Renal: glomerular disease Flashcards
nephritic syndrome
hematuria, proteinuria, azotemia, oliguria, edema, HTN
azotemia
increased BUN and Cr d/t dec GFR
nephrotic syndrome
proteinuria >3.5 g/d, edema, hyperlipidemia, lipiduria
rapidly progressive GN
ARF in days, hematuria, dysmorphic RBC and RBC casts and proteinuria, nephritis
acute renal failure sx
oliguria or anuria with azotemia
chronic renal failure sx
s/s of uremia (impaired renal excretory function + biochemical and endocrine abnormalities)
focal vs diffuse
focal is
segmental vs global
segmental is only part of glomerulus
global is all of glomerulus
sclerosis in kidney
increased ECM
primary renal causes of nephrotic syndrome
minimal change dz
focal segmental
membranous
membranoproliferative
secondary/systemic causes of nephrotic syndrome
amyloid
diabetes
SLE
minimal change disease epi
m/c nephrotic syndrome in kids, M>F
20% adults with nephrotic syndrome, M=F
minimal change dz pathogenesis
aka lipoid nephrosis
unknown cause, a/w recent URI or allergen exposure
? T-cell dysfxn -> lymphokines -> epithelial damage -> loss of charge and size selection -> albuminuria
*Selective loss of LMW proteins
minimal change dz clinical
edema and albuminuria with exacerbations and remissions
tx w empirical steroids, biopsy if no response
adults need biopsy to establish cause of nephrotic syndrome
minimal change dz histo
LM: normal
IF: normal
EM: fusion of foot processes
minimal change dz tx and prognosis
> 90% remit on steroids but recur
may remit spontaneously
few fail to respond to steroids or cytotoxic agents -> renal failure
*consider genetic d/o involving glomerular slit diaphragm (NPHS2 for podocin) if no response
FSGS epi and s/s
5-10% nephrotic syndromes in kids, up to 35% in adults (m/c cause)
heavy non-selective proteinuria
may have microscopic hematuria, reduced GFR, HTN
FSGS pathogenesis
idiopathic (HIV, heroin, podocin or cytoskeletal mutations), drug-induced, or inherited
may be a/w obesity or systemic dz
? in spectrum with MCD
epithelial cell damage d/t IgM and C3 deposits -> loss of size selectivity and charge
FSGS histo
segmental collapse of some glomerular tufts
hyalinosis (eos, PAS+ deposits on endothelial surface of GBM)
hypercellular mesangium with foam cells
adherence to Bowman’s capsule
IF: IgM and C3 in mesangium and subendothelial, thick GM
FSGS prognosis
most progress to RF slowly
some respond to steroids or cytotoxics
20% rapid decline -> RF in 2 yrs
25-50% recurrence after transplant