begin demeclocycline, 600-1200 mg/d Begin intravenous conivaptan, 20 mg over 30 minutes, then 20 mg over 24 hours for no more than 4 days |
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Hypernatremia
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Hypernatremia is defined as a serum sodium concentration greater than 145 meq/L (145 mmol/L). This relatively common condition always indicates hypertonicity and cell shrinkage and is an independent risk factor for mortality in the intensive care unit. Manifestations of hypernatremia include lethargy, weakness, fasciculations, seizures, and coma.
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Evaluation of a patient with hypernatremia should begin by assessing for a cause of
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Evaluation of a patient with hypernatremia should begin by assessing for a cause of inadequate water intake. Inadequate water intake usually occurs in patients in an altered state of consciousness or with impaired mental status who are unaware of thirst or unable to communicate the need for water, such as the elderly and critically ill. Infants and young children who have restricted access to water also may consume inadequate amounts of water, and a reduced sensation of thirst is a normal feature of increasing age. A specific lesion of the hypothalamus affecting the thirst center is a rare cause of hypernatremia.
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Polyuria i
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Polyuria in adults is characterized by a urine volume that exceeds 50 mL/kg body weight daily and is associated with frequent urination. Polyuria can be caused by osmotic diuresis, also known as solute diuresis, or water diuresis. A urine osmolality greater than 300 mosm/kg H2O (300 mmol/kg H2O) in a patient with polyuria is suggestive of osmotic diuresis. Polyuria associated with osmotic diuresis occurs in patients with poorly controlled diabetes mellitus; mannitol administration; and high-protein enteral feeding, which is specifically associated with urea diuresis.
Once osmotic diuresis is excluded, the cause of water diuresis must be assessed. Water diuresis may represent appropriate water loss, which occurs in primary polydipsia, or inappropriate water loss, which occurs in conditions such as central or nephrogenic diabetes insipidus. |
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Central and nephrogenic diabetes
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Central and nephrogenic diabetes insipidus are both characterized by severe, frequent nocturia as well as an absence of change in urine osmolality in response to water deprivation. Patients with central and nephrogenic diabetes insipidus also tend to have a mild negative water balance and a serum sodium concentration greater than 140 meq/L (140 mmol/L).
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Central diabetes insipidus
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Central diabetes insipidus also is characterized by an abrupt onset of symptoms, whereas symptoms in nephrogenic diabetes insipidus typically manifest gradually. In addition, patients with central diabetes insipidus often have a predilection for ice water.
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Central Diabetes Insipidus
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IdiopathicHead traumaPost neurosurgeryCranial neoplasmPituitary infiltrative diseases (histiocytosis, sarcoidosis)
Central nervous system infections Sheehan pituitary necrosis Brain death |
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Nephrogenic Diabetes Insipidus
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Electrolyte disturbances (hypokalemia, hypercalcemia)Vasopressinase production by placenta during pregnancy Drugs (lithium, foscarnet, amphotericin B, demeclocycline,Chronic tubulointerstitial diseases (Sjögren syndrome, amyloidosis, sickle cell nephropathy, multiple myeloma, sarcoidosis)
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Manage chronic kidney disease in a patient with hyperkalemia.
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Manage chronic kidney disease in a patient with hyperkalemia.
Key Point * Discontinuation of medications that interfere with the renin-angiotensin-aldosterone system, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and NSAIDs, is warranted to help correct hyperkalemia in the setting of renin-angiotensin inhibition. Discontinuation of ibuprofen and initiation of |
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Thiazide diuretics are largely ineffective in individuals with an
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Thiazide diuretics are largely ineffective in individuals with an estimated glomerular filtration rate below 30 mL/min/1.73 m2.
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Diagnose pentamidine-induced hyperkalemia.
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Diagnose pentamidine-induced hyperkalemia.
Key Point * Hyperkalemia due to impaired kidney potassium excretion commonly develops in patients treated with pentamidine, amiloride, triamterene, and trimethoprim. The most likely cause of this patient’s |
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Causes of hypokalemia associated with normal total body potassium content include
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Causes of hypokalemia associated with normal total body potassium content include a laboratory error or pseudohypokalemia, which may develop in patients with leukemia and elevated leukocyte counts. In this setting, leukocytes may extract potassium from the serum, which can lead to a decreased serum potassium concentration despite normal total body potassium content. In the absence of these circumstances, a low serum potassium concentration in the presence of normal total body potassium content and no evidence of gastrointestinal or kidney potassium losses suggests a shift of potassium from the extracellular to the intracellular space
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A urine potassium concentration of less than 20 meq/L (20 mmol/L) is suggestive of extrarenal losses, whereas a concentration higher than this value
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In the absence of a cellular shift, a low serum potassium concentration can be caused by losses via the gastrointestinal tract or skin, kidney potassium losses, or inadequate dietary intake of potassium. A urine potassium concentration of less than 20 meq/L (20 mmol/L) is suggestive of extrarenal losses, whereas a concentration higher than this value is suggestive of kidney losses.
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Causes of hyperkalemia
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Hyperkalemia occurs when abnormalities develop in the regulatory mechanisms that excrete excess potassium quickly or redistribute excess potassium into cells until it is excreted. For example, after consumption of a high-potassium meal, the kidneys alone cannot excrete potassium at a sufficiently rapid rate to prevent life-threatening hyperkalemia; in healthy persons, rapid shifting and storage of excess potassium into the cells are needed until the kidneys have successfully excreted the potassium load.
