Medstudy Nephrology

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RTA, diarrhea, carbonic anhydrase inhibitors, hyperalimentation with TPN

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Causes of non-anion gap metabilic acidosis

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High anion gap acidosis, obtundation/intoxication, osmolal gap (usually > 20)

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Alcohol Poisoning (ethanol, ethylene glycol, methanol)

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Ketosis without acidosis, fruity smell, obtundation

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Isopropyl alcohol

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Idiopathic hypercalciuria, IgA nephropathy, thin basement membrane disease, early Alport syndrome

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Causes of persistent asymptomatic hematuria

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Gross hematuria, edema, hypertension, renal insufficiency

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Acute post-streptococcal glomerulonephritis

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Ages 5-15, boys > girls, latency period of 1-2 weeks post-infection (3-6 wks if skin infection), smoky or coca-cola colored urine, low C3 level (resolves after 6-8 wks), check throat cx or ASO, DNase B provides best sens/spec

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Acute post-streptococcal glomerulonephritis

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Most common cause of gross hematuria

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IgA nephropathy

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Recurrent, painless macroscopic hematuria, occurs concomitantly with infection, no specific lab tests, tx with ACE-I, fish oil, ?steroids, immunosuppresion (if have crescentic disease)

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IgA nephropathy

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Purpuric rash (esp on buttocks, abdomen, and lower extremities), abdominal pain, arthralgias, glomerulonephritis with IgA deposition, peak incidence ages 4-5, more common in winter/spring with preceding infection

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Henoch-Schonlein Purpura (anaphylactoid purpura)

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Asymptomatic hematuria, mild proteinuria, 10% with acute nephritic syndrome, renal involvement within 8 wks of disease onset, majority improved in 4 weeks

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HSP nephritis

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Most common cause of chronic glomerulonephritis in children and young adults, thickening of GBM and hypercellularity

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Membranoproliferative glomerulonephritis

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20-30% present with acute nephritic syndrome, similar to APSGN, PERSISTENTLY decreased C3, 20-40% present with incidental findings of proteinuria and hematuria, 30-50% present with nephrotic syndrome, tx is 3-10 yrs of steroids

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Membranoproliferative glomerulonephritis

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Presence of cresents in majority of glomeruli, 3 types: immune complex nephritis, pauci-immune disease, anti-GBM disease

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Rapidly progressive glomerulonephritis

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Isolated renal disease but can have associated pulmonary hemorrhage, young men, previous URI/influenza, +smoking history, linear deposits of IgG and C3 in GBM, plasmapharesis is main tx

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Anti-glomerular basement membrane disease (Anti-GBM aka Goodpasture's)

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ANCA-associated focal necrotizing glomerulonephritis, allergic asthma, vasculitis associated with eosinophilic infiltrates, peripheral blood eosinophilia

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Churg-Strauss Syndrome

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Flu-like illness, myalgias, fever, anorexia, weight loss, purpura or urticaria, arthritis/arthralgias, pulmonary hemorrhage (due to necrotizing granulomas), nephritis (hematuria, proteinuria, renal insufficiency), cANCA positive, tx with steroids or cyclophosphamide

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Wegener Granulomatosis

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Flu-like syndrome, pulmonarry hemorrhage, absence of lung granulomas, pANCA elevation

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Microscopic Polyarteritis

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Proteinuria > 3.5gm/24 hrs, albumin < 3, edema, hypercholesterolemia, frequent infections, thrombotic disease (up to 20% have silent thrombotic event) esp in renal vein or sagittal sinus

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Nephrotic Syndrome

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Morning eyelid swelling, microscopic hematuria (20%), oval fat bodies, C3 normal to high, tx is salt restriction and steroids, usually idiopathic but can be assoc with infection, NSAIDs, Hodgkin disease, atopy

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Minimal Change Nephrotic Syndrome

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Most common glomerular cause of ESRD, segment of glomerulus collapses with mesangial sclerosis, nephrotic syndrome that does not respond to steroids, hypertension, boys > girls, onset between 2-7 yrs, bx needed for diagnosis, tx high dose steroids and cyclophosphamide

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Focal Segmental Glomerulosclerosis

