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95 Cards in this Set
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Nephritic Clinical Symptoms
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Hematuria, proteinuria, hypertension. RBC casts, and acanthocytes are pathognomonic
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Nephrotic clinical sympotoms
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Proteineria, hypocomplementemia, hyperlipidemia, edema, > 3.5 gm protein/day
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Prerenal azotemia
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Increased BUN w/o tubular necrosis - from decreased GFR
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Chronic Renal Failure - Na balance
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Na excess & Hypervolemia
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Chronic Renal Failure and K balance
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Little chenge unless GFR < 5mL
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Chronic Renal Failure: CV & Pulm abnormalities
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CHF, Pulmonary Edema, Hypertension,
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Chronic Renal Failure: Hematologic Abn.
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Dec RBC #, WBC function, clotting.
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Minimal Change Disease: Epidemiology
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Especially found in children
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Minimal Change Disease: LM
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Normal
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Minimal Change Disease: IF
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IgM (maybe)
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Minimal Change Disease: EM
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Effacement of podocytes, no immune dep.
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Minimal Change Disease: Definition
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Fusion of Epithelial foot processes, typically ~1wk after infection. Explosive edema, foam cells.
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FSGS:LM
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Segmental sclerosis of glomeruli
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FSGS: IF
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Focal & Segmental IgM, C1q
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FSGS: EM
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Foot process fusion, sclerosis, hyalinosis
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Membranous nephropathy: Epidemiology
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Most common nephritis in adults, male, esp 40, 60 (nephrotic), assoc. w/ renal vein thrombosi
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Membranous Nephropathy: LM
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(late) GBM thickening
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Membranous Nephropathy: IF
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Granular, IgG, C3
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Membranous Nephropathy: EM
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Supepithelial deposits, GBM expansion
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Membranoporliferative Definition
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Complement mediate (type I: classic & alternate, type II(DDD): alternate) nephritic/nephrotic disease.
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Membranoproliferative: Epidemiology
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2nd, 3rd decade.
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Membranoproliferative: LM
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Hypercellular glomeruli, duplicated GBM's (tramtracks)
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Membranoproliferative: IF
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Type 1: C3, IgG, IgM. Type II: C3 in capillary and mesangium
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Membranoproliferative: EM
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Type 1: Subendo Type II: Dense GBM
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IgA Nephropathy: Definition
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Nephritic disease - IgA deposits in Mesangium. Red or cola colored urine 1-2 d after infection.
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Iga Nephropathy: LM
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Focal proliferative w/ diffuse mesangial widening
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Goodpastures (anti-GBM): Definition
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Ab's against GBM that can also affect lung. Assoc. w/ smoking, hydrocarbon exposure, cocaine. (NEPHRITIC)
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Wegeners Definition
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P-ANCA abs cause Nephritic, pauci immune disease
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Microscopic Polyangiitis
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P or C ANCA abs cause Nephritic, pauci immune disease.
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Churg Straus
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Eosinophilia causes nephritic disease.
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Post infectious GN
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Nephritic disease 1-2 weeks after infection (esp Strep).
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Post infectious GN - Clinical Signs
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Periorbital Edema, Urine RBC's, RBC casrs, hypocomplementemia
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Post infectious GN - IF
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IgG/C3
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Post infectious GN - EM
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Electron dense humps
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Post Infectious GN - LM
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Hypercellular glomeruli w mesangial proliferation
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Alports (Hereditary Nephritis)
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Genetic disorder in Type IV collage (a-5 chain) causes Nephritic
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Alports - EM
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Irregular thickening of BM , foam cells
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SLE GN (LM, EM)
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Renal depositions in lupus (LM: wire loops, EM: fingerprints). 5 types
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Diabetic Nephropathy LM/EM
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Hypertrophy of mesangial matrix. Kimmelsteil wilson nodules, glomerulosclerosis, thickening of BM.
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3 primary and 2 pathognomonic
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Diabetic Retinopathy
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ALWAYS found w/ diabetic nephropathy.
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Nephritic Syndrome: Pathognomonics
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RBCs in urine, acanthocytes.
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Crescents in glomeruli indicate:
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RPGN
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Preferential passing in slit membrane
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Negatives, acids blocked.
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Causes of FSGS
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SO HARM (sickle/sleep apnea, obesity, HIV, addiction, addiction, reflux, minimal change
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SLE Membranous vs Diffuse
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Membranous : Karryhrexis wire loops, crescents, diffuse segmental prolif, subeNdothilial prolife DIFFUSE: Mesangial Prolif, SubePithelial
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Membranoproliferative - risk factors
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CIVLL (Chronic infection, virus, leuk, lymph
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thyroidization of tubules
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indicative of chronic pyelonephritis.
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Reflux chronic pyelonifrites - organization
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Polar. (obstructive has multiple scars)
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Cavitary Ring Shadow
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Analgesic induced nephropathy.
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Which type of diabetes is more like to cause nephropathy?
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Type I
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Where do high affinity antibodies end up in the glom.
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mesangium
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Where fo high valency antigens end up in the glomerulus
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Mesangium
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Where do deposits end up in antigen excess
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Capillary wall
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What disease is from circulating immune complexes depositing?
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Lupus.
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Which diseases activate the alternate pathway (C3_
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Post Strep, Lupus, IgA, MP
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Who's got C3NeF
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MP II
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Flea bitten kidney (petechial hemorrhage)
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Post Infectious GN
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Which lupus has more decrease in complement
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Diffuse
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Clinical presentation of acute renal failure
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Hyperkalemia, Oliguria, Acidosis, Creatine (inc), Dec Urine
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What is Ang II's effect on GFR
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Increase via efferent constriction
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What are prostaglandin's effect on GFR
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Increase via blocking constriction of afferent
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Causes of Vascular Intrinsic Renal Failure
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HARMS - HUS/TTP, Atheroembolic/antiphospholipd diseas, Radiation, Mal hypertension, Scleroderma
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Why do crushing injuris cause ATN?
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Myoglobin (and hemoglobin) are nephrotoxic.
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Causes of ATN
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Toxic, ischemic
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Causes of Interstitial Intrinsic Renal Failure
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MAID - Malig, Autoimmune, Infect/idio, Drug
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Which diuretics are potassium wasting?
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Loop
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Which adrenergic causes a decrease in K+
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Beta agonists
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Sevelamer
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Phosphate binder
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5 levels of kidney disease
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GFR 1. >90 2. 60-89 3. 30-59 4. 15-29 5. <15
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How are acute and chronic kidney rejection mediated?
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Humoral & Cellular, by IgM, C3/C1q
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Which renal transplantation rejections are irreversible?
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Hyperacute and chronic
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What is indicitave of hyperacute rejection?
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PMN infiltration, sludging, fibrin.
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What is indicitave of actue rejection?
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Petechiae, lymphocytes, monocytes, perivascular infiltration, tubulitis
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What is indicative of chronic rejection
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Plasma cells, mesangial expansion, fibrosis, fibrointimal prolif
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Explain cyclosporin toxicity
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Acute changes: Necroses,vacuolar degeneration, cellular infiltration, HUS. Chronic - Hyalinization, fibrosis
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Which (2) diseases are most likely to recur in a renal transplant
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MPII, IgA
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Which disease is most likely to occur in a transplant (not recur)
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Membranous GN
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What is characteristic of ischemic ATN
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Hypotension, Patchy lesions, tubulorrhexis, casts
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What is characteristic of toxic ATN
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Diffuse lesions.
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What causes toxic ATN
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MAOI - Metals, Ab's, Organix Solvents, Immunosuppresants
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What are the phases of ATN
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Oliguric (hyperkalemia, acidosis, fluid retention), Early diuretic (hypokalemia, fluid loss), late diuretic (recovery)
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What distinguishes hematogenous from reflux pyelonephritis?
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Reflux is polar.
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What's indicative of Analgesic Nephropathy?
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Necrosis of papillae, cavetary ring shadow
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How is Drug Induced TIN mediate
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NSAID's causea Type I Hypersens response (IgE) --> Histology shows eosinophils
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What clinically differentiates Malignant Hypertension from Benign Hypertension
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Presence of renin in malignant hypertension, and malignant hypertensive patients are younger
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Onion skin lesions in vessels are indicative of which hypertension?
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Malignant.
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3 classes of disease that cause secondary hypertenstion
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Glomerular, Tubulointerstitial, Vascular
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What are the differences in the cysts in dom vs rec polycystic kidney
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Dom - all over. Rec - Just in collecting duct (fusiform)
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Fibrocystin mutation is what disease
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ARPKD
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Clinical presentations of medullary sponge
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HIS BAG - Hematuria, infection, stones, benign, asymptomatic, gravel
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Nephrocystin mutation is which disease
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Medullary cystic disease complex
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MCDC clinical manifestations
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Nephronophthisis, Uremia, CRF, Salt wasting, Polyuria
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What genes are involved in ADPKD?
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PKD1,2,3
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EGFR and ADPKD
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EGFR dedifferentiates into fetal form and presents on the luminal side in ADPKD
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How do you treat ADPKD
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Tyrosine Kinase inhibition
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