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47 Cards in this Set

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Acute kidney injury classification

1) oliguric (<400cc/24 hrs)


worse prognosis


can give them fluid challenge to convert from oliguric --> non-oliguric




2) non-oliguric (>400cc/24 hrs)

Prerenal vs intrarenal

BUN/creatinine ratio




pre-renal: >20


urine Na will be very low




intra-renal: 10


urine Na can be high (indicates tubular injury)

Glomerulonephritis

has RBCs in urine




can be described as dysmorphic RBCs or erythrocyte casts




order following Abs:


dsDNA, ANA, antistreptolysin O, HIV serology, complement level, cryoglobulins, p-ANCA (microscopic PAN), c-ANCA (Wegener's), anti-GBM

Chronic kidney issues on u/s

will find small kidneys




normal size kidneys on u/s indicate an acute process

Reasons for dialysis

refractory hyperkalemia




profound metabolic acidosis




AMS




refractory fluid overload




uremic pericarditis (BUN consistently >100)

Acute tubular necrosis

minimal proteinuria with muddy brown casts




can be due to drugs (eg NSAIDs)




cannot hold onto Na so urine Na will be high

Acute interstitial nephritis

allergic reaction




eosinophilia, eosinophiluria w/ or w/o rash




may or may not have eosinophils but must have WBC casts in urine




hx of prior catheterization p/w AKI --> chol emboli & look for violaceous reticular rash or livedo reticularis




should do urine cx to r/o pyelo bc of WBC in urine

Enlarged kidneys on u/s

obstructive uropathy




diabetes




amyloidosis




HIV nephropathy




polycystic kidney disease

Hyperphosphatemia and hypocalcemia

can be seen in pts with CKD




tx hyperphosphatemia with calcium acetate, calcium carbonate, or sevelamer




hypocalcemia bc of vitamin D def (low 1,25 Vit D)

Lowering K+

sodium polystyrene sulfonate (Kexellate) also lowers K+




insulin (with glucose or HCO) will transport K+ intracellular thereby reducing serum K+ --> most rapid way of lowering K+




very high K+ with EKG changes --> CaCl or Ca gluconate IV with insulin

Essential HTN

need 3 independent visits with BP >140/90 or 1 reading of >160/100




single high reading does not warrant medication




6 months of diet, exercise, reduced etoh then if no improvement --> medication (diuretic first then add ACEI, ARB, or CCB)

BP goals

<140/90




if >160/100 --> start with 2 meds (diuretic + ACEI)




if >140/90 and diabetes --> start with 2 meds

b-blocker side effects

depression


memory loss


impotence


fatigue


may mask Sxs of hypoglycemia in diabetics


Raynaud phenomenon & can worsen PVD

ACE inhibitors

first choice for:


DM


CHF


previous MI


chronic renal failure with proteinuria


use in any pt with nephrotic syndrome




contraindicated in:


hyperkalemia


pregnancy


b/l renal artery stenosis

Hypertensive urgency vs emergency

urgency:


>180/120 with NO end organ damage (aSx)




cont home meds if not on meds, observe, reduce with ACEI in office, then d/c with 2 meds




emergency:


>180/120 with end organ damage (eg SOB, chest pain, encephalopathy, retinopathy, AKI)




admit, IV b-blocker, CCB, diuretics, or nitroglycerin

Left ventricular hypertrophy on EKG

S wave in V1 & R wave in V5 >35mm

W/u of suspected renal artery stenosis

duplex u/s of renal artery




Magnetic resonance angiography




renal artery arteriography (gold standard)

Tx of renal artery stenosis

balloon angioplasty




repeat angioplasty if first fails




surgical repair if angioplasty not possible or effective




tx with ACEI if angioplasty doesnt work & surgery is not an option ONLY in unilateral renal artery stenosis

Causes of renal artery stenosis

fibromuscular dysplasia


young woman <30




atherosclerotic dz


older male

Serum osmolality vs urine osmolality

major osmoles in serum are glucose and Na




increase in urine osmolality in euvolemic & hyponatremic pt --> too much ADH




ADH --> increases urine osmolality




if no reason for high ADH (dehydration, bleed, liver failure, etc) --> high urine osmolality (>100) indicates SIADH

Causes of hyponatremia

hypovolemic:


addison dz


GI losses


burns


diuretic use with free water intake




euvolemic:


SIADH


psychogenic polydipsia


hypothyroid




hypervolemic:


CHF


nephrotic syndrome


cirrhosis

Causes of SIADH

pulmonary


small cell carcinoma




CNS




neoplasm




medications


SSRI

Tx of SIADH

mild (Na >120):


restrict water




severe (Na <120):


give saline and diuretic




emergent level (Na <110) or severe sxs (coma or seizures):


hypertonic saline




if Na rises too fast --> central pontine myelinolysis




if Na is lowered rapidly --> cerebral edema

Kidney stone

tx with hydration until it passes




if >5cm or hydration doesnt work, need to remove with intervention bc cant pass it (eg shock wave lithotripsy)




renal u/s is almost 100% sensitive for stones in kidney (but not if in ureter) but best imaging test is abd CT




after stone passes, need to fig out why stone formed




most common is Ca stones and less common uric acid --> serum Ca and uric acid + 24hr urine Ca, oxalate, citrate, uric acid, Mg, Phos

Kidney stone composition

Ca oxalate - 70%


Ca phosphate - 10%


Struvite - 10-15% (occurs in setting of repeated UTI with Proteus)


Uric acid - 5-10%


Cysteine - 1%




recurrences in 50-80%




alkaline urine predisposes to calcium stones




acidic urine predisposes to uric acid stones

Chronic metabolic alkalosis

weakness


fatigue


muscle cramps


diminished reflexes


hypokalemia




anyone with metabolic alkalosis will have high aldosterone

Mg, K, Ca

all go together and hypomagnesaemia leads to hypokalemia and hypocalcemia




should correct hypomagnesaemia first bc it acts as co-factor for other 2

Aldosterone

decreases K and H+ in blood




Conn syndrome --> tumor secretes aldo




Bartter syndrome --> inability of loop of Henle to reabsorb KCl leading to secondary hyperaldo

Metabolic alkalosis and urine Cl

urine Cl <20 --> GI loss, prior diuretic, adenoma




urine Cl >20 --> check BP


normal BP --> Bartter or Gitelman syndrome, hypokalemia, hypomag, active diuretic use


high BP --> check plasma renin and aldo level

Periorbital edema

indicates either nephrotic syndrome or cirrhosis

Oval fat bodies in urine

means pt has nephrotic syndrome

Nephrotic syndrome

edema


proteinuria (>3.5g/24 hr)


hypoalbuminemia


hyperlipidemia


lipiduria




most common cause in adults is FSGS




most common cause of nephrotic range proteinuria is DM




also assoc with SLE, HIV, and amyloid





Nephrotic syndrome w/u

albumin


BUN/creatine


lipid profile


protein:creatine ratio


UA


HgA1c




if all c/w nephrotic syndrome --> renal bx with EM

DDx for nephrotic syndrome

1) minimal change dz


assoc with Hodgkins




2) membranous nephropathy


assoc with breast cancer & B-cell lymphomas


have increased thrombotic risk




3) FSGS


assoc with HIV & African Americans




4) membranoproliferative


assoc with Hep C

Tx of nephrotic syndrome

low risk - ACEI




high risk - immunosuppressors w/ or w/o steroids




dialysis and/or transplant maybe indicated with advanced dz




DO NOT GIVE STEROIDS ALONE

Painless hematuria w/u

thinking nephritic syndrome




UA


BUN/creatine


HIV testing


serology for C3, C4, ANA, ANCA, anti-GBM


urine protein/creatine ratio


cholesterol




renal u/s and/or CT scan

DDx of glomerulonephritis

IgA nephropathy


post-infectious GN


rapidly progressive GN




systemic dz that can cause:


goodpasture


wegener's


SLE




dx via a renal bx

Frothy urine

implies proteinuria

Renal Tubular Acidosis Type 1 (distal)

inability to excrete acid at distal tubule resulting in alkaline urine




urinary loss of K+ due to failure of H/K ATPase




results in hypokalemia, hyperchloremic metabolic acidosis




assoc with autoimmune dz (eg SLE, Siogren)




can cause kidney stones (Ca stones) bc of alkaline urine




tx with HCO-

Renal Tubular Acidosis Type 2 (proximal)

inability to reabsorb HCO- in prox tubule




body loses HCO- in urine until supply is so depleted that distal tubule can absorb the rest




initially urine pH is basic then becomes acidic




normally p/w hypokalemia and serum HCO- 18-20




common cause is MM




tx with high dose HCO- and thiazide diuretics and K+

Renal Tubular Acidosis Type 4 (distal)

hypoaldosterone like state results in decreased K+ excretion




results in normal anion gap metabolic acidosis with hyperkalemia (only RTA that has hyperkalemia)




affects distal tubule




tx with fludrocortisone

DDx for normal anion gap metabolic acidosis

RTAs


diarrhea


acetazolamide (carbonic anhydrase inhibitors)

Diarrhea vs distal RTA

calculate urinary anion gap:




urine Na + urine K - urine Cl




diarrhea is negative




RTA is positive or 0

DDx for AMS with no focal neurologic findings

drugs


infections


metabolic

AMS initial w/u

dextrose/thiamine/naloxone




CBC


BMP


UA


CXR


ABG


EKG


blood etoh level

Ethylene glycol vs methanol AGMA

ethylene glycol: forms oxalate crystals in urine


ataxia, confusion, hallucinations, coma




methanol: causes blindness




tx both w/fomepizole OR ethyl alcohol

UV fluorescence and ethylene glycol

if u take pt urine & shine UV light, will see green fluorescent substance