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Immune deposits of IgG and C3 in GBM or subepithelial area of capillary wall, 50% of cases are due to secondary cause, renal bx required for dx

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Membranous Nephropathy

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Complement levels in post-infectious, membranoproliferative GN, cryoglobulinemic GN, SLE, shunt nephritis, subacute bacterial endocarditis

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Low Complement

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Complement levels in RPGN, mesangial proliferative GN, Wegener granulomatosis, and Goodpasture syndrome

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Normal Complement

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Complement level in minimal change, focal sclerosis, membranous, diabetic nephropathy, or amyloid nephropathy

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NEVER have low complement

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Endothelial and glomerular injury resulting in microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency

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Hemolytic Uremic Syndrome

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N/V/D, abd pain, onset 6 days after diarrhea, pallor, renal insufficiency, irritability/sleepiness, seizures in 20%, coma in 15%

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Hemolytic Uremic Syndrome

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Tx is dialysis in 50%, volume control, antibx and antimotility agents contraindicated, poor prognosis if anuria > 2 wks, neutrophil > 20K, coma, atypical forms

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Hemolytic Uremic Syndrome

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X-linked, AR, or AD, mutation in genes coding for type IV collagen, sensorineural hearing loss and ocular defects, boys dev microhematuria with proteinuria, HTN, and renal failure, dx via kidney bx - lamellation in the basement membrane

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Alport Syndrome

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AD inheritance, multiple family members with hematuria and RBC casts, no family hx of renal failure

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Benign familial hematuria (Thin glomerular basement membrane disease)

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Wilms tumor, XY gonadal dysgenesis, ambiguous genitalia, nephropathy, renal lesion is diffuse mesangial sclerosis

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Denys-Drash Syndrome

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X-linked deficiency of alpha-galactosidase A, in boys it causes structural and fxnal abnormalities of kidney, heart, and nervous system

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Fabry disease

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AD inheritance, hypoplasia/absence of patellae, dysplasia of elbows, iliac horns, and renal disease, localized to chromosome 9

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Nail-Patella Syndrome

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AR inheritance, obesity, retinitis pigmentosa, hypogenitalism, polydactyly, mental retardation, cystic dysplasia of the kidney

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Laurence-Moon-Bardet-Biedl Syndrome

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AR inheritance, cystic dysplasia of the kidney, hepatic fibrosis, occipital encephalocele, postaxial polydactyly

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Meckel-Gruber Syndrome

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Ectasia of cortical ducts within inner medulla giving a sponge-like appearance, frequent UTIs, renal stones, linear striations from dilated collecting ducts and enlarged calices on pyelogram

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Medullary Sponge Kidney

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Polyuria, polydipsia, anemia, FTT, salt-losing nephropathy, no differentiation between cortical and medullary areas on U/S, extrarenal manifestations include: inability to move eye horizontally, retinitis pigmentosa, and cerebellar aplasia with coloboma

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Juvenile Nephronopthisis Type 1 (NPH1)

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AR inheritance, chromosome 6, bilateral kidney enlargement, transformation of collecting ducts into fusiform cysts, hepatic fibrosis, oligohydramnios, "Potter facies," HTN, recurrent UTIs, growth failure, osteodystrophy, hyperechogenicity on renal US

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Autosomal Recessive PKD

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These drugs work by causing a diauresis with bicarbonate wasting resulting in metabolic acidosis

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Carbonic anhydrase inhibitors (Acetazolamide)

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These drugs work by blocking absorption of Na+ in the ascending loop, they also increase Ca++ excretion

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Loop Diuretics

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This hormone facilitates active resorption of Na+ in the distal tubule and thus excretion of K+ and H+ causing metabolic alkalosis

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Aldosterone

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This hormone works at the collecting duct and increaes the permeability of the collecting duct to water allowing free water to resorb into the hypertonic renal medulla

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Antidiuretic Hormone (ADH)

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These drugs inhibit Na+ entry into the distal cells and thereby block the K+ and H+ secretory process (K+ sparing)

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Triamterene and amiloride

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These drugs decrease the Na+ and Cl- absorption at the early distal tubule and cortical thick ascending limb after much of the filtered NaCl has been resorbed in the PCT and ascending limb, decrease Ca++ excretion

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Thiazides

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Similar mechanism to acetazolamide - decreasing bicarb resorption in proximal tubule, frequently caused by Fanconi syndrome, acidic urine, treat with Na+ restriction

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Type 2 RTA

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Fanconi syndrome, drugs, heavy metal poisoning, metabolic disorders, MM

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Causes of type 2 RTA

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Affects Na/K/H exchange mechanism, effect similar to spironolactone or hypoaldosteronism, (hyperkalemic, hyperchloremic)

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Type 4 RTA

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Obstructive uropathy, interstitial renal disease, multicystic dysplastic kidneys, type 1 pseudohyperaldosteronism, diabetic nephropathy, 21 hydroxylase deficiency, renal transplant

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Causes of type 4 RTA

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Defect in H secretion in distal tubule, hypokalemia, acidosis, causes renal stones due to decreased citrate excretion and hypercalciuria

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Type 1 RTA

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Amphotericin B, toluene, lithium, SLE, Sjogrens, chronic active hepatitis

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Causes of type 1 RTA

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What gives metabolic acidosis with low urine sodium?

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Diarrhea induced volume contraction

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Think of this in pts with pre-renal azotemia after starting ACE-I/ARB

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Renal artery stenosis (fibromuscular dysplasia) or atherosclerotic disease

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Hypocomplementemia, increased ESR, eosinophilia, rash, but NO RBC casts

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Atheroembolic renal disease

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Rhabdomyolysis, hemoglobinuria, heavy metals, contrast dye, drugs (aminoglycosides, amphotericin B, platinums, cyclosporine)

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Causes of ATN

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Causes proximal tubule damage resulting in non-oliguric ATN, delayed 7-10 days after start of therapy

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Aminoglycosides

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Magnesiuria and hypomagnesemia are most common effects

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Cisplatin

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Isoosmolar urine, large muddy brown granular casts, urine Na > 20

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ATN

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Causes proximal tubule damage resulting in non-oliguric ATN, delayed 7-10 days after start of therapy

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Aminoglycosides

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Magnesiuria and hypomagnesemia are most common effects

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Cisplatin

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Isoosmolar urine, large muddy brown granular casts, urine Na > 20

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ATN

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Hyperphosphatemia, hyperkalemia, hypocalcemia, urine myoglobin, elevated CPK

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Rhabdomyolysis

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Urine eosinophils, RBCs (but no casts), WBCs, WBC casts, beta-2 microalbuminuria, caused by abx (esp beta lactams), NSAIDs, SLE, sarcoid, infection, transplant rejection, if due to abx triad of fever, rash, and eosinophilia, if due to NSAIDs can have nephrotic range proteinuria

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Acute Interstitial Nephritis

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Pts present with frequent pain, proteinuria, and elevated Cr, caused by drugs, heavy metals, renal outlet obstruction, Sjogrens, HbSS, associated with papillary necrosis from chronic analgesic abuse

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Chronic Interstitial Nephritis

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Think about this in pts spilling glucose in urine but with normal serum glucose

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Chronic Tububulointerstitial Disease, Type 2 RTA, and pregnancy

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Drugs that decrease GFR by blocking prostaglandins that vasodilate the afferent arteriole, also decrease renin release exacerbating hyperkalemia in pts with hyporeninemic hypoaldosteronism

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NSAIDs

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Decreases T cell proliferation (but not fxn) without affecting bone marrow, side effects are tremors, nephro/hepato/CNS toxicity, HTN, gum hypertrophy, metabolized by P450 system

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Cyclosporine

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Decreases T cell proliferation without affecting bone marrow, nephro/hepato/CNS toxicity, diabetogenic

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Tacrolimus

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Side effects are hyperlipidemia, thrombocytopenia, delayed wound healing

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Sirolimus

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Affects bone marrow leading to leukopenia, serum levels increased with allopurinol

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Azathioprine

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Newer agent, less bone marrow suppression, increased GI side effects

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Mycophenolate Mofetil

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Screen all pregnant women with lupus for these and why

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Lupus Anticoagulant (spontaneous abortion) and SSB antibodies (neonatal heart block)