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157 Cards in this Set
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Nephrotic diseases by location of immune deposits |
1. Subendothelial: Type I membranoproliferative glomerulonephritis 2. Intramembranous: Type II membranoproliferative glomerulonephritis 3. Subepithelial: membranous glomerulonephritis 4. No immune deposits: minimal change disease, FSGS, systemic causes (diabetes/amyloid) |
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List the six nephrotic glomerulonephritis disorders |
Effacement of foot processes: 1. Minimal change disease 2. FSGS
Immune complex disorder: 3. Membranoproliferative glomerulonephritis (types I & II) 4. Membranous glomerulonephritis
Systemic causes: 5. Diabetes 6. Amyloidosi |
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Nephrotic syndrome: clinical, physical exam and laboratory findings |
Clinical findings: flank pain
Physical exam: edema (esp. periofrbital), sometimes HTN
Serum laboratory findings: - Hypercholesterolemia/hyperlipidemia - Hypoalbuminemia - Hypercoaguability (antithrombin III wastingf)
Urine laboratory findings: - Lipid casts - Proteinuria > 3.5 g/24 hr |
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Nephrotic syndrome: clinical consequences |
1. Renal failure 2. Hypercoagulability, thromboosis 3. Malnutrition and infection from protein loss 4. Hypocalcemia (less albumin binding) 5. Hyperlipidemia |
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What is meant by "hyperfiltration injury"? |
When some glomeruli are injured, increased pressure on the healthy glomeruli can accelerate their degeneration as well.
Additionally, in disorders like diabetic glomerulonephritis, narrowing of the efferent arteriolar lumen creates comparable hyperfiltration pressures on the existing glomeruli. |
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Physiology of edema in nephrotic syndrome |
Underfill pathway: hypoalbuminemia --> edema
Overflow pathway: Renin/angiotensin/aldosterone system detects lower volume status --> renal sodium retention --> propagation of edema |
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Hallmark of fatty cast on urinalysis |
Polarized maltese crosses |
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Epidemiology of minimal change disease |
Most common glomerulonephritis in children |
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Clinical course of miimal change disease |
Excellent response to steroids |
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Etiology of minimal change disease |
Usually idiopathic; association with non-Hodgekin's lymphoma |
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Pathology of minimal change disease |
H&E: normal Immunoflorescence: normal EM: effacement of foot processes |
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Clinical manifestations of minimal change disease |
Nephrotic system manifestations with SELECTIVE albumin proteinuria (light chains and immunoglobulins are not lost in urine) |
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Epidemiology of focal segmental glomerulosclerosis |
Most common nephrotic syndrome in adults, particularly in Hispanics and AfricanAmericans |
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Etiology of focal segmental glomerulosclerosis |
- Idiopathic - Reflux nephropathy - Heroin use - Sickle cell disease - HIV |
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Pathology of focal segmental glomerulosclerosis |
H&E: focal segmental eosinophilic glomerular sclerosis Immunoflorescence: non-specific findings due to trapping of complement and immunoglobulins (not immune complex deposition) EM: flattened "effaced" foot processes |
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Pathophysiology of focal segmental glomerulosclerosis |
1. Podocyte injury --> denudation and exposure of capillaries --> hyperfiltraiton injury 2. Anti-apolipoprotein L1 (APOL1_ antibodies have been implicated |
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Clinical course of focal segmental glomerulosclerosis |
Steroid resistance/dpeendence. High rate of recurrence, even w/renal transplant. 50% progression to ESRD. |
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Membranous glomerulonephritis: epidemiology |
Most common in caucasian adults |
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Membranous glomerulonephritis: physiology |
1. Primary: may involve native podocyte antigen phospholipase A2 receptor (PLA2R)
2. Secondary: circulating immune complexes from: - Malignancy - Lupus - Hep B >> Hep C - Medications (NSAIDs, penicillins) |
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Membranous glomerulonephritis: clinical course |
50% progress to ESRD, 50% have complete or partial remission w/corticosteorids |
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Membranous glomerulonephritis: pathology |
Electron microscopy: subepithelial depositsx w/spike & dome formation
H&E: thickening glomerular basement membrane, rigid open capillaries
Silver stain: open areas of glomerulus on Jones stain
Immunoflorescence: granular IgG & C3 |
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Nephrotic syndromes with low serum complement |
Membranous and membranoproliferative glomerulonephropathies |
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Membranoproliferative glomerulonephritis: etiology |
1. Primary: idiopathic
2. Secondary: - Hep C >> Hep B (Type I) - Infected ventriculoatrial shunt - Subacute bacterial endocarditis - Cryoglobulinemia |
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Membranoproliferative glomerulonephritis: pathology |
H&E: Mesangial proliferatio with thickening and duplication of BM ("tram tracks")
Immunoflorescence: granular C3 and IgG deposits
EM: - Type II: intramembranous deposits |
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Distinctive serum chemistry of membranoproliferative glomerulonephritis |
Serum C3 nephritic factor (type II only) |
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Which disorder has both a nephrotic and a nephritic version? |
Membranoproliferative glomerulonephritis |
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Physiology: type I vs type II membranoproliferative glomerulonephritis |
Type I: activation of classical complement pathway Type II: activation of alternative complement pathway |
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Epidemiology of diabetic nephropathy |
Most common cause of kidney disease leading to ESRD |
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Diabetic nephropathy: pathophysiology |
Diabetes --> hyperglycemia --> non-enzymatic glycosylation of BM --> preferential narrowing of efferent arteriolar lumen --> hyperfiltration injury |
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Diabetic nephropathy: pathology |
H&E: Kimmelstiel-Wilson nodules, thickened glomerular BM, hypertensive findings (hyaline arterioloscelerosis) |
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Diabetic nephropathy: clinical course |
Immediate presentation in T1DM, insidious onset in TIIDM
Control of hyperglycemia and hypertension and/or pancreatic transplantation can reverse nephropathy. ACEi's are particularly helpful given vasodilatory effect on efferent arteriole. |
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Amyloidosis nephropathy: etiology and pathology |
Etiology: lamda light-chain amyloidosis
Pathology: - H&E: mesangial nodules - EM: randomly arranged fibrils - Immunoflorescence: congo red apple-reen birefringence |
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Clinical features, physical exam findings and laboratory findings in nephritic sydnrome |
Clinical finding: flank pain
Physical exam: - Edema (esp. periorbital) - HTN - Reduced GFR
Laboratory findings: - Hematuria/dysmorphic RBCs/RBC casts (defining feature of nephritic syndrome) - May have low-grade proteinuria, but <3.5 g/24 hr |
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IgA nephropahty: epidemiology |
Most common glomerulonephritis worldwine, esp. southeast Asians and Hispanics |
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IgA nephropahty: pathogenesis |
Immune defect resulting in: - Defective galactosylation of IgA1 - Decreased clearance of IgA1 - Increased IgA production |
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IgA nephropahty: pathology |
H&E: mesangial inflammation and proliferaiton EM: Subendothelial IgA deposits |
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IgA nephropahty: clinical presentaiton |
Accompanied by mucosal infection (i.e. URI); onset in a few days. Also associated with celiac disease and cirrhosis. |
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IgA nephropahty: clinical course |
Progression to ESRD in 20-50% of cases. |
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Acute proliferative post-streptococcal (post infectious) glomerulonephritis: etiology |
Delayed reaction to nephitogenetic antigen (aM protein virulence factor), most commonly as a result of streptococcal strains.
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Acute proliferative post-streptococcal (post infectious) glomerulonephritis: clinical course |
Supportive care; children usually recover, adults may progress to RPGN |
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Acute proliferative post-streptococcal (post infectious) glomerulonephritis: pathology |
H&E: neutrophilic infiltration with globular appearance Immunoflorescence: IgG, C3 and IgM granular, chunky, "starry sky" appearance EM: subepithelial "humps" |
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EM immune deposits in nephritic disorders |
1. Subendothelial IgA deposits: IgA nephropathy 2. Subepithelial humps: post-infectious glomerulonephritis |
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Rapidly progressing glomerulonephritis: pathology |
H&E: glomeruli dwith characteristic macrophage/fibrin crescents secondary to BM rupture
Immunoflorescence: depends on subtype Anti-GBM/Goodpasture's: linear Immune complex disease :granular Pauci-immune: nonspecific immunoflorescence findings |
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What is the most severe glomerulonephritis? |
Rapidly progressing (crescentic) glomerulonephritis |
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Rapidly progressing glomerulonephritis: etiolgoy |
1. Anti-GBM/Goodpasture's: antibodies against alpha 3 chain of collagen IV
2. Immune complex: - Lupus - Vasculitities - Post-infectious - IgA nephropathy |
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Distinguishing between etiologies of rapidly progressing glomerulonephritis |
1. Immunoflorescence 2. ANCA (indicates immune complex disorder) 3. Pulmonary involvement: Goodpasture's, UNLESS there is concomitant nasopharyngeal disease (then it's Polyangitis with Granulomatosis) 4. Normal complement --> Pauci immune |
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Alport's disease: definition, clinical manifestations, and pathology |
Definition: X-linked inherited nephritis involving defective collagne IV synthesis.
Clinical manifestations: nephritis accompanied by hearing loss and occular disturbances.
Pathology: multi-layering of lamina denas |
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Henoch-Schoenlein purpura |
IgA nephropathy with skin involvement |
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Prognostic indicators in ATN |
Worse prognosis w/olguria (<400 mL/day) |
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ATN: pathogenesis |
1. Predisposition to ischemia: medullary interstitium & loop of henle is particularly susceptible to ischemia due to paucity of vasa recta 2. Susceptibility to toxic injury, as concentrations are highest in the tubules 3. Reperfusion injury dure to calcium and oxygen free radicals 4. Decreased GFR due to tubular obstruction and increased hydrostatic pressure in Bowman's capsule |
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Why does ATN lead to a buildup of toxins in the interstitial space? |
ATN --> tubular damage --> indiscriminate substance reabsorption into the interstitium |
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Risk factors for ATN |
1. DM 2. Cirrhosis 3. CKD 4. S/p cardiac surgery |
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How is the location of ischemic vs. toxic ATN different? |
Ischemic: PCT + ascending limb Toxic: PCT + descending limb |
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Etiology of ischemic ATN |
Disruption in renal blood flow: s/p MI. s/p surgery, etc. |
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Etiology of toxic ATN |
1. Aminoglycoside antibiotics 2. Hemoglobin (massive transfusion reaction) 3. Myoglobin (rhabdomyolysis) 4.Cis platinum (chemo) 5. Etylene gycol |
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IV contrast nephropathy |
Most common form of ATN; stimulates afferent arteriole vasoconstriction, so produces both toxic and ischemic injury. |
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Ethylene glycol induced ATN: pathology |
Vacuolization in renal tubule cells & birefringent dumbbell-shaped crystal |
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Gross pathology of ATN |
Nephromegaly + swelling & redness of the renal parenchyma |
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Pathological cascade in ATN |
1. Reversible injury - Interstitial edema - Blebbing - Apoptosis: decrease in ATP and increase in cytosolic Ca2+ - Loss of cellular polarity (basolateral Na+/K+ ATPase can often be found on luinal surface)
2. Irreversible changes - Decreased adhesion, deatchment from BM and sloughing of cells - Luminal obstruction w/intercellular debris --> increased intratubular pressure and decreased GFR - RTE and granular cast formation - Rupture of tubular BM (ischemic injury only)
3. Regenerative changes: mitotic bodies in tubular epithelium. Removal of large bodies of urine + loss of concentrating ability --> polyuria, which is followed by a fall in creatinine. |
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Clinical manifestations of AIN
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Rise in creatinine w/constitutional symptoms (fever, rash, etc.) Often manifests 2-3 weeks after exposure, unless it is a secondary exposure. |
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Laboratory findings of AIN |
- Hematuria - Urine leukocyte esterase - Leukocyturia often including eosinophils - Urine WBC casts - Mild proteinuria - Serum eosinophilia |
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Etiologies of AIN |
Idiopathic or medication induced - Antibiotics - NSAIDs - DIruetics - Anticonvulsants - Herbal medications (Aristolochic acid - snake bites, RA) |
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Pathogenesis of AIN |
Drug or unk antigen forms a hapten, that elicits immunologic response when bound to tubular cells --> IgE-mediated or T-cell mediated attack of tubules or BM |
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Is the severity of AIN dose-dependent? |
NO! |
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AIN: pathology |
1. Leukocytes in interstitium (esp. eosinophils 2. Sparing of glomeruli 3. Immunolforescence: antibodies to tubular BM, esp. when pencillin-related 4. Interstitial fibrosis and scaring if chronic |
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Pathology of Aristocholic acid AIN |
Paucity of immune cells |
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Analgesic nephropathy: etiology |
10-20 years analgesic use: phenacetin, aspirin, caffeine and/or acetominophen. |
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Analgesic nephropathy: pathology |
Chronic AIN + renal papillary necorsis |
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Analgesic nephropathy: clinical manifestations |
1. Renal colic pain and obstruction from tubular obstruction 3. UTI 4. Extrarenal symptoms: headache, GI, HTN |
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Pathology of urate nephropathy |
Uric acid stones grossly, microphytus (deposition of uric acid stones in inerstitium) and mononuclear giant cell reaction on histopath if chronic. |
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Etiologies of chronic hypercalcemic tubulointerstitial nephritis |
1. Multiple myeloma 2. Hyperparathyroidism 3. Metastatic disease to bone |
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Pathophysiology of chronic hypercalcemic tubulointerstitial nephritis |
Calcium stones --> tubular damage --> inability to concentrate urine -- > chronic tubulointerstitial nephritis |
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Bence Jones proteinura: definition and pathophysiology |
Definition: cast nephropathy seecondary to multiple myeloma
Pathogenesis: light chain proteinuria that bind to Tamm-Horsfall proteins --> obstruciton, inflammation, giant cell reaction
Chronic tubulointerstitial nephritis --> hypercalcemia, hyperuricemia and amyloidosis |
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Pathology of myeloma cast nephropathy |
Elongated, dilated tubules filled w/proteinaceous material produced by malignant cells |
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Renal cell carcinoma: risk factors (7) |
1. Male gender 2. Age > 60 3. HTN & obesity 4. Smoking 5. Heavy metals (cadminium) 6. Acquired polycystic kidney disease from dialysis ESRD 7. Tuberous sclerosis |
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Renal cell carcinoma: clinical presentation |
- Triad: costovertebral pain, hematuria and palpable abdominal mass - Often asymptomatic growth - Mets to bone and lung |
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Renal cell carcinoma: paraneoplastic syndromes (6) |
1. Polycythemia 2. HTN 3. Hypercalcemia 4. Hepatic dysfunction 5. Masculinization/feminization 6. Cushing's syndrome |
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Renal cell carcinoma: staging |
Stage 1: small, local Stage 2: large, local Stage 3: invasion of renal vein or peripheral tissue Stage 4: extrarenal or ipsilateral adrenal spread |
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Clear cell carcinoma: origin |
PCT |
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Clear cell carcinoma: indicdence |
70-80% RCCs |
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Clear cell carcinoma: gross pathology |
- Well circumscribed, solitary mass - Yellow orange color (lipid accumulation) - Often hemorrhagic - Dramatic invasion of renal vein |
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Clear cell carcinoma: cytopathology (sporadic form) |
Twohit inactivation of both VHL alleles (chromosome 3) to form cysts, plus additional mutations for carcinoma.
Normal VHL function: degradation of HIFalpha > inhibition of transcription of VEDF, TGFalpha and IGF1 |
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Clear cell carcinoma: inherited form |
VonHippelLindau Disease: autosomal dominant inheritance of one defective VHL allele.
Carcinogenesis thus only requires a single VHL hit to produce cysts, and the additional mutations to produce carcinoma.
Renal presentation is multifocal, bilateral clear cell RCC at an earlier age (3545 YO) |
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Papillary renal cell carcinoma: origin |
Mixed morphology from PCT and DCT |
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Papillary renal cell carcinoma: incidence |
10-15% RCCs |
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Papillary renal cell carcinoma: gross pathology |
Cystic, wellcircumscribed, sometimes hemorrhagic mass. Often bilateral/multifocal, even in spontaneous forms. |
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Papillary renal cell carcinoma: histopathology |
Papillary formations with foamy macrophage papillary core |
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Papillary renal cell carcinoma: cytogenetics (sporadic form) |
- Trisomy 7, 16 or 17 - Loss of Y chromosome - MET activation (rare) |
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Papillary renal cell carcinoma: inherited forms |
1. Hereditary papillary RCC (HPRCC) - Autosomal dominant MET activation - Cytopathology: MET activation (constitutive activity of hepatocyte growth factor receptor linked tyrosine kinase) + trisomy 7 - Multiple, bilateral papillary RCCs, but no extrarenal tumors
2. Hereditary Leimyomatosis and RCC (HLRCC) - Krebs cycle fumarate hyratase tumor suppressor gene inactivation --> no accumulation of fumarate --> no inhibition of HIF-alpha --> transcription of VEGF, TGF-alpha, IGF-1 - Associated with uterus and skin leiomyomatosis - 1/3 of patients develop solitary papillary RCC |
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Which renal cell carcinoma is most common in ESRD dialysis patients? |
Papillary RCC |
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Chromophobe renal cell carcinoma: incidence |
5% of RCCs |
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Chromophobe renal cell carcinoma: origin |
Intercalated cells of the collecting duct |
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Chromophobe renal cell carcinoma: prognosis |
Excellent (80-95% 5 yr survival) |
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Chromophobe renal cell carcinoma: gross pathology |
Tan-mahogany, well-circumscribed masses |
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Chromophobe renal cell carcinoma: histopathology |
- Pale cytoplasm (but still more eosinophilic than clear cell) - Concentrated around vasculature - Perinuclear halos - Raisinoid, irregular, wrinkled nuclei |
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Chromophobe renal cell carcinoma: sporadic cytopathology |
Monoploidy (hypodiploidy) |
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Chromophobe renal cell carcinoma: inherited form |
Birt-Hog-gDube syndroeme: BHD gene mutation causing defective folliculin. Manifests w/chromophobe RCC, skin and lung tumors.a |
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Collecting duct RCC: risk factors |
Medullary subtype w/African Americans w/sickle cell trait |
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Collecting duct RCC: incidence |
Rare (1% RCCs) |
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Collecting duct RCC: prognosis |
Poor (25% 2 yr survival) |
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Collecting duct RCC: gross path |
Pale gray-white masses |
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Oncocytoma: origin |
Intercalated cells of the collecting duct |
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Oncocytoma: gross appearance |
Tan-mahogany mass w/pale central scar |
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Oncocytoma: histopathology |
Nesting pattern w/eosinophilic, granular cytoplasm (from lots of mitochondria) |
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Oncocytoma: prognosis |
Completely benign, but must be distinguished from chromophobe RCC |
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Renal papillary adenoma |
Same as papillary RCC but <0.5 cm large |
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Angiomyolipoma: etiology |
Sporadic or syndromic (tuberous sclerosis, in the context of neuro and developmental deficits). |
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Angiomyolipoma: prognosis |
Benign, but run risk of hemorrhage |
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Angiomyolipoma: histopathology |
Consists of blood vessels, smooth muscle and fat |
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Papillary RCC: prognosis |
Fair (50-85% 5year survival) |
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List the benign kidney tumors |
1. Oncocytoma 2. Renal papillary adenoma 3. Angiomyolipoma |
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Risk factors for urinary bladder tumors (7) |
1. Male gender 2. Age >60 3. Smoking 4. Industrial carcinogens (aromatic hydrocarbons, dyes, etc.) 5. Shcistosoma hematobium 6. Drugs (analgesics, etc.) 7. Radiation therapy for other UG disease |
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Clinical presentation of urinary bladder tumors |
Painless hematuria, sometimes w/obstruciton |
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Inherited urinary bladder tumors |
There are none (all sporadic) |
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Staging of urinary bladder tumors |
- In situ (Tis/Ta) - Invasion to lamina propia (T1) - Invasion to detrusor muscle (T2) - Invasion into perivascular soft tissue (T3) - Invasion to adjacent organs (T4) |
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Papillary uroepithelial tumors: prognosis |
Vast majority are noninvasive. They do, however, often recur after resection. |
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Papillary uroepithelial tumors: cytopathology |
Activation of pro-oncogene HRAS & FGFR3. Rare progression to high-grade lesion requires Rb or P53 mutations. |
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Papillary uroepithelial tumors: histopathology |
Papilloma: normal uroepthelium w/papilalry architecture.
PUNLMP: thick uroepithelium (>7 layers) and papillary architecturea
Low-grade Papillary uroepithelial carcinoma: minimal but definitive cytologic atypia (hyperchromatic nuclei, thick urothelial lining, etc.
High-grade papillary urothelial carcinoma: definitive atypia including loss of cell polarity, nuclear pleiomorphism, mitotic figures, etc. |
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Schistosoma hematobium carcinogenesis? |
Causes squamous cell carcinoma and frequently produces urinary stones. |
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Flat uroepithelial tumors: gross appearance |
Flat mucosal reddening; often multifocal |
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Flat uroepithelial tumors: histopathology |
Discohesion, denuding and shedding |
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Flat uroepithelial tumors: cytopathology |
p53, Rb, 8-8p and 17p mutations |
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Flat uroepithelial tumors: prognosis |
Initially benign, but will often progress to invasive subtypes |
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Etiologies of urinary obstruction |
1. Intratubular/intraluminal: stones 2. Intramural: bladder tumor 3. Extrinsic compression: BPH, pelvic mass 4. Functional obstruction: neurogenic bladder |
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Pathogenesis of urinary obstruction |
1. Early: compensated GFR (afferent arteriolar vasoconstriciton/efferent arteriolar vasodilation)
2. Mid: decompensated GFR, decreased Na+ delivery --> thromboxane A2 --> propagation
3. Late: GFR severely impaired. Intratubular pressure returns to normal due to tubular dilation and lymphatic drainage.
4. Post-obstructive: osmotic diuresis, impaired sodium & water handling and ADH insensitivity --> polyuria. Watch out for hypovolemia and hyperkalemia, and replace electrolytes & fluid if necessary. |
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Historical features, physical exam findings and laboratory findings with urinary obstruction |
1. Historical features: - Unilateral: flank pain/fullness; severe if etiology = stone - Bilateral: suprapubic pain/fullness, small-volume frequent urination of obstruction is partial, anuria if total bilateral obstruction.
2. Physical exam features: - Flank or suprapubic tenderness -
3. Laboratory findings - High BUN/creatinine if obstruction is bilateral (will likely be compensated if unilateral) - Confusing urine electrolytes - Hematuria and urine crystals if stones is the etiology - Hyperkalemia - Metabolic acidosis - Post-voidal residual > 100 - Stones/hydronephrosis on ultrasound & CT |
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Treatment of urinary obstruction |
1. Relief of obstruction (complete obstruction --> irreversible damage if obstruction isn't relieved in at least a week)
2. Permanent measures: percutaenous nephrostomy tube, uretal stent |
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Urolithaisis/nephrolithaisis: epidemiology |
- White dudes from the south - Higher male incidence in summer, higher female incidence in early winter - Onset at age 20-30; high rate of recurrence |
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Urolithaisis/nephrolithaisis: predisposing congenital factors (4) |
1. Horseshoe kidney 2. Medullary sponge kidney 3. Polycystic kidney disease 4. Cysteinuria |
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Urolithaisis/nephrolithaisis: pathogenesis |
1. Supersaturation (mulitfactorial) 2. Nucleation: attachment to epithelial surface 3. Growth (years/months/weeks): encouraged by urinary stasis. |
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Factors that encourage supersaturation (--> stone formation) |
1. Hypercalciuria - Diet: high sodium, low carbohydrate - Hyperparathyroidism - Renal tubular acidosis - Sacroidosis
2. Hyperoxaluria - Diet: high oxalate, low calcium - Colonic disorders (Crohn's, ileal bypass, etc.) - Primary congenital hyperoxaluria TI & TII |
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Factors that inhibit supersaturation (--> stone formation) |
- Citrate - Magnesium - Nephrocalcin - Tamm-Horsfall protein |
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Urolithaisis/nephrolithaisis: clinical manifestations |
- Abrupt onset of severe, colicky flank pain that radiates to groin - Gross or microscopic hematuria - Nausea/vomiting - Ileal immotility (rarely) - Low-grade fever |
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Urolithaisis/nephrolithaisis: laboratory findings |
- Hematuria - +/- crystals in urine - Elevated WBC count |
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Urolithaisis/nephrolithaisis: stone appearance |
- Calcium oxalate: envelope - Uric acid: rhomboid - Struvite: coffin lids - Cysteine: hexagonal |
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Treatment of calcium oxalate stones (4) |
- Increase in fluid intake - Dietary sodium, protein and oxalate restriction - Thiazide diuretics to decrease Ca2+ excretion - Calcium and potassium citrate supplementation |
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Treatment of uric acid stones (5) |
- Increase in fluid intake - Urine alkalization - Purine restriction in diet - Gout: Allopurinol, NOT Probenecid - Calcium oxalate stone prophylaxis (uric acid can form nidus for calcium oxalate stones) |
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Etiology, clinical manifestations and treatment of struvite stones |
Etiology: urea-splitting bacteria (Proteus/Providencia)
Clinical manifestations: stone (hematuria, severe pain) + basic urine
Rx: surgical removal + antibiotics |
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#1 difference between clinical appearance of urinary stone vs. pyelonephritis |
High-grade fever with pyelonephritis; low grade fever w/stones |
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Mortality from AKI |
50% |
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Complications of AKI |
1. Hypervolemia 2. Uremia 3. Electrolyte abnormalities: - Hyperkalemia - Metabolic acidosis - Hypocalcemia - Hyperphosphatemia |
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Pathophysiology of each category of AKI etiologies |
Recall starling forces equation:
1. Prerenal: decrease in glomerular capillary filtration pressure --> decreased ∆P 2. Intrinsic renal: luminal occlusion --> increased Bowman's space pressure --> decreased ∆ 3. Postrenal: luminal occlusion --> increased Bowman's space pressure --> decreased ∆ |
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Separating etiologies in AKI |
1. Prerenal: evidence of volume depletion and sodium avidity - History: orthostatic hypotension - Physical exam: decreased skin turgor, dry mucous membranes, hypotension, tachycardia - Lab: high BUN/creatinine, low fractional excretion of sodium, low urine sodium, bland urine sediment.
2. Intrinsic renal: inability to concentrate urine --> high urine sodium and FeNa, low serum osmolality, normal BUN:Creatinine, exciting urine sediment
3. Postrenal: postvoidal residual >150 mL |
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Etiologies of prerenal AKI |
1. Hypovolemia: - Gastrointestinal Na+/H2O losses - Renal Na+/H2O losses - Third spacing - Bleeding
2. Systemic hypoperfusion: - Vasodilation (shock) - CHF - Decreased blood osmolality: nephrotic syndrome, cirrhosis, hepatorenal syndrome
3. Decreased renal perfusion: bilateral renal artery stenosis, NSAIDs, ACEIs |
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Etiologies of intrinsic renal AKI and their distinctive findings |
1. Vascular: renal vein thrombosis, vasculiitis, etc.: ANCA & other distinctive serum chemistry
2. Primary or secondary glomerular disease: RBC casts
3. ATN (ischemic or toxic): Granular casts ("muddy brown")
4. AIN: WBC casts |
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Hepatorenal syndrome: definition, pathophysiology and distinction from cirrhosis |
Definition: decrease in intravascular volume due to poor oncotic pressure
Pathophysiology: third spacing and compensatory mechanisms, as well as vasodilation that disproportionately affects splanchnic vessels and promotes third pacing.
Distinction from cirrhosis: refractory to volume repletion |
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Epidemiology of CKD |
Higher among African Americans and Native Americans |
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CKD staging |
Stage 1: GFR >90 mL/min Stage 2: GFR = 60-90 mL/min Stage 3: GFR = 30-60 mL/min Stage 4: GFR = 15-30 mL/min Stage 5: GFR <15 mL/min
Stage 1 and stage 2 are nbd. Stage 3 requires management and may begin to clinically manifest Stage 4 may need dialysis Stage 5 is ESRD |
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Pathophysiology of CKD |
- Initial insult = pathogenesis - Disease propogates even after withdrawal of initial insult due to compensatory hemodynamic changes and hyperfiltration damage & progressive sclerosis in the good nephrons |
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CKD etiologies (6) |
1. Diabetes mellitus 2. Hyperensive nephrosclerosis 3. Chronic glomerulonephritis 4. Tubulointerstitial diseae 5. Polycystic kidney disease 6. Renal vascular disease |
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Clinical manifestations of CKD |
1. Hypervolemia (edema & HTN)
2. Electrolyte abnormalities arising from renal tubular excretion and reabsorption: - Hyponatremia - Hyperkalemia - Metabolic acidosis
3. Hormonal defects: - Anemia - Prolonged bleeding time - Renal osteodistrophy
4. Proteinuria secondary to glomerular damage (+/-)
5. Uremia |
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Renal osteodystrophy pathphysiology |
Dysregulation of calcium that results from: - Decreased GFR leading to decreased phosphorous excretion - Decreased vitamin D metabolism leading to hypocalcemia - Hyperphosphatemia + hypocalcemia leading to hyperparathyroidism - Metabolic acidosis leading to increased bone reabsorption
Resulting in: Bony abnormalities, slow bone growth, bone pain, frequent fractures. Precipitation of calcium in vessels (calciphylaxis), causing ulcers |
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Treatment of renal osteodystrophy |
Phosphate binders, vitamin D |
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Uremia symptoms |
1. Constitutional: fatigue, lethargy 2. GI: nausea, vomiting, anorexia 3. Cardiac; pericardial effusion & pericarditis 4. Neuro: sleep disturbances, neuropathies, confusion, depression, muscle twitches 5. Skin: pruritis 6. Sexual dysfunction |
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How do you distinguish between HTN and DM CKD? |
More proteinuria earlier on with diabetic nephropathy |
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Management of CKD |
1. Delay progression - BP control <140/90 (130/80 w/proteinuria) - Control of proteinuria with ACEIs/ARBs & protein restriction - Avoidance of nephrotoxic agents
2. Treat complications - Renal osteodystrophy: calcium, phosphate, Vitamin D - Erythropoetin replacement and iron supplementation |
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How good is hemodialysis at replicating kindey function |
Operates at about 15% normal GFR :( |