Causes of hyperkalemia include pseudohyperkalemia, excessive dietary intake of potassium, cellular redistribution, and decreased kidney excretion of potassium. |
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Pseudohyperkalemia
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Pseudohyperkalemia is an in vitro phenomenon caused by the mechanical release of potassium from cells during phlebotomy or specimen processing or in the setting of marked leukocytosis and thrombocytosis.
Next: Excessive Dietary Intake |
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Hypophosphatemia
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Hypophosphatemia is defined as a serum phosphate concentration less than 3 mg/dL (1 mmol/L). The glomerulus freely filters approximately 90% of plasma inorganic phosphate, and the proximal tubule reabsorbs nearly 80% of the filtered load. Phosphate crosses the apical membrane of the proximal tubular cell via the type IIa sodium-phosphate cotransporter. Low dietary phosphate intake and decreased parathyroid hormone levels increase cotransporter expression, whereas high dietary phosphate intake and elevated parathyroid hormone levels decrease cotransporter expression.
Hypophosphatemia is common in hospitalized patients, particularly those with sepsis and trauma. Severe symptomatic hypophosphatemia is relatively rare and most often develops in patients with chronic alcoholism. Hypophosphatemia may manifest as severe weakness, rhabdomyolysis, hemolysis, and a leftward shift of the oxygen dissociation curve. |
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Selected Causes of Hypophosphatemia
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Cellular Redistribution
Respiratory alkalosis Administration of glucose and insulin (refeeding) Correction of metabolic acidosis Intestinal Malabsorption Vitamin D deficiency Fat malabsorption Increased Kidney Excretion Hyperparathyroidism Fanconi syndrome Vitamin D–resistant rickets Osmotic diuresis Decreased Phosphate Intake |
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Hypophosphatemia tx
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Phosphate supplementation is indicated only for patients who are symptomatic or who have a condition resulting in chronic phosphate wasting. Oral phosphate therapy is the preferred treatment of hypophosphatemia. Intravenous phosphate can precipitate with calcium and produce various adverse effects, including hypocalcemia, acute kidney injury, and potentially arrhythmias. Intravenous phosphate replacement therapy therefore should be reserved for patients with a serum phosphate level below 1.5 mg/dL (0.5 mmol/L) and warrants close monitoring of serum phosphorus levels
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Hyperphosphatemia
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Hyperphosphatemia is defined as a serum phosphate concentration greater than 4.5 mg/dL (1.4 mmol/L). Acute hyperphosphatemia is typically caused by tissue breakdown, which occurs in rhabdomyolysis or tumor lysis syndrome.
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Diagnose hypophosphatemia in a patient with chronic alcoholism.
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Diagnose hypophosphatemia in a patient with chronic alcoholism.
Key Point * In the hospital setting, patients with chronic alcoholism may have normal serum phosphorus levels on admission to the hospital but often develop severe hypophosphatemia over the first 12 to 24 hours. Severe hypophosphatemia rarely manifests |
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The sudden development of hypophosphatemia may cause
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The sudden development of hypophosphatemia may cause confusion, rhabdomyolysis, hemolytic anemia, and severe muscle weakness that can lead to respiratory failure. Treatment involves preventing the serum phosphorus level from decreasing below 1 mg/dL (0.32 mmol/L). Oral phosphate is the preferred treatment in this setting, but intravenous administration may be needed if oral therapy cannot be tolerated.
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Hypercalcemia
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=may manifest as decreased neuromuscular excitability that causes decreased muscular tone. Hypercalcemia is most commonly caused by alterations in calcium absorption from the gut and bone resorption due to primary hyperparathyroidism, malignancy, and granulomatous diseases. Primary hyperparathyroidism and thiazide diuretic use also may cause this condition
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Hypokalemia
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Hypokalemia can cause diffuse muscle weakness, gastrointestinal tract atony, respiratory failure, and cardiac arrhythmias. In chronic hypokalemia, muscle weakness is unusual in patients with a serum potassium level above 2.5 meq/L (2.5 mmol/L) but may be precipitated by a sudden decrease in potassium. However, the risk of profound hypokalemia is low in a patient receiving potassium supplementation. Furthermore, hypokalemia would not explain this patient’s mental status changes.
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f hyponatremia
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Early signs of hyponatremia typically include nausea, vomiting, and headaches; progressive manifestations include impaired mental status and seizures. These symptoms are not compatible with this patient’s presentation.
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* Metabolic acidosis is characterized by a
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* Metabolic acidosis is characterized by a low serum pH, a decreased serum bicarbonate concentration, and a respiratory compensation resulting in a decreased arterial PCO2.
* |
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The presence of either a low albumin level or an unmeasured cationic light chain results
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The presence of either a low albumin level or an unmeasured cationic light chain results in a low anion gap.
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Metabolic acidosis of extrarenal origin is suggested by
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Metabolic acidosis of extrarenal origin is suggested by a large, negative urine anion gap, whereas metabolic acidosis of kidney origin is suggested by a positive urine anion gap.
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Treatment of proximal renal tubular acidosis may require
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Treatment of proximal renal tubular acidosis may require sodium bicarbonate, and the addition of a thiazide diuretic may be warranted.
