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Glomerulonephritis, ischemia, malignant hypertension |
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Tubulointerstital inflammation, acute pyelonephritis, transplant rejection |
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Advanced renal disease/chronic renal failure |
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APSGN, RPGN, Bergers IgA, Alport syndrome |
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Both Nephritic and nephrotic |
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Diffuse proliferative glomerulonephritis (DPGN) Membranoporliferative glomerulonephritis (MPGN) |
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Massive proteinuria >3.5 g/day (frothy), hyperlipidemia, fatty casts, edema Assoc with thromboembolism and inc risk of infection FSGS, Membranous nephropathy, minimal change disease, amyloidosis, diabetic glomerulonephropathy |
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LM- segmental sclerosis and hyalinosis EM- effacement of foot processes (similar minimal change) *Most common cause of nephrotic syndrome in adults Assoc: HIV, heroin, massive obesity, interferon treatment, CKD due to congenital absence or removal |
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LM- diffuse capillary and GBM thickening EM- *Spike and dome deposits in subepithelium IF- granular Assoc with drugs, infection, SLE, solid tumors |
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EM- foot process effacement Selective loss of albumin (NOT globulins) caused by GBM poyanion loss May be triggered by recent infection or an immune stimulus Most common in children *responds to corticosteroids |
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LM- congo red stain shows apple green birefringence Assoc with MM, TB, RA |
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Type 1-Subendothelial IC deposits with granular IF; *tram tract appearance due to GBM splitting from mesangial growth Assoc with HBV and HCV Type 2- intramembrane IC deposits (dense deposits) Can also present as nephritic syndrome Assoc with C3 nephritic factor |
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Diabetic glomerulonephropathy |
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Definition
Nonenzymatic glycosylation of GBM, Inc permeability, thickening NEG of efferent arterioles > Inc GFR, mesangial expansion LM- mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis *(Kimmelstiel Wilson lesion) |
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Acute Post strep glomerulonephritis |
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Definition
LM- enlarged and hyper cellular glomeruli, neutrophils; *Lumpy-bumpy appearance EM- subepithelial immune complex humps IF- granular appearance due to IgG, IgM and C3 deposition along GBM and mesangium Peripheral and periorbital edema, dark urine, hypertension |
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LM and IF- crescents made of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes and macrophages *Goodpastures (T2 HS Rxn, linear IF, Ab to GBM - hematuria and hemptysis) Wegeners - cANCA Microscopic polyangiitis - pANCA |
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Due to SLE or MPGN "Wire lupus" LM- wire looping of capillaries EM- subendothelial IgG and C3 deposits *Most common cause of death in SLE |
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Related to Henoch-Schonlein purpura LM- mesangial proliferation IF- IgA based IC deposits in mesangium Often presents with a URI or acute gastroenteritis |
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Mutation in type 4 collagen > split BM X linked Glomerulonephritis, deafness and less commonly, eye problems |
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80% - most common CaPO4 precipitates at high pH Ca oxalate precipitates at low pH Radiopaque Oxalate crystals can result from ethylene glycol or Vit C abuse Tx: thiazides and citrate |
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Ammonium magnesium phosphate kidney stone |
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Definition
15% - second most common Inc pH Radiopaque Infection with urease pos bugs (Proteus, Staph, Klebsiella) Hydrolyze urea to ammonia > urine alkalinization *staghorn calculi |
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Dec pH, radiolucent Visible only on CT and US (not XR) Often seen in diseases with inc cell turnover (leukemia) Tx: alkalinize the urine |
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Back up of urine into the kidneys Dilation of renal pelvis and calyces prox to obstruction Parenchymal thinning in chronic, severe cases |
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Dec pH, radiopaque Most often secondary to cystinuria Hexagonal crystals Tx with alkalization of urine |
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Originates from proximal tubule cells > polygonal clear cells Filled with lipids and carbohydrates Men 50-70, inc with obesity and smoking Invades renal vein then IVC and spreads hematogenously Mets to liver and bone *Gene deletion on chromasome 3, VHL |
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Most common renal malignancy of early childhood Contains embryonic glomerular structures Huge palpable flank mass and/or hematuria Deletion of TSG WT1 on c11 May be part of Beckwith-Weidman syndrome or WAGR complex |
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Wilms tumors, Aniridia, Genitourinary malformation and MR |
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Transitional cell carcinoma |
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Most common tumor of the urinary tract system Painless hematuria (no casts) suggests bladder cancer Assoc: Phenacetin, Smoking, Aniline dyes and cyclophosphamide |
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Affects cortex with sparing of glomeruli Fever, CVA tenderness, nausea and vomiting White cell casts in urine are classic |
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Requires predisposition to infection, like vesicourteral reflux, or chronically obstructing kidney stones Coarse, asymmetric corticomeduallry scarring, blunted calyces *tubules can contain eos casts (thyroidization) |
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Drug induced interstitial nephritis |
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Definition
Acute interstitial renal inflammation Pyuria and azotemia (eosinophils) Drugs act as hapetens, inducing hypersensitivity 1-2 weeks post drug administration *diuretics, penicillin, sulfonamides, rifampin, nsaids (months) Fever, rash, hematuria and CVA tenderness |
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Diffuse cortical necrosis |
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Definition
Acute generalized cortical infarction of both kidneys Likely due to vasospasm and DIC *obstetric catastrophies and septic shock |
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Most common cause of intrinsic renal failure 1. Inciting event 2. Maintenance phase- oliguric, lasts 1-3 weeks, hyperkalemia 3. Recovery phase- polyuric; BUN and serum createnine fall, risk of hypokalemia Renal ischemia, crush injury, drugs, toxins |
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Sloughing of renal papillae Gross hematuria and proteinuria Recent infection or immune stimulus Assoc: DM, acute pyelo, Chronic phenacetin use, SCA |
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In normal nephron, BUN is reabsorbed but Cr is not ARF: abrupt decline in renal function with inc Cr and Inc BUN over a period of several days |
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Dec RBF, leads to dec GFR Na, H2O, and urea are retained to conserve volume Urine osm: >500 Urine Na: <20 FeNa: <1% Serum BUN/Cr: > 20 (urea resorption) |
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ATN, Acute glomerulonephritis, toxins, or ischemia Patchy necrosis leads to debris obstructing tubules and fluid back flow across necrotic tubule > dec GFR Urine has epithelial/granular casts Urine Osm: <350 Urine Na: >40 FeNa: >2% Serum BUN/Cr: < 15 (resorption is impaired) |
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Outflow obstruction Develops only with bilateral obstruction Urine Osm: <350 Urine Na: >40 FeNa: >2% Serum BUN/Cr: >15 |
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Inc BUN and Inc Cr Nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction |
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Failure of Vit D hydroxylation, hypocalcemia, and hyperphosphatemia > secondary hyperparathyroidism Hyperphosphatemia > dec serum Ca by causing tissue calcs Sub periosteum thinning of bones |
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Bilateral cysts that destroy the parenchyma AD mutation in PKD1 or PKD2 Death from chronic kidney disease or HTN Assoc: berry aneurysm, MV prolapse, benign hepatic cysts |
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Infntile presentation in parenchyma Congenital hepatic fibrosis Significant renal failure in utero can lead to Potter's syndrome HTN, portal HTN and progressive renal insufficiency |
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Inherited causing tubuloinsterstital fibrosis and progressive renal insufficiency with inability to concentrate urine Shrunken kidneys on US, poor prognosis |
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Osmotic diuretic in PCT; increases tubular fluid osmolarity, producing inc urine flow and dec IOP/ICP Use: drug overdose, ICP/IOP increase T- pulmonary edema, dehydration, CI'd in anuria, CHF |
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CA inhibitor Self limited NaHCO3 diuresis and reduction in HCO3 store Use- glaucoma, metabolic alkalosis, altitude sickness, pseudo tumor cerebra Tox- Hyperchloremic metabolic acidosis, NH3 tox, sulfa allergy |
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Loop diuretic, works at thick ascending limb of LOH Inhibits Na/K/Cl transporter. Abolishes hypertonicity of medulla Stimulates PGE release (vasodilatory), inhibited by NSAIDs Loops lose calcium Use- edematous states, HTN, hypercalcuria T- Ototox, Hypokalemia, dehydration, sulfa allergy, nephritis, gout |
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Same action as Furosemide (loop) Use- diuresis in patients allergic to sulfa T- similar to furosemide. Never use or gout |
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Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of nephron Dec Ca excretion Use- HTN, CHF, hypercalcuria, nephrogenic diabetes insipidus Tox- hypokalemic metabolic acidosis, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia |
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Spironolactone, eplerenone,triamterene, Amiloride Works at CD Spir and Ep are competitive aldosterone R antagonists Triam and Amil act by blocking Na channels in CCT Use- hyperaldosteronism, K depletion, CHF Hyperkalemia Tox- Hyperkalemia, endocrine effects (gynecomastia) |
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Acidemia- CA blockers, K sparing, Alkalemia- Loops and thiazides |
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Captopril, lisinopril, enalapril Inhibit ACE > dec GFR by preventing constriction at eff arteriole Renin levels increase due to loss of feedback Prevents Inactivation of bradykinin, a potent vasodilator Use- HTN, CHF, proteinuria, diabetic renal disease *prevents heart remodeling from CHF T- cough, angioedema, teratogen, Cr increase, Hyperkalemia, Hypotension *avoid in bilateral renal artery stenosis because ACEI will further decrease GFR |
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