Kidney Pathology Flashcards
[diagnosis: glomerular response to injury]
acute, proliferation of mesangium/endothelial cells (hypercellularity), crescent formation
PSGN
[diagnosis: glomerular response to injury]
deposition of electron-dense material, synthesis of protein component of GBM, additional layers of BM matrices,
membranous nephropathy
[diagnosis: glomerular response to injury]
deposition of homogenous eosinophilic material, deposition of collagen
FSGS
[diagnosis]
hematuria, azotemia, edema, hypertension, variable proteinuria
nephritic syndrome
[diagnosis]
acute nephritis, proteinuria, acute renal failure
RPGN
[diagnosis]
> 3.5g/day proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria
nephrotic syndrome
[diagnosis]
azotemia, uremia progressing for months to years
chronic renal disease
[diagnosis]
Glomerular hematuria and/or subnephrotic proteinuria
isolated urinary abnormalities
[diