LECOM Path Ch 20 Kidney
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| 4 stages of renal failure | Deminished renal reserve, Renal insufficiency, Chronic renal failure, End-stage renal disease
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| Progression to renal failure usually ensues when GFR is reduced to | 30-50% of normal
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| Acute Nephritic, after infection, Sub-epithelial humps, granular IgG and C3 in GBM, diffuse proliferation | PSGN
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| Diffuse nephritis, global hypercellularity, Granular IF | PSGN
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| Rapidly progressive glomerulonephritis, Linear IgG and C3 and/or fibrin crescents, proliferative, maybe crescenteric | Goodpasture
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| RPGN Type I mediated by | Anti-GBM
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| RPGN Type II mediated by | Immune complex
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| RPGN Type III mediated by | Pauci Immune
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| Type I RPGN that cross reacts with lung BM | Goodpasture
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| Elevated titer in Type III RPGN | ANCAs
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| Ruptures of the GBM on EM, inflammatory and parietal cell proliferation in Bowman space | RPGN/ cresenteric
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| Escape of this into bowman’s space is a leader in crescent development | fibrinogen
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| MCC of nephrotic syndrome in children | Minimal-Change Disease
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| Nephrotic syndrome Dx with | >3.5g of daily proteinuria
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| Membranous Nephropathy mediated by | chronic immune-complex mediated
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| Nephrotic, Diffuse thickening of capillary walls, tubular epithelial cells with protein reabsorption droplets, diffuse GBM granular staining, sub-epi deposits on EM | membranous Nephropathy
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| Pathognomonic finding of spikes on GBM w. silver stain Dx? | Membranous Nephropathy
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| Membranous nephropathy vs Minimal Change disease: difference in onset | Minimal change is selective proteinuria and responds to corticosteroids
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| Nephrotic, Diffuse effacement of podocytes on EM, but look normal on light microscopy. Dx? | Minimal-Change Disease
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| Most characteristic thing about Minimal-Change disease is | it’s response to corticosteroid therapy
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| Effacement of podocytes with normal glomeruli Dx? | minimal change
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| MCC of nephrotic syndrome in adults in the US is | Focal Segmental Glomerulosclerosis (FSGS)
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| MC location of lesion is FSGS | juxtamedullary glomeruli
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| Disease states that can cause FSGS (5) | HIV, IV drug use, Sickle Cell, morbid obesity, loss of renal tissue
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| Hylinosis and sclerosis of some viewed glomeruli and only some of the capillaries | FSGS
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| Retraction of entire glomerular tuft, proliferation and hypertrophy of glomerular visceral epithelial cells. Dx and most characteristic lesion of? | Collapsing glomerulopathy of FSGS and in HIV-nephropathy
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| MC lesion in HIV nephropathy | collapsing variant of FSGS
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| Alteration in the GBM, proliferation of glomerular cells, and leukocyte infiltration | membranoproliferative glomerulonephritis (MPGN)
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| Other name of Type II primary MPGN | dense-deposit disease
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| Type I MPGN is Dx when finding | immune complexes in the glomerulus and activation of both compliment pathways
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| Type II MPGN is Dx when finding | decreased serum C3 but normal C1 and C4
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| Is there IgG deposits found in Dense Deposit Disease? | no, only C3 and properdin
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| 70% of Pts w/ DDD have this circulating antibody | C3NeF
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| “Tram-tracking” or duplication of the basement membrane is seen in what disease | MPGN
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| Large hypercellular glomeruli, GBM thickened, IgG and C3 in granular pattern in subendothelial location. Dx? | MPGN Type I
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| Large hypercellular glomeruli, dense-ribbon like GBM, C3 in basement membrane granular or linear, and circular rings of C3 in mesangium. Dx? | MPGN Type II aka DDD
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| Causes of Secondary MPGN (all type I)(7) | SLE, HBV, HCV, HIV, alpha 1 antitrypsin, leukemia or lymphoma
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| Frequent cause of recurrent gross or micro hematuria, probably MC glomerulonephritis worldwide | IgA nephropathy
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| Which subclass forms Ab in IgA nephropathy | IgA1
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| Which pathway is activated in IgA nephropathy | alternative compliment pathway
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| 2 causes of secondary IgA nephropathy | celiac disease and liver disease
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| Teen presents with gross hematuria after respiratory infection a week before. Dx and outlook? | IgA nephropathy, variable
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| Classic findings in IgA nephropathy | mesangial widening with IgA and C3 in the mesangium
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| Hematuria with progression to renal failure, eye disorders Dx? And what else will be found with sensitive testing | Alport Syndrome and hearing deficiency
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| Cause of Alport Syndrome | defective collagen IV synthesis; a5 in X-linked variety
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| On EM of 2 brothers glomeruli: irregular foci of thickening alternating with attenuation of the GBM, splitting and lamination of the lamina densa “basket weave” appearance. Dx? | Alport syndrome
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| 2 diseases linked to defective type IV collagen | Alport and Thin Basement Membrane Lesion/Benign Familial Hematuria
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| Gross appearance of kidneys in Chronic glomerulonephritis | symmetrically contracted, diffusely granular cortical surface
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| Findings in a dialysis kidney (5/6) | arterial intimal thickening, calcifications, calcium oxalate crystals, cystic disease, increased renal adenomas and adenocarcinomas
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| Purpuric skin lesions on extensor surfaces of arms and legs and buttock; abdominal pain, GI bleed; non-migratory arthralgias; renal abnormalities | Henoch-Schonlein Purpura
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| Mesangial proliferation, IgA and C3 deposition in the mesangium. 2 DDx and what would differentiate | IgA nephropathy or Henoch-Schonlein Purpura; subepidermal hemorrhages and necrotizing vasculitis of small vessels, and GI manifestation
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| Arteriolar manifestation of diabetic nephropathy | hylanizing arteriolar sclerosis
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| Capillary basement membrane thickening, diffuse mesangial sclerosis, nodular glomerulosclerosis | diabetic nephropathy
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| Normal or enlarged kidneys with deposition of AL or AA type chains. Dx? | amyloid kidney
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| MCC of acute renal failure | AKI or ATN
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| 4 types of ATN/AKI: due to | ischemia, Direct toxic injury, Acute tubulointerstitial nephritis from drug hypersensitivity, urinary obstruction
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| 2 critical events in AKI | tubule cell injury and persistant/severe disturbance in blood flow
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| In AKI, loss of cell polarity causes what | abnormal ion transport, increase Na+ to distal tubules, causes vasoconstriction
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| What causes luminal obstruction in AKI | detached injured cells
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| Patchy tubular necrosis, in short lengths around straight segments of proximal tubule and ascending limb of Loop of Henle. Type of AKI? | Ischemic
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| Extensive necrosis along proximal convoluted tubule. Type of AKI | Toxic AKI
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| 2 areas most susceptible in ischemic AKI | straight portion of proximal tubule and ascending thick limb in medulla
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| Area most susceptible to toxic AKI | proximal convoluted tubule
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| 3 stages of AKI | initiation, maintenance and recovery
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| Findings in initiation phase of AKI | slight decline in urine output and rise in BUN
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| 5 findings of maintenance phase of AKI | sustained decrease in urine to 40-400ml/d; salt/water overload; rising BUN; hyperkalemia; metabolic acidosis
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| 6 Findings in recovery stage of AKI | increased urine output; loss of large amounts of water, sodium and potassium(hypokalemia); increase infection risk;BUN/Creatinine return to normal
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| Acute vs Chronic tubulointerstitial nephritis: interstitial edema, eos and neuts, focal tubular necrosis | Acute
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| Acute vs Chronic tubulointerstitial nephritis: mononuclear leukocytes, interstitial fibrosis, widespread tubular atrophy | chronic
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| (4 bugs) MCC of UTI (85%) | gram neg bacilli; E.coli; Proteus; Klebsiella; Enterobacter
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| MCC of clinical pyelo | ascending infection
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| Acute pyelonephritis with reflux: damage is mostly seen where? | upper and lower poles
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| Patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, and tubular necrosis Dx? | acute pyelonephritis
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| 3 complications in Acute Pyelo and their special circumstances | Papillary (coag)Necrosis: in Pt’s with DM and obstruction; Pyonephrosis: complete obstruction; Perinephric abscess: extension through renal capsule
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| What finding differentiates kidney from bladder Infx? | leukocyte casts
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| Cause of emerging pyelonephritis in transplant Pt’s | polyomavirus
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| Only 2 tubulointerstitial diseases that affect the renal calyces | chronic pyelonephrosis and analgesic nephropathy
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| 2 types of chronic pyelo | reflux and obstructive
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| MC type of chronic pyelo | reflux
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| Asymmetric scarring of kidney with coarse, discrete corticomedulary scars overlying blunted or deformed calyces, with flattened papilla | chronic pyelo
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| What do tubules look like in chronic pyelo | atrophy in some and hypertrophy or dilation in others
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| Foamy macrophages with plasma cells, lymphs and PMN cells in large yello/orange nodule in kidney. Not renal cell carcinoma. Dx and w. what Infx? | Xanthogranulomatous pyelonephritis; Proteus infx
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| Acute Drug induced interstitial nephritis: common drugs(3) and onset | synthetic penicillin, diuretics, NSAIDS, 15 days after drug exposure
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| Kindey injury in acute drug induced nephritis is cause by | IgE and/or cell mediated immune reaction; not the drug ie dose independent
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| Kindey interstitium edema and mononuclear infiltration; eos and neuts in clusters with plasma cells, normal glomeruli Dx? | acute drug induced interstitial nephritis
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| Analgesic nephropathy is cause by what 2 events, in order | papillary necrosis, then cortical tubulointerstitial nephritis from urine obstruction
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| 2 drugs causing Analgesic Nephropathy and their action | acetaminophen/phenacetin depletes glutathione causing ROS damage and aspirin inhibits vasodialation by PG
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| Normal or slightly small kidneys, cortical atrophy over papillary necrosis which are in various stages Dx? | Analgesic nephropathy
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| Cancer associate w/ analgesic pephropathy | transitional papillary carcinoma of the renal pelvis
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| Pink/blue tubular casts, angulated and/or fractured, surrounded by macrophages. Dx? | Bence-Jones proteinuria / Myeloma Kidney
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| Normal or slightly shrunken kidneys, leather grain on the outside | Benign nephrosclerosis
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| Medial and intimal thickening of small arteries in kidney with hyaline arteriosclerosis, microscopic subcapsular scars with sclerotic glomeruli | benign nephrosclerosis
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| Pts with malignant HTN with show what type of arterial disease in the kidney | malignant /accelerated nephrosclerosis
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| Early malignant nephrosclerosis shows (3) | fibrinoid necrosis of arterioles and small arteries, swelling of vascular intima, intravascular thrombus
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| Typical arteriopathy in malignant HTN that causes further narrowing of the lumen | hyperplastic arteriolosclerosis
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| “flea bitten kidney” Dx? | malignant nephrosclerosis
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| This finding represents an acute event in a person with HTN | fibrinoid necrosis of arterioles
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| Interlobular arteries and arterioles with proliferation of concentric smooth muscle cells, collagen, and clear layers Dx? 2 names and what it correlates with | onion-skinning, hyperplastic arteriolitis; renal failure
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| Initial cause of HTN with constriction of renal artery is due to | increased plasma renin
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| MCC of renal artery stenosis | plaque at the origin
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| MC location, age and sex for fibromuscular dysplasia of renal artery | medial thickening, 20-40yo, women, distal or medial portion of the artery
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| Typical HUS is most often associated with | consumption of food with Shiga-like toxin
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| MCC of TTP | deficiency of ADAMTS13, which regulates vWF
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| 2 MCC of Atypical HUS | mutation in compliment-regulatory proteins; or acquired endothelial injury
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| Initiating event in TTP vs HUS | TTP: platelet aggregation by vWF multimers; HUS: endothelial injury
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| What is usually present and causative in the majority of TTP Pts? | antibodies to ADAMTS13
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| Child Diarrhea then Sudden onset of bleeding, hematemesis, melena, severe oliguria, hematuria, microangiopathic hemolytic anemia, thrombocytopenia and HTN Dx? | typical HUS
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| MC deficiency in atypical HUS | factor H, compliment regulatory protein
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| How to differentiate TTP and HUS? | normal ADAMTS13 in HUS
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| Better outcome typical or atypical HUS? | typical
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| Fever, neurologic symptoms, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. CNS involvement is a dominant feature | TTP
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| Massive necrosis after an obstetrics emergency is usually limited to where? Dx? | cortex; diffuse cortical necrosis
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| Renal infarcts are usually of what type | white
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| Wedge shaped area of gray white color, depressed scar on cortex Dx? | renal infarct
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| Adult Polycystic Kidney Disease: Inheritance, cyst locations, outcome | AD; large multicystic kidneys, liver cysts, berry aneurysms; chronic renal failure at 40-60yo
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| Childhood Polycystic Kidney Disease: Inheritance, cyst locations, outcome | AR; enlarged, cystic kidneys at birth; variable, death in infancy or childhood
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| Medullary Sponge Kidney: Inheritance, cyst locations, outcome | none; medullary cysts on excretory urography; benign
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| Familial Juvenile Nephronopthisis: Inheritance, cyst locations, outcome | AR; corticomedullary cysts, shrunken kidneys; progressive renal failure starts in childhood
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| Adult-Onset medullary cystic disease: Inheritance, cyst locations, outcome | AD; Corticomedullary cysts, shrunken kidneys; chronic renal failure in adulthood
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| Simple Cysts: Inheritance, cyst locations, outcome | none; single or multiple cysts in normal sized kidney; benign
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| Acquired Renal Cystic Disease: Inheritance, cyst locations, outcome | none; Cystic degeneration in end-stage kidney disease; Dialysis dependant
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| MC mutation in ADPKD | PKD1
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| Better or worse prognosis with PKD1 mutation in ADPKD? | worse
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| Gene affected in ARPKD | PKHD1
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| Bilaterally Enlarged kidneys with smooth external appearance; numerous small cysts on section with dilated elongated channels at right angles to the cortex Dx? | ARPKD
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| Extra-renal disease with ARPKD | liver cysts with portal fibrosis
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| Extra-renal disease with ADPKD | cysts in the liver, intracranial berry aneurysm, mitral valve prolapse
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| Multiple cystic dilations of the collecting ducts in the medulla | Medullary sponge kidney
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| MC malignant kidney tumor in adults | renal cell carcinoma
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| MC malignant kidney tumor in children | Wilms tumor
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| On autopsy small tumor with the cortex, pale yellow, discrete, well circumscribed nodules, complex branching cuboidal cells Dx? | Renal Papillary Adenoma
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| Angiomyolipomas are present in 25-50% of Pts with | tuberous sclerosis
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| Clinical importance of angiomyolipoma? | likes to spontaneously hemorrhage
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| Solitary tumor in kidney, tan/brown, well-encapsulated, large eosinophilic cells, small round benign nuclei, lots of mitochondria. Dx? And what cell they come from | Oncocytoma; intercalated cells
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| Most significant risk factor for renal cell carcinoma | tobacco
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| MC type of renal cell carcinoma | Clear Cell Carcinoma
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| Loss of VHL on 3p leads to what tumor | hereditary and sporadic Clear Cell Carcinoma
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| Trisomy 7 leads to what renal tumor | sporadic and hereditary Papillary carcinoma
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| Mutated/activated MET leads to what renal tumor | sporadic and hereditary Papillary carcinoma
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| Renal tumor with pale eosinophilic cells, perinuclear halo, in solid sheets. Dx? | Chromophobe renal Carcinoma
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| Renal tumor: nest of malignant cells enmeshed within a prominent fibrotic stroma. Typically in the medulla | Collecting duct / Bellini Duct carcinoma
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