Group1 Flashcards
principle causes of ESRD (2)
44% diabetes, 27% HTN
glomerular barrier parts (3)
fenestrated capillary endothelium, basement membrane, podocyte foot processes with slit diaphragms made up of nephrin
normal urine proteins (amount, % of two major) and what level of proteinuria is nephrotic?
Normal urine has < 150 mg/day proteins: 45% Tamm Horsfall (secreted by TAL epithelium), 35% albumin (escapes reabsorption in PCT); if urine has more than 3.5 g/day it must be glomerular in origin
selective proteinuria: urine findings, mechanism, pathophys
pathophys: minimal change disease; mechanism: foot process effacement (loss of charge barrier?); urine: albumin, transferrin, no IgG (too big)
non-selective proteinuria
pathophys: most glomerulopathy other than min change disease; mechanism: foot process effacement (loss of size barrier?); urine: albumin, transferrin, IgG
proximal tubular dysfn proteinuria: urine findings, mechanism, pathophys
mech: decr reabs of filtered protein; pathophys: tubulo-interstitial dis, Fanconi; urine: <3 g day proteinuria (B2 microglobulin, lysozyme, albumin) along w/ other signs of PCT dysfn (glucose, bicarb, AA, etc.)
overload proteinuria: urine findings, mechanism, pathophys
pathophys: plasma cell dyscrasias (multiple myeloma); mech: incr # small, abnormal filterable serum proteins, these proteins can cause PCT toxicity/cast formation (prevent reabs of albumin); urine: <3 g day (non-glomelular), normal urine dipstick for protein (altho poss incr albumin), lots of IgG light chains (Bence Jones protein)
orthostatic proteinuria: urine findings, pathophys
pathophy: not pathological (seen in healthy teens/young adults); <2 g day proteinuria that appears in first morning urine when pt becomes upright
functional proteinuria
not pathological, seen in pts w/ high fever, CHF, cold exposure, resolves w/ resolution of precipitating event
best method for long term follow-up of proteinuria
spot urine protein:creatinine ratio
spot urine protein:creatinine ratio
best method for long-term follow-up; detects all protein; Upr/Ucr ~ 24 hr protein excretion (nl <.15) b/c Ucr ~ 1000 mg/day; this underestimates Upr in muscular men and overestimates Upr in elderly pts, but still useful for tracking vs time b/c Ucr shouldn’t change
nephrotic syndrome
non-inflammatory glomerulopathy (seen in CKD); syndrome: glomerular proteinuria (>3.5 g/day), hypoproteinemia, edema, hyperlipidemia
diff dx of edema (5)
proteinuria, renal failure, CHF, liver failure, protein malnutrition
complications of nephrotic syndrome (3)
hypercoagulability (due to loss of antithrombin proteins), infection, atherogenesis
histopathologies of nephrotic syndrome (3)
minimal change disease; focal segmental glomerulosclerosis; membranous glomerulopathy
mechs of injury in nephrotic syndrome (3)
minimal change -> unclear (T/B mediated); FSGS -> podocyte injury; MGN -> in-situ immune complex to some antigen on podocytes
minimal change disease: type of what, LM/FM/EM, etiology, demographics, tx (2), prognosis (3)
type of histopath in nephrotic syndrome; normal cx on LM, negative FM, but EM shows foot process effacement; etiology either primary (poss B/T cell mediated) or secondary (NSAIDs, lymphoma); seen mostly in kids; tx w/ corticosteroids for 6 weeks (90-95% remission) -> may give kids steroid trial rather than biopsy if they have nephrotic syndrome w/o HTN and hematuria and w/ normal GFR and C3; 33% never relapse after tx, 33% occasionally relapse, and 33% frequently relapse (>3 in 6 mos)
FSGS: type of what, LM/FM/EM, pathogenesis, FSGS factor, demographics (2)
type of histopath in nephrotic syndrome; LM has focal (some glomeruli) segmental (parts of these glomeruli) scleroris (too much ECM) w/ segmental collapse w/ adhesions to Bowman’s capsule, FM has IgM and C3 in mesangium of collapsed segments, EM has foot process effacement, focal podocyte injury or denudation of GBM, collapse of cap loops w/ accumulation of hyalin; pathogenesis: final common pathway for glom injury, due to podocyte injury w/ loss of podocytes in urine -> segmental sclerosis; may be due to uPAR (circulating factor, explains why transplanted kidneys can get FSGS in FSGS pts); common in elderly (infantile FSGS is monogenetic)
uPAR
circulating FSGS factor (explains why pts w/ FSGS can get FSGS in donated kidneys)
what disease has no findings on LM or FM but has foot process effacement on EM?
minimal change disease
what disease is assoc w/ injury and loss of podocytes?
FSGS
what disease has FM of IgM and C3 in mesangium?
FSGS
what disease has EM of foot process effacement, focal podocyte injury or denudation of GBM, collapse of capillary loops w/ accumulation of hyalin
FSGS
what nephrotic syndrome is common in kids?
minimal change disease