* |
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Treatment of hypokalemic distal renal tubular acidosis includes
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Treatment of hypokalemic distal renal tubular acidosis includes correction of hypokalemia followed by administration of alkali therapy.
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The primary treatment of hyperkalemic distal renal tubular acidosis is to
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The primary treatment of hyperkalemic distal renal tubular acidosis is to correct the hyperkalemia.
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Accumulation of D-lactate produces an
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Accumulation of D-lactate produces an anion gap metabolic acidosis that is associated with normal serum lactate levels.
* |
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Ethylene glycol and methanol poisoning are characterized by a
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Ethylene glycol and methanol poisoning are characterized by a severe anion gap metabolic acidosis accompanied by an osmolal gap greater than 10 mosm/kg H2O (10 mmol/kg H2O).
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Fomepizole is the agent of choice
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* Fomepizole is the agent of choice to inhibit alcohol dehydrogenase and prevent formation of toxic metabolites in patients with ethylene glycol and methanol poisoning.
* |
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An unexplained anion gap metabolic acidosis in the presence of recent acetaminophen ingestion should raise suspicion for
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An unexplained anion gap metabolic acidosis in the presence of recent acetaminophen ingestion should raise suspicion for pyroglutamic acidosis.
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* Saline-responsive metabolic alkalosis is characterized by
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* Saline-responsive metabolic alkalosis is characterized by a low effective arterial blood volume and a urine chloride level less than 15 meq/L (15 mmol/L).
* |
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The preferred treatment of metabolic alkalosis in patients with volume expansion i
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The preferred treatment of metabolic alkalosis in patients with volume expansion is to remove the underlying cause of the persistent mineralocorticoid activity or block actions of mineralocorticoid at the level of the kidney.
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* Acute compensation for respiratory alkalosis is
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* Acute compensation for respiratory alkalosis is characterized by a 2 meq/L (2 mmol/L) decrease in serum bicarbonate for each 10 mm Hg decrease in the arterial PCO2.
* |
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Chronic compensation for respiratory alkalosi
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Chronic compensation for respiratory alkalosis is characterized by a 5 meq/L (5 mmol/L) decrease in serum bicarbonate for each 10 mm Hg decrease in arterial PCO2.
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* Respiratory alkalosis may cause lightheadedness and palpitations and symptoms that resemble those
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* Respiratory alkalosis may cause lightheadedness and palpitations and symptoms that resemble those of hypocalcemia, including paresthesias and carpopedal spasm.
* |
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Reassurance and rebreathing into a paper bag or other closed system are indicated for patients with
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Reassurance and rebreathing into a paper bag or other closed system are indicated for patients with respiratory alkalosis associated with the hyperventilation syndrome.
* |
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Primary respiratory acidosis is characterized by the presence of
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Primary respiratory acidosis is characterized by the presence of acidemia and hypercapnia.
* |
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Serum bicarbonate concentrations higher or lower than the expected compensation suggest the presence of
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Serum bicarbonate concentrations higher or lower than the expected compensation suggest the presence of a mixed respiratory and metabolic acid-base disorder.
* |
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Patients with acute respiratory acidosis are primarily at risk for
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Patients with acute respiratory acidosis are primarily at risk for hypoxemia rather than hypercapnia or acidemia.
* |
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Excessive oxygen may worsen hypoventilation in patients with
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Excessive oxygen may worsen hypoventilation in patients with chronic respiratory acidosis.
* |
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Correction of induced posthypercapnic metabolic alkalosis can usually be achieved with
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Correction of induced posthypercapnic metabolic alkalosis can usually be achieved with saline and discontinuation of loop diuretics if these agents are being used.
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An elevated osmolal gap suggests the presence of
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An elevated osmolal gap suggests the presence of an unmeasured osmole and is most commonly caused by ethanol. The osmolal gap is also elevated in the presence of ethylene glycol, methanol, and isopropyl alcohol. However, isopropyl alcohol does not cause an elevated anion gap metabolic acidosis (methanol and ethylene glycol poisoning) and is not associated with retinal abnormalities (methanol poisoning) or kidney failure (ethylene glycol poisoning).
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toluene
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This patient’s confusion and disorientation are consistent with ethylene glycol poisoning, diabetic ketoacidosis, and alcoholic ketoacidosis; however, these conditions would be associated with an anion gap metabolic acidosis. Toluene, an industrial solvent that can be abused as an inhalant, may cause confusion and disorientation in addition to metabolic acidosis, hypokalemia, hypophosphatemia, rhabdomyolysis, and elevated creatine kinase level. The absence of metabolic acidosis and hypokalemia makes toluene poisoning unlikely.
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Metabolic acidosis
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Metabolic acidosis Acute: PCO2 = (1.5) [HCO3] + 8
Chronic: PCO2 = [HCO3] + 15 Failure of the PCO2 to decrease to expected value = complicating respiratory acidosis; excessive decrease of the PCO2 = complicating respiratory alkalosis Quick check: PCO2 = value should approximate last two digits of pH |
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Metabolic alkalosis
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Metabolic alkalosis For each ↑ 1 meq/L in [HCO3], PCO2 ↑ 0.7 mm Hg
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Respiratory acidosis
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Acute: 1 meq/L ↑ [HCO3] for each 10 mm Hg ↑ in PCO2
Chronic: 3.5 meq/L ↑ [HCO3] for each 10 mm Hg ↑ in PCO2 Failure of the [HCO3] to increase to the expected value = complicating metabolic acidosis; excessive increase in [HCO3] = complicating metabolic alkalosis |
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Respiratory alkalosis
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Acute: ↓ 2 meq/L [HCO3] for each 10 mm Hg ↓ in PCO2
Chronic: 4-5 meq/L ↓ [HCO3] for each 10 mm Hg ↓ in PCO2 Failure of the [HCO3] to decrease to the expected value = complicating metabolic alkalosis; excessive decrease in [HCO3] = complicating metabolic acidosis |
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Proximal or type 2 RTA should be suspected in patients with a
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Proximal or type 2 RTA should be suspected in patients with a normal anion gap metabolic acidosis, a normal UAG, hypokalemia, and an intact ability to acidify the urine to a pH of less than 5.5 while in a steady state. In the steady state, the serum bicarbonate concentration is usually between 16 and 18 meq/L (16 and 18 mmol/L).
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Proximal RTA can be an isolated finding but most commonly is accompanied by generalized dysfunction of the proximal tubule, which manifests as
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Proximal RTA can be an isolated finding but most commonly is accompanied by generalized dysfunction of the proximal tubule, which manifests as glycosuria, phosphaturia, uricosuria, aminoaciduria, and tubular proteinuria and is known as Fanconi syndrome (Table 10 ). Proximal RTA is not associated with nephrolithiasis or nephrocalcinosis. However, osteomalacia can develop as a result of chronic hypophosphatemia and/or deficiency in the active form of vitamin D. Patients with proximal RTA may develop osteopenia due to acidosis-induced demineralization of bone.
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Causes of Hypokalemic Distal Renal Tubular Acidosis Primary
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Causes of Hypokalemic Distal Renal Tubular Acidosis Primary
Idiopathic Familial |
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Causes of Hypokalemic Distal Renal Tubular Acidosis
Secondary |
Causes of Hypokalemic Distal Renal Tubular Acidosis
Secondary Autoimmune disorders Hypergammaglobulinemia Sjögren syndrome Primary biliary cirrhosis Systemic lupus erythematosus Genetic disorders Ehlers-Danlos syndrome Marfan syndrome Hereditary elliptocytosis Drugs and toxins Amphotericin B Toluenea Disorders associated with nephrocalcinosis Hyperparathyroidism Hypervitaminosis D Idiopathic hypercalciuria Tubulointerstitial diseases Obstructive uropathy Kidney transplantation |
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Hyperkalemic distal RTA (type 4 RTA) should be suspected in patients with a
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Hyperkalemic distal RTA (type 4 RTA) should be suspected in patients with a normal anion gap metabolic acidosis associated with hyperkalemia and a slightly positive UAG (Table 12 ). Patients in whom this condition is caused by a defect in mineralocorticoid activity typically have a urine pH higher than 5.5.
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he primary goal of treatment in patients with hyperkalemic distal RTA is to
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he primary goal of treatment in patients with hyperkalemic distal RTA is to correct the hyperkalemia. A decrease in the serum potassium level often results in correction of the acidosis by restoring kidney ammonium production and therefore increasing the buffer supply for distal acidification. Alkali therapy with sodium bicarbonate may treat the acidosis and hyperkalemia in patients with hyperkalemic distal RTA.
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tx inhyperkalemic distal RTA
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Drugs known to interfere in the synthesis or activity of aldosterone should be discontinued. In patients who do not have hypertension or fluid overload, administration of a synthetic mineralocorticoid such as fludrocortisone is an effective treatment for aldosterone deficiency; in patients with hypertension, a thiazide diuretic would be an appropriate alternative treatment. In addition, loop diuretics are indicated in patients with an estimated GFR of less than 30 mL/min/1.73 m2; these agents increase distal sodium delivery, which stimulates potassium and hydrogen secretion in the collecting duct.
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Renal Tubular Acidosis of Kidney Insufficiency
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Renal Tubular Acidosis of Kidney Insufficiency
Patients with chronic kidney disease (CKD) initially develop a normal anion gap metabolic acidosis associated with normokalemia as the GFR decreases below 30 mL/min/1.73 m2. In patients with a GFR of less than 15 mL/min/1.73 m2, an anion gap metabolic acidosis usually develops and reflects a progressive inability to excrete phosphate, sulfate, and the sodium salts of various organic acids. Initiation of sodium bicarbonate once the serum sodium level decreases to less than 22 meq/L (22 mmol/L) achieves correction of the metabolic acidosis in patients with CKD. |
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Ileal Conduits
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Ileal Conduits
Surgical diversion of the ureter into the intestine may lead to the development of a normal anion gap metabolic acidosis due to systemic reabsorption of ammonium and chloride from the urinary fluid and exchange of chloride for bicarbonate through activation of the chloride-bicarbonate exchanger on the intestinal lumen. The likelihood of developing metabolic acidosis associated with ileal conduits increases with the amount of time the urine is in contact with the bowel and the total surface area of bowel that is exposed to urine. |
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Pyroglutamic Acidosis
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Pyroglutamic Acidosis
Pyroglutamic acidosis occurs in critically ill patients who receive therapeutic doses of acetaminophen; in this setting, acetaminophen metabolism and oxidative stress associated with critical illness lead to a decrease in glutathione levels, which causes pyroglutamic acid to accumulate. Pyroglutamic acidosis manifests as an anion gap metabolic acidosis accompanied by mental status changes ranging from confusion to coma. An unexplained anion gap metabolic acidosis in the presence of recent acetaminophen ingestion should raise suspicion for this condition. |
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Aspirin poisoning
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Aspirin poisoning leads to increased lactic acid production. The accumulation of lactic acid, salicylic acid, ketoacids, and other organic acids results in an anion gap metabolic acidosis. Salicylates also have a concomitant direct stimulatory effect on the respiratory center. Increased ventilation lowers the arterial PCO2, which contributes to the development of a respiratory alkalosis.
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Salicylate poisoning manifests as
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Salicylate poisoning manifests as either a respiratory alkalosis or an anion gap metabolic acidosis in adults, whereas affected children usually only have an anion gap metabolic acidosis. Clinical manifestations of salicylate poisoning in adults may include tinnitus, tachypnea, tachycardia, excessive sweating, and nausea and vomiting. Patients with severe toxicity may develop hyperthermia, pulmonary edema, hematemesis, and mental status changes.
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In addition to supportive therapy, initial management of salicylate
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In addition to supportive therapy, initial management of salicylate poisoning includes correcting the systemic acidemia and increasing the urine pH. Increasing the systemic pH leads to an increase in the ionized fraction of salicylic acid, which results in decreased accumulation of the drug in the central nervous system. An alkaline urine pH also favors increased urine excretion of the salicylate. Hemodialysis is warranted in patients with serum salicylate concentrations above 80 mg/dL (5.8 mmol/L) or in the setting of severe clinical toxicit
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Metabolic alkalosis develops when
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Metabolic alkalosis develops when a decrease in acid or increase in alkali results in the addition of new bicarbonate, which may be generated by kidney or extrarenal mechanisms, to the blood. To maintain a metabolic alkalosis, the capacity of the kidney to correct the alkalosis must be impaired or the capacity to reabsorb bicarbonate must be enhanced, and at least one of the following features is usually required: decreased effective arterial blood volume (EABV), hypokalemia, or hypochloremia (Figure 9 ). Treatment is focused on correction of the mechanism responsible for metabolic alkalosis.
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Metabolic alkalosis is generally benign. However, alkalemia can lead to
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Metabolic alkalosis is generally benign. However, alkalemia can lead to respiratory depression and decreased delivery of oxygen to the tissues and a high blood pH can cause decreased tissue perfusion. Therefore, aggressive correction of the alkalosis is particularly important in critically ill patients, in whom perfusion of the heart and brain is essential
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Classification of Metabolic Alkalosis
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Low EABV Low EABV High EABV
Urine Chloride (meq/L) <15 >15 >15 Response to Saline Saline responsive Saline resistant Saline resistant |
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Assessment of the EABV can help to determine whether a metabolic alkalosis is saline resistant
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Assessment of the EABV can help to determine whether a metabolic alkalosis is saline resistant (Table 14 ). If the EABV can be restored with saline, the metabolic alkalosis can be easily corrected; however, numerous types of metabolic alkalosis respond poorly to saline. Saline-resistant metabolic alkalosis is generally maintained by a combination of increased mineralocorticoid levels, increased distal sodium delivery, and hypokalemia.
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Saline-Responsive Metabolic Alkalosis Associated with a Decreased Effective Arterial Blood Volume
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* Gastrointestinal Acid Loss
* Diuretic Use |
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Diuretic Use
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Diuretic Use
Thiazide and loop diuretics commonly cause a metabolic alkalosis that is generated in the distal nephron by the combination of high aldosterone levels and enhanced distal delivery of sodium. If diuretics are stopped and the patient remains on a low-sodium diet, the alkalosis will be maintained because the patients are usually volume contracted and hypokalemic. Saline infusion is indicated to correct this condition. |
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Treatment of Saline-Resistant Metabolic Alkalosis
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Decreased EABV
Thiazide and loop diuretics-- tx Discontinue causative drug; replete EABV Magnesium deficiency tx Replete magnesium deficit Gitelman syndrome tx Amiloride, triamterene, or spironolactone; potassium supplements and magnesium supplements Bartter syndrome tx Amiloride, triamterene, or spironolactone; potassium supplements; magnesium supplements if needed I ncreased EABV Renin-secreting tumor txRemove tumor Primary hyperaldosteronism tx Remove tumor; spironolactone for BAH Glucocorticoid-remediable aldosteronism tx Dexamethasone Liddle syndrome tx Amiloride or triamterene |
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Respiratory Alkalosis
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Primary respiratory alkalosis is characterized by an arterial PCO2 of less than 35 mm Hg. Liver failure is a common cause of primary respiratory alkalosis. Salicylate poisoning and elevated progesterone levels associated with pregnancy also may cause this condition. In hospitalized patients, respiratory alkalosis is the presenting manifestation of gram-negative sepsis.
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Primary respiratory alkalosis must be differentiated from secondary respiratory alkalosis, which is a compensatory mechanism in the setting of primary metabolic acidosis
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Acute respiratory alkalosis is characterized by an acute decrease in the arterial PCO2, which results in a bicarbonate-chloride shift in the erythrocytes and a decrease in the serum bicarbonate concentration by 2 meq/L (2 mmol/L) for every 10 mm Hg decrease in the arterial PCO2.
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Primary respiratory alkalosis must be differentiated from secondary respiratory alkalosis, which is a compensatory mechanism in the setting of primary metabolic acidosi
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Chronic respiratory alkalosis is characterized by a 2- to 3-day process during which a transient bicarbonate diuresis occurs. At steady state, the serum bicarbonate concentration decreases by 4 to 5 meq/L (4 to 5 mmol/L) for each 10 mm Hg decrease in the arterial PCO2.
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In order to maintain a normal extracellular fluid volume in the setting of increased urinary loss of sodium bicarbonate, the kidney retainsPatients with chronic respiratory alkalosis therefore typically have
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In order to maintain a normal extracellular fluid volume in the setting of increased urinary loss of sodium bicarbonate, the kidney retains sodium chloride. Patients with chronic respiratory alkalosis therefore typically have hyperchloremia. These patients also have a 3- to 5-meq/L (3- to 5-mmol/L) increase in the serum anion gap because of the greater fixed negative charge on serum albumin as well as an increased serum lactate concentration; this increase in lactate production is caused by the stimulatory effect of high serum pH on phosphofructokinase, which regulates the rate of glycolysis.
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Clinical ManifestationsBoth primary and secondary respiratory alkalosis
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Both primary and secondary respiratory alkalosis often initially manifest as tachypnea. Acute hypocapnia decreases cerebral blood flow and causes binding of free calcium to albumin in the blood. Mild respiratory alkalosis may cause lightheadedness and palpitations. More profound respiratory alkalosis may cause symptoms that resemble those of hypocalcemia, including paresthesias of the extremities and circumoral area and carpopedal spasm. Patients with ischemic heart disease may occasionally develop cardiac arrhythmias, ischemic electrocardiographic changes, and angina pectoris.
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Primary respiratory alkalosis is treated by
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Primary respiratory alkalosis is treated by correcting the underlying cause. Reassurance is indicated for patients with respiratory alkalosis associated with the hyperventilation syndrome. In addition, rebreathing into a paper bag or other closed system causes the arterial PCO2 to increase, resulting in partial correction of hypocapnia and symptomatic improvement.
Respiratory alkalosis frequently develops as a complication of the hypoxia that occurs at high altitudes. Administration of oxygen or a return to lower altitudes can reverse the respiratory alkalosis that develops in this setting. |
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Respiratory Acidosis
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Primary respiratory acidosis is characterized by the presence of acidemia and hypercapnia. The development of respiratory acidosis is usually multifactorial. Major causes of carbon dioxide retention include disease or a disorder of a component of the respiratory system, including the central and peripheral nervous systems, respiratory muscles, thoracic cage, pleural space, airways, and lung parenchyma.
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Acute respiratory acidosis is associated with
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Acute respiratory acidosis is associated with an increase in the plasma bicarbonate concentration by 1 meq/L (1 mmol/L) for every 10 mm Hg elevation in the arterial PCO2. After 24 to 48 hours, proximal tubular cells increase hydrogen secretion, which results in accelerated bicarbonate reabsorption and increased kidney excretion of sodium chloride. Chronic respiratory acidosis is characterized by a 3.5 meq/L (3.5 mmol/L) increase in bicarbonate for each 10 mm Hg elevation in the arterial PCO2. Serum bicarbonate concentrations higher or lower than these values suggest the presence of a mixed respiratory and metabolic acid-base disorder.
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Primary respiratory acidosis develops as a result of
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Primary respiratory acidosis develops as a result of ineffective alveolar ventilation and is suggested by a PCO2 higher than 45 mm Hg. However, a PCO2 less than this value may indicate respiratory acidosis in a patient with primary metabolic acidosis that is not adequately compensated by alveolar ventilation. This condition must be differentiated from primary respiratory acidosis. The differential diagnosis of acute and chronic respiratory acidosis includes various conditions of the respiratory system
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Differential Diagnosis of Respiratory Acidosis
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nhibition of the medullary respiratory center
Disorders of the chest wall and the respiratory muscles Airway obstruction Disorders affecting gas exchange across the pulmonary capillaries Increased carbon dioxide production Mechanical ventilation |
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Respiratory Acidosis clin
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Carbon dioxide diffuses and equilibrates across the blood-brain barrier much more rapidly than bicarbonate, which results in a more rapid decrease in cerebrospinal fluid and cerebral interstitial pH. Therefore, acute respiratory acidosis is typically significantly more symptomatic than acute metabolic acidosis.
Respiratory acidosis may manifest as hypercapnic encephalopathy, a clinical syndrome with initial symptoms that include irritability, headache, mental cloudiness, apathy, confusion, anxiety, and restlessness that can progress to asterixis, transient psychosis, delirium, somnolence, and coma. Severe hypercapnia may cause decreased myocardial contractility, arrhythmias, and peripheral vasodilatation, particularly when the serum pH decreases below 7.1. |
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Acute respiratory acidosis is associated
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Acute respiratory acidosis is associated with an increase in the plasma bicarbonate concentration by 1 meq/L (1 mmol/L) for every 10 mm Hg elevation in the arterial PCO2. After 24 to 48 hours, proximal tubular cells increase hydrogen secretion, which results in accelerated bicarbonate reabsorption and increased kidney excretion of sodium chloride. Chronic respiratory acidosis is characterized by a 3.5 meq/L (3.5 mmol/L) increase in bicarbonate for each 10 mm Hg elevation in the arterial PCO2. Serum bicarbonate concentrations higher or lower than these values suggest the presence of a mixed respiratory and metabolic acid-base disorder.
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Primary respiratory acidosis develop
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Primary respiratory acidosis develops as a result of ineffective alveolar ventilation and is suggested by a PCO2 higher than 45 mm Hg. However, a PCO2 less than this value may indicate respiratory acidosis in a patient with primary metabolic acidosis that is not adequately compensated by alveolar ventilation. This condition must be differentiated from primary respiratory acidosis. The differential diagnosis of acute and chronic respiratory acidosis includes various conditions of the respiratory system
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tx Patients with acute respiratory acidosi
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Patients with acute respiratory acidosis are primarily at risk for hypoxemia rather than hypercapnia or acidemia. Therefore, initial therapy should focus on establishing and securing a patent airway in order to provide adequate oxygenation.
Excessive oxygen may worsen hypoventilation in patients with chronic respiratory acidosis and should be avoided in this population. When mechanical ventilation is required, the arterial PCO2 should be decreased slowly and with caution to minimize the risk of inducing posthypercapnic metabolic alkalosis due to the high serum bicarbonate concentration. In order to normalize the acid-base status, the kidneys must excrete this bicarbonate. However, this excretion will not occur when the EABV is reduced either because of sodium depletion secondary to restricted salt intake or diuretic therapy or because of a sodium-retentive state, such as heart failure or cirrhosis. Correction of the superimposed metabolic alkalosis can usually be achieved with saline and discontinuation of loop diuretics if these agents are being used. However, patients with edema and with heart failure may require acetazolamide to correct the alkalosis. |
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contrast-induced nephropathy.
Key Point * Before radiocontrast is used, the cardiac output and kidney perfusion should be optimized when possible to decrease the risk of contrast-induced nephropathy. |
Contrast-induced nephropathy is characterized by an increase in the serum creatinine level 24 to 48 hours after contrast administration. Risk factors for this condition include age greater than 75 years, heart failure, hypertension, diabetes mellitus, and chronic kidney disease.
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administr diuretics before contrast
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Diuretics are associated with an increased risk of acute kidney injury and should be withheld before contrast administration in patients with normal or near-normal volume status. However, withholding diuretics would not be appropriate for a patient with heart failure. When cardiac catheterization can be safely delayed, use of diuretics to correct significant hypervolemia before contrast administration helps to optimize cardiac output and thus kidney perfusion and decreases the risk of contrast-induced nephropathy. Serum electrolyte levels, kidney function, and volume status also should be closely monitored to avoid overdiuresis.
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contrast administration/.NSAIDs and metformin
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Discontinuation of NSAIDs and metformin also is indicated in patients undergoing procedures that involve contrast administration. These agents can be reinitiated once kidney function has been shown to be stable for several days after contrast exposure.
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contrast administration/fenoldopam
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fenoldopam does not reduce the risk of contrast-associated acute kidney injury. Therefore, this agent is not recommended to prevent contrast-induced nephropathy.
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angiotensin-converting enzyme inhibitors/ contrast administration
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Before contrast administration, angiotensin-converting enzyme inhibitors should be discontinued in most patients with acute kidney injury but can be continued in those with stable kidney function
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Isotonic bicarbonate or saline/ contrast administration
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Isotonic bicarbonate or saline administered both before and after contrast administration helps to prevent contrast-induced nephropathy but would not be initially appropriate in this patient with heart failure. Isotonic saline may have equal efficacy to isotonic bicarbonate in the prevention of contrast-induced nephropathy.
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* Acute kidney injury is a common condition characterized by an
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* Acute kidney injury is a common condition characterized by an abrupt decline in kidney function that occurs over hours to days.
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* Risk factors for acute kidney injury include
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* Risk factors for acute kidney injury include preexisting chronic kidney disease, diabetic nephropathy, heart failure, liver disease, hypovolemia, and age over 50 years.
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* Evaluation of patients with suspected acute kidney injury should include
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* Evaluation of patients with suspected acute kidney injury should include a history of nephrotoxic exposures.
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* Kidney ultrasonography is indicated for all patients with
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* Kidney ultrasonography is indicated for all patients with acute kidney injury, and kidney biopsy should be considered when the diagnosis remains unclear after excluding prerenal and postrenal disease.
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prerenal azotemia
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Physical examination findings consistent with extracellular fluid volume depletion are absent in up to 50% of patients with prerenal azotemia, and this condition may develop in patients with normal or increased extracellular fluid volume.
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Acute tubular necrosis
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Acute tubular necrosis usually occurs after a sustained period of ischemia or exposure to nephrotoxic agents and is most commonly associated with muddy brown casts on urinalysis and a fractional excretion of sodium above 2%.
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Contrast-induced nephropathy
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Contrast-induced nephropathy is characterized by an increase in the serum creatinine level 24 to 48 hours after contrast administration and is usually associated with recovery of normal kidney function in 1 to 2 weeks.
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The most effective intervention to decrease the incidence and severity of contrast-induced nephropathy is
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The most effective intervention to decrease the incidence and severity of contrast-induced nephropathy is volume expansion with either isotonic saline or sodium bicarbonate.
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Rhabdomyolysis
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Rhabdomyolysis most commonly develops after exposure to myotoxic drugs, infection, excessive exertion, or prolonged immobilization.
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most effective intervention to limit nephrotoxicity in patients with rhabdomyolysis.
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* Expansion of the extracellular fluid volume with isotonic saline is the most effective intervention to limit nephrotoxicity in patients with rhabdomyolysis.
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Urinalysis findings in patients with acute interstitial nephritis may include
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Urinalysis findings in patients with acute interstitial nephritis may include leukocyte casts, eosinophils, and a protein-creatinine ratio below 2.5 mg/mg.
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Acute kidney injury in patients with scleroderma renal crisis often improves afte
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Acute kidney injury in patients with scleroderma renal crisis often improves after angiotensin-converting enzyme inhibitor therapy.
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Urinary tract obstruction should be strongly suspected in patients with acute kidney injury
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Urinary tract obstruction should be strongly suspected in patients with acute kidney injury who have known obstructive prostatic disease or pelvic malignancy and may manifest as significantly decreased urine output or polyuria.
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Kidney ultrasonography in most patients with urinary tract obstruction reveals
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Kidney ultrasonography in most patients with urinary tract obstruction reveals hydronephrosis.
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Patients with acute kidney injury caused by urinary tract obstruction have a favorable prognosis when obstruction is relieved within
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Patients with acute kidney injury caused by urinary tract obstruction have a favorable prognosis when obstruction is relieved within 1 week of onset.
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Diagnosis of abdominal compartment syndrome is established in patients who have
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Diagnosis of abdominal compartment syndrome is established in patients who have an intravesicular pressure greater than 20 mm Hg as measured through a bladder catheter who also have new-onset organ system failure.
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Surgical decompression of the abdomen is usually required in patients with
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Surgical decompression of the abdomen is usually required in patients with abdominal compartment syndrome and often promptly improves kidney function.
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Cardiorenal syndrome refers to kidney dysfunction that develops in the setting of acute
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Cardiorenal syndrome refers to kidney dysfunction that develops in the setting of acute decompensated heart failure.
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Cholesterol crystal embolization
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Cholesterol crystal embolization may cause acute kidney injury in patients with aortic atherosclerotic plaques and most often develops after angiography or aortic surgery.
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Patients with cholesterol crystal embolization may have
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Patients with cholesterol crystal embolization may have cutaneous manifestations, abdominal pain, gastrointestinal bleeding, pancreatitis, and retinal artery emboli.
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what management indicated for individuals with cholesterol crystal embolization.
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Management of risk factors such as dyslipidemia and hypertension as well as smoking cessation and glycemic control in patients with diabetes are indicated for individuals with cholesterol crystal embolization.
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Hepatorenal syndrome
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Hepatorenal syndrome manifests as azotemia caused by significantly impaired kidney perfusion in patients with worsening liver dysfunction.
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what is recommended for patients with spontaneous bacterial peritonitis to decrease the risk of hepatorenal syndrome.
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Albumin infusions are recommended for patients with spontaneous bacterial peritonitis to decrease the risk of hepatorenal syndrome.
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what to order in P with suspected hepato renal sundrome to assess whether there is a component of prerenal azotemia.
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In patients with suspected hepatorenal syndrome, volume expansion with albumin should be performed to assess whether there is a component of prerenal azotemia.
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what adjunctive therapy for patients with hepatorenal syndrome until liver transplantation can be performed in eligible patients.
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Vasopressors can be used as adjunctive therapy for patients with hepatorenal syndrome until liver transplantation can be performed in eligible patients.
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Tumor lysis syndrome
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Tumor lysis syndrome usually develops after initiation of chemotherapy and occasionally occurs spontaneously in patients with a high tumor burden.
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Allopurinol or off-label usage of rasburicase
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Allopurinol or off-label usage of rasburicase may help to prevent tumor lysis syndrome in at-risk patients.
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the most appropriate management of tumor lysis syndrome
what s indicated in patients who are oliguric or have life-threatening hyperkalemia. |
Hydration with isotonic saline is the most appropriate management of tumor lysis syndrome, and early intervention with dialysis is indicated in patients who are oliguric or have life-threatening hyperkalemia.
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what s an important clue to the diagnosis of myeloma cast nephropathy.
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* In patients with a negative dipstick urinalysis for protein, sulfosalicylic acid testing of the urine may detect light chains and is an important clue to the diagnosis of myeloma cast nephropathy.
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what should be used with caution in patients with myeloma and kidney dysfunction.
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Bisphosphonates should be used with caution in patients with myeloma and kidney dysfunction.
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Patients with HIV infection have an increased risk of acute kidney injury most often caused by
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Patients with HIV infection have an increased risk of acute kidney injury most often caused by certain opportunistic infections.
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Highly active antiretroviral therapy mayslow the progression of HIV-associated nephropathy and usually does not
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slHighly active antiretroviral therapy may slow the progression of HIV-associated nephropathy and usually does not cause acute kidney injury.
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Sodium phosphate–containing bowel preparation solutions may
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Sodium phosphate–containing bowel preparation solutions may cause acute kidney injury and should be avoided, particularly because of the availability of safer alternatives such as polyethylene glycol electrolyte solution.
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