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Goljan Renal Path 1

What are podocytes? visceral epithelial cells
What are the spaces between the podocytes called? split pores
Which cells synthesize the glomerular BM? visceral epithelial cells (podocytes)
What keeps albumin out of urine? strong negative charge of Glomerular BM
What is responsible for charge of GBM? Heparan Sulfate (strong negative charge)
damage to visceral epithelial cell results in what? damage to BM and leaking of albumin into urine --> nephrotic syndrome
linear pattern outlining BM on Immunofluorescence goodpasture syndrome
subendothelial immune complex deposits in glomeruli on EM (granular) lupus
subepithelial immune complex deposits in glomeruli EM (granular) post-strep glomerulonephritis
only glomerulonephritis one can diagnose with IF IgA glomerulonephritis
granular pattern on IF. what does it mean? immunocomplex type III disease (membranous glomerulonephritis = immune complexes)
anti BM antibodies is what type of immune complex disease? Type II
RBC casts in urine is unique to what class of diseases nephritic syndromes
serum ANA shows rim pattern. what does that mean? anti-DNA --> lupus
crescentic glomerulonephritis is most commonly seen in what syndrome? goodpasture's syndrome
cholesterol casts in urine that when polarized look like maltese crosses. what is the diagnosis? nephrotic syndrome
why does lipoid nephrosis occur (Minimal change disease)? loss of negative charge of GBM
Nephrotic syndrome associated with HIV FSGS
glomerular problem in HBV diffuse membraneous glomerulonephritis
glomerular problem in HCV Membranoproliferative glomerulonephritis
vasculitis associated with HBV polyarteritis nodosa
large golf-ball appearing glomeruli on H&E diabetic nephropathy
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
ACE inhibitors do what to glomerular arterioles? less angiotensin II dilates efferent arteriole
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
properties of BUN blood urea nitrogen - secreted and reabsorbed in PCT
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)
normal BUN and Cr levels BUN: 9-10 Cr: 1 mg/dl
normal BUN/Cr 10
pre-renal azotemia normal kidneys, but reduced Cardiac Output (e.g. CHF), ergo, GFR decreases. BUN/Cr >20
most common cause of acute renal failure ischemic acute tubular necrosis
Cardiac output decreases and oliguria, what do you worry about most? ischemic acute tubular necrosis
Acute tubular necrosis associated with? renal ischemia (eg shock), crush injury (myoglobinuria), toxins
Acute renal failure values: BUN/Cr Prerenal: >20 Renal: <15 Postrenal: >15
Acute renal failure values: Urine Osmolality Prerenal: >500 Renal: <350 Postrenal: <350
Acute renal failure values: Urine Na Prerenal: <10 Renal: >20 Postrenal: >40
Created by: Asclepius