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103 Cards in this Set

  • Front
  • Back
prerenal azotemia etiology
acute renal failure due to
hypovolemia (dehydration, burns, diuretic, vomitting, diarrhea, sweating, hemorrhage)
hypotension (shock, anaphylaxis)
third-spacing of fluids (peritonitis)
osmotic diuresis
low aldosterone (Addison)
low cardiac output (CHF)
low albumin (nephrotic syndrome)
renal artery stenosis
hepatorenal syndrome (hepatic failure, vasoconstriction of afferent)
ACEi-induced (in susceptible patients, vasodilation of efferent)
prerenal azotemia diagnosis
BUN/creatinine ratio 20:1
low urine sodium (<20)
high urine osmolality (>500)
low fractional Na (<1%)
specific gravity >1.010 (RAA system retains water and concentrates urine)
postrenal azotemia etiology
renal failure due to bilateral obstruction to urine flow
bladder stone or clot
bladder cancer
prostate hypertrophy or cancer
bilateral ureteral disease (retroperitoneal fibrosis)
neurogenic bladder
postrenal azotemia pathogenesis
bilateral obstruction to urine outflow leads to postrenal azotemia
if obstruction takes a long time it can lead to tubular necrosis
postrenal azotemia diagnosis
BUN/creatinine ratio can go as high as 20:1 but then starts to decrease
there's also concentrated urine and low fractional Na
need to find distended bladder on physical
OR bilateral hydronephrosis on renal sonogram or CT
OR large volume of urine after Foley catheter
acute tubular necrosis etiology
any cause of hypoperfusion or hypodrainage (pre or postrenal azotemia) can lead to tubular necrosis if prolonged;
acute tubular necrosis phases
prodromal (between injury and acute renal failure)
oliguric or anuric
post oliguric (polyuria due to tubular death and lack of urine concentration function)
acute tubular necrosis diagnosis
BUN/creatinine ration close to 10:1
low urine osmolarity (<350)
high urine sodium (>40)
high fractional Na (>1%)
brown pigmented granular casts and epithelial casts
acute tubular necrosis management
no effective medical therapy, just hydration and if life-threatening, dyalisis
dopamine or diuretics cannot reverse it
allergic interstitial nephritis etiology
accounts for 10-15% of intrinsic renal failure
due to drug allergy in 70%
penicillins, cephalosporins, sulfas, NSAIDs, allopurinol, rifampin, quinolones, CCBs, PPIs
also caused by leptospira, legionella, CMV, ricketsia and strep
allergic interstitial nephritis presentation
fever (90%)
rash (25-50%)
hemolysis (95%, nonspecific)
eosinophilia, eosinophiluria, proteinuria, increased IgE
allergic interstitial nephritis diagnosis
initial test is urinalysis looking for WBCs then Hansel or Wright stain for eosinophils
also eosinophilia, eosinophiluria, proteinuria (<2g/24h), increased IgE
allergic interstitial nephritis management
remove offending agent; if persistent failure then short course of steroids
renal failure from pigments etiology
hemoglobin and myoglobin are toxic to tubules and also precipitate
rhabdomyolisis can be caused by crush injury, seizures, severe exertion, statins, hypokalemia, hypophosphatemia, ABO incompatibility
renal failure from pigments diagnosis
best intitial test --> urinalysis looking for positive blood dipstick but absence of red cells
confirm by extremenly high CPK levels
also rapidly rising creatinine
most important test is EKG or potassium level looking for peaked T waves which can lead to arrhythmia death
renal failure from pigments management
if EKG abnormalities --> calcium chloride or gluconate is best initial therapy
hydration, manitol and urine alkalinization
acute renal failure from oxalate
most commonly by ethylene glycol overdose in suicide attempt
intoxicated patient with anion gap metabolic acidosis and renal insuficiency
confirm with oxalate crystals in urinalysis
treat with ethanol or fomepizole, dyalisis and bicarbonate
acute renal failure from urate
seen in tumor lysis syndrome of leukemia/lymphoma patients
treat with allopurinol and alkalinization of urine before chemo
confirm with uric acid crystals in urinalysis
renal failure from calcium
hypercalcemia is most common in hyperparathyroidism
surgical resection of parathyroids indicated if renal impairment
aminoglycoside renal toxicity
10-20% of drug-induced nephrotoxocity and usually reversible; due to high trough levels, not peak levels therefore give once a day to allow same bactericidal effect (peak level) and low trough levels (less toxicity)
amphotericin B renal toxicity
leads to renal insufficiency and distal tubular acidosis after several days from cumulative dosing; find high creatinine; stop medication
atheroembolic renal failure
usually angioplasty patient after several days
presents with eosinophilia, low complement, bluish discoloration of fingers and toes, livedo reticularis
contrast agent renal failure
onset is faster than other toxics (12-24 hours)
rise in creatinine in 3-5 days
BUN/creatinine ratio may be as high as 20:1
diabetics, hypertensives and myeloma patients are predisposed
nephrotoxic drugs
contrast agents
NSAID nephropathy
mechanisms: interstitial nephritis, direct toxic, papillary necrosis, membranous GN, inhibition of vasodilatory prostaglandins

risk factors are elderly, hypertension, diabetes or other renal impairment

diagnose with history of NSAIDs + rise in BUN/creatinine and sterile pyuria
papillary necrosis
risk factors are sickle cell, diabetes, urinary obstruction, chronic pyelonephritis and acutely precipitated by NSAIDs

flank pain, hematuria, pyuria, fever and necrotic cells in urinalysis
most accurate diagnosis is bumpy countours of renal pelvis on CT
prevention of contrast-induced renal failure
most importantly is hydration; then bicarbonate and N-acetyl cysteine have been shown to decrease it
glomerulonephritis general presentation
hematuria with dysmorphic red cells, edema, hypertension, proteinuria <2gm/24h
biopsy is extremely important for specific Rx
glomerulonephritis from vascular causes
glomerulonephritis from glomerular disease
postinfectious GN
IgA nephropathy
diabetes (nodular or diffuse glomerulosclerosis)
Wegener glomerulonephritis presentation
glomerulonephritis associated with rhinitis, sinusitis, nasal ulcers, cough and hemoptysis
it's systemic and also affects skin, joints, eyes
nonspecific: ↑ESR, anemia, leukocytosis

best initial test: c-ANCA (anti-proteinase-3)
most accurate: biopsy of kidney or lung looking for granulomas

treat with cyclophosphamide + steroids
Churg-Strauss glomerulonephritis
glomerulonephritis with respiratory symptoms similar to Wegener
eosinophilia and adult-onset asthma are characteristic
best initial tests are ↑eosinophils and p-ANCA (antimyeloperoxidase)
definitive is lung biopsy showing granulomas
treat with cyclo + steroids
Goodpasture syndrome
glomerulonephritis + hemoptysis, cough and shortness of breath
no other organs are affected
best intial test: anti-basement membrane Abs to type IV colagen
confirm with biopsy showing hemosiderin-ladden macrophages (in lungs) and linear Ig deposits (kidneys)
treat with plasmapheresis and steroids
polyartheritis nodosa
involves every organ except lungs
kidney involvement presents as GN and renal insufficiency
there are systemic nonspecific signs
abdominal and joint pain are prominent
best initial tet is p-ANCA (present only in minority)
biopsy is confirmatory (usually sural nerve)
treat with cyclo + steroids
Henoch-Schonlein purpura
palpable purpura, arthralgias, abdominal pain and GN/renal insufficiency due to systemic IgA deposition

biopsy is confirmatory but not performed in majority of patients because it's self-limited

treatment is supportive, steroids if severe
IgA nephropathy (Berger)
most common glomerulopathy worldwide
IgA deposition that affects only kidney causing GN
presents as hematuria 1-2 days following viral illness or pharyngeal infection
40-50% progress to end-stage renal disease
initial test --> IgA (↑ in 50%)
confirm with kidney biopsy showing IgA deposits
no proven effective therapy
postinfectious glomerulpnephritis
due to any organism but mostly from throat or skin infection with group A strep
hematuria, red cell casts, proteinuria, edema, hypertension
initial test: ASO and anti-hyaluronic acid test
biopsy --> humps on electron micro and granular IgG/C3 deposits on IF
treat hypertension and proteinuria with ACEi or ARBs and penicillin for infection
thrombotic thrombocytopenic purpura
pentad for clinical diagnosis
hemolytic anemia, uremia, thrombocytopenia, fever, neurologic findings
intravascular hemolysis with schistocytes and fragmented RBCs, ↑LDH, ↑reticulocytes, ↓haptoglobin

mild disease resolves, if severe --> plasmapheresis
don't transfuse platelets or give antibiotics
hemolytic uremic syndrome
E. coli 0157:H7
triad for clinical diagnosis --> hemolytic anemia, uremia, thrombocytopenia
intravascular hemolysis with schistocytes and fragmented RBCs, ↑LDH, ↑reticulocytes, ↓haptoglobin
mild disease resolves, if severe --> plasmapheresis
don't transfuse platelets or give antibiotics
renal diasease associated with hep B or C, joint pain, neuropathy and purpura; no GI involvement (different from HSP); ↑ESR, ↓complement and confirmation with cryoglobulins; treat underlying hepatitis with interferon and ribavirin; if severe --> pulse steroids and plasmapheresis
diabetic nephropathy
directly proportional to duration of diabetes
nodular (Kimmelstein-Wilson) or diffuse glomerulosclerosis
screen for microalbuminuria and creatinine level
treat with ACEi or ARB
lupus nephritis
asymptomatic proteinuria or hematuria or severe renal disease requiring dialysis
initial test is dsDNA
confirm and determine treatment with kidney biopsy
if sclerosis --> no therapy needed
if proliferative --> steroids with mycophenolate
Alport syndrome
glomerular disease + congenital eye problems and sensorineural hearing loss
rapidly progressive glomerulonephritis
can be due to other glomerular diseases or idiopathic in which there's crescent formation
amyloidosis etiology
AL type is from Ig light chains in multiple myeloma
AA is from rheumatoid arthritis, IBD, myeloma
amyloidosis presentation
restrictive cardiomyopathy, arrhythmias, heart blocks
carpal tunnel syndrome
amyloidosis diagnosis
biopsy of involved organ such as kidney shows green birefringence in Congo red stain
amyloidosis treatment
control underlying disease; melphalan and prednisone can control protein production
nephrotic syndrome etiology
primary: membranous GN, Nil, membranoproliferative, focal-segmental GN
1/3 associated with diabetes, hypertension or myeloma
any glomerulonephritis can convert to nephrotic syndrome if severe enough
nephrotic syndrome presentation
proteinuria >3.5g/24h, edema, hyperlipidemia, hypoalbuminemia
can have hyperlipiduria (maltese cross) and hypercoagulable states (arterial or venous thrombosis from loss of antithrombin, proteins C and S)
nephrotic syndrome diagnosis
initial test is proteinuria >3.5g/24h or albumin/creatinine ratio >3.5 on urinalysis
renal biopsy is most accurate
nephrotic syndrome management
treat underlying disease
if primary --> steroids
if unresponsive --> cyclo or mycophenolate
ACEIs for all with proteinuria
membranous glomerulonephritis
most common nephrotic syndrome in adults
associated with lymphoma, breast cancer, endocarditis, chronic hepatitis, lupus
treat with steroids
Nil lesion
minimal change disease most common in children, 15% adults
electron micro shows fusion of foot processes
responds to steroids
membranoproliferative glomerulonephritis
nephrotic syndrome associated with chronic hepatitis and hypocomplement
immunofluorescensce detects mesangial IgM deposits
steroid-resistant, dipyridamole and aspirin are useful
focal segmental glomerulonephritis
nephrotic syndrome associated with heroin use and HIV; limited response to steroids; ESRD over 5-10 years
things to check for in urinalysis
proteinuria, hematuria, nitrites, bacteriuria, casts
urine dipstick detects only albumin not Ig light chains
found in glomerular or tubular disease, glomerulonephritis, diabetes, fever, CHF, severe exercise, orthostatic
microalbuminuria is 30-300g/24h in diabetic nephropathy
found in diseases of bladder or kidney; stones, cancer, bleeding disorders, trauma, cyclo, glomerulonephritis, cystitis, prostatitis
gram negative bacteria reduce nitrate to nitrite and is marker for infection
if isolated, has limited significance unless pregnant since they can develop pyelonephritis; >100,000 colonies indicates urinary infection
hyaline casts
dehydration; not necessarily disease
red cell casts
broad, waxy casts
chronic renal failure
granular/muddy casts
acute tubular necrosis
white cells in urinalysis
pyelonephritis, interstitial nephritis
indications for dyalisis
life-threatening abnormalities such as refractory fluid overload, acidosis, pericarditis, encephalopathy, other neuropathies, hyperkalemia, uremia (nausea, vomitting, bleeding diathesis)
end-stage renal disease etiology
diabetic nephropathy
glomerulonephritis (15%)
cystic disease (5%)
interstitial nephritis (5%)
requires dialysis
anemia as ESRD complication
normo normo anemia from decreased production of erythropoietin; replace EPO
hypocalcemia as ESRD complication
from decreased production of 1,25 dihydroxy vitamin D (1-hydroxylase); vitamin D replacement
hyperphosphatemia as ESRD complication
from decreased ability to excrete
treat with calcium carbonate or calcium acetate
cinacalcet in refractory cases
