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Goljan Renal Path 1

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
What are podocytes?   visceral epithelial cells  
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What are the spaces between the podocytes called?   split pores  
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Which cells synthesize the glomerular BM?   visceral epithelial cells (podocytes)  
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What keeps albumin out of urine?   strong negative charge of Glomerular BM  
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What is responsible for charge of GBM?   Heparan Sulfate (strong negative charge)  
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damage to visceral epithelial cell results in what?   damage to BM and leaking of albumin into urine --> nephrotic syndrome  
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linear pattern outlining BM on Immunofluorescence   goodpasture syndrome  
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subendothelial immune complex deposits in glomeruli on EM (granular)   lupus  
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subepithelial immune complex deposits in glomeruli EM (granular)   post-strep glomerulonephritis  
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only glomerulonephritis one can diagnose with IF   IgA glomerulonephritis  
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granular pattern on IF. what does it mean?   immunocomplex type III disease (membranous glomerulonephritis = immune complexes)  
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anti BM antibodies is what type of immune complex disease?   Type II  
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RBC casts in urine is unique to what class of diseases   nephritic syndromes  
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serum ANA shows rim pattern. what does that mean?   anti-DNA --> lupus  
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crescentic glomerulonephritis is most commonly seen in what syndrome?   goodpasture's syndrome  
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cholesterol casts in urine that when polarized look like maltese crosses. what is the diagnosis?   nephrotic syndrome  
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why does lipoid nephrosis occur (Minimal change disease)?   loss of negative charge of GBM  
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Nephrotic syndrome associated with HIV   FSGS  
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glomerular problem in HBV   diffuse membraneous glomerulonephritis  
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glomerular problem in HCV   Membranoproliferative glomerulonephritis  
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vasculitis associated with HBV   polyarteritis nodosa  
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large golf-ball appearing glomeruli on H&E   diabetic nephropathy  
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what happens to the GFR and creatinine clearance in early diabetic nephropathy?   hyalinization of efferent arterioles, so Cr clearance and GFR increase. Also nonenzymatic glycosylation of BM cause microalbuminuria  
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ACE inhibitors do what to glomerular arterioles?   less angiotensin II dilates efferent arteriole  
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mesangial cells split BM on EM. C3 deposited adjacent to but not within dense deposits. serum C3 is very low. what is the diagnosis?   Type II membranoproliferative glomerulonephritis  
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properties of BUN   blood urea nitrogen - secreted and reabsorbed in PCT  
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properties of Creatinine   end-product of creatine - only filtered in kidney, neither reabsorbed nor secreted in kidney (can be in other places in very high levels)  
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normal BUN and Cr levels   BUN: 9-10 Cr: 1 mg/dl  
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normal BUN/Cr   10  
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pre-renal azotemia   normal kidneys, but reduced Cardiac Output (e.g. CHF), ergo, GFR decreases. BUN/Cr >20  
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most common cause of acute renal failure   ischemic acute tubular necrosis  
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Cardiac output decreases and oliguria, what do you worry about most?   ischemic acute tubular necrosis  
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Acute tubular necrosis associated with?   renal ischemia (eg shock), crush injury (myoglobinuria), toxins  
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Acute renal failure values: BUN/Cr   Prerenal: >20 Renal: <15 Postrenal: >15  
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Acute renal failure values: Urine Osmolality   Prerenal: >500 Renal: <350 Postrenal: <350  
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Acute renal failure values: Urine Na   Prerenal: <10 Renal: >20 Postrenal: >40  
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