aluminum-containing binders should not be used due to dementia and bone abnormalities risk
osteodystrophy as ESRD complication
osteitis fibrosa cystica
bone cysts due to ↓vitamin D --> secondary hyperparathyroidism
manage by improving calcium and treating hyperPTH
hypertension and atherosclerosis as ESRD complication
acceleratd atherosclerosis not known why
most common COD for dialysis patients
hypertension goal is 130/80
infection as ESRD complication
second most common COD
white cells don't function well under uremia
staph is most common due to catheters
bleeding as ESRD complication
uremia-induced platelet dysfunction increases bleeding time
treated with desmopressin to increase vWB and factor VIII
minor signs present in ESRD
decreased libido
glucose intolerance
not indications for dialysis
dietary treatment in ESRD
restricted Na, K, protein, magnesium, phosphate
renal transplant
live related donor 95%/1 year, 72%/5years
cadaver donor 88%/1 year, 58%/5 years
dialysis alone 30-40%/5 years
average wait for transplant is 2-4 years
graft rejection prevention with cyclosporine, tacrolimus, mycophenolate
renal tubular acidosis type I etiology
problem in distal tubules
usually sporadic or secondary to autoimmune disease, ampB, lithium, NSAIDs, nephrocalcinosis, sickle cell, familial, chronic hepatitis
renal tubular acidosis type I presentation
inability to develop ↑[H+] in urine
urine pH >5.4
secondary hyperaldosteronism
renal tubular acidosis type I diagnosis
Acid load test: give amonium chloride which should lower urine pH, with disease urine pH remains high; serum bicarbonate ~10; hypokalemia
differentiate RTA from diarrhea acidos
urine anion gap = (Na + K) - Cl
both have normal serum anion gap metabolic acidosis but diarrhea has negative urine anion gap (↑ urine Cl-) and RTA type I cannot excrete H+ so Cl- will be low and urine anion gap is positive
renal tubular acidosis type I treatment
oral bicarbonate because proximal tubule reabsoprtion is intact and potassium replacement
renal tubular acidosis type II etiology
inability to absorb bicarbonate in proximal tubules
Fanconi, Wilson, amyloidosis, myeloma, acetazolamide, vitD deficiency, secondary hyperPTH, chronic hypocalcemia
renal tubular acidosis type II presentation
initial urine pH is basic but then becomes <5.4
serum bicarbonate 18-20
malabsorption of glucose, amino acids, urate, phosphate
renal tubular acidosis type II diagnosis
sodium bicarbonate IV is not reabsorbed; basic urine in presence of acidemia; bicarbonate in urine
renal tubular acidosis type II treatment
potassium, thiazides and large amounts of HCO3
difference between type I and type II RTA
type I is inability to excrete H+ and has nephrolithiasis
type II inability to reabsorb HCO3 and has osteomalacia/rickets
renal tubular acidosis type IV etiology
aldosterone deficiency or adrenal insensitivity to angiotensin II
diabetes (50%)
sickle cell
renal failure
renal tubular acidosis type IV presentation
asymptomatic hyperkalemia
mild to moderate renal failure
hyperchloremic (nonanion gap) metabolic acidosis
renal tubular acidosis type IV diagnosis
high urine sodium with oral salt restriction is diagnostic
renal tubular acidosis type IV treatment
fludrocortisone has mineralocorticoid effect
types of kidney stones
calcium oxalate (70%)
calcium phosphate (10%)
Mg/aluminum/phosphate (struvite)
uric acid
causes of hypercalciuria
increased absorption: vitamin D intoxication, ↑vitamin D from sarcoidosis or granulomatous diseases; familial, idiopathic; resorptive: hyperPTH, multiple myeloma
causes of hyperoxaluria
primary familial, enteric; fat malabsorption binds calcium and leaves oxalate to be reabsorbed
causes of uric acid stones
acid tubules and high uric acid from gout, hematologic malignancies, Crohn
radiolucent on x-rays
causes of struvite stones
infections with urease-producing proteus, pseudomonas, klebsiella; highly alkaline urine
nephrolithiasis presentation
constant flank pain, hematuria, pain radiating to groin
stones < 5mm should pass spontaneously
nephrolithiasis diagnosis
plain x-ray is rarely used
ultrasound, spiral CT
strain the urine
check serum and urine calcium
never do intravenous pyelogram
nephrolithiasis treatment
analgesia, hydration, bed rest
shockwave lithotripsy for stones <2cm but fragments may obstruct
percutaneous removal (anesthesia and hospital stay)
adult polycystic kidney disease presentation
flank pain, hematuria, palpable mass, UTIs, calculi
hepatic cysts (40%)
colonic diverticula
intracraneal aneurysm
mitral valve prolapse
adult polycystic kidney disease diagnosis and treatment
ultrasound and CT; treatment is nonspecific with management of hypertension, UTIs and calculi
simple cysts
cysts with irregular walls or debris should be aspirated to exclude malignancy
dialysis can cause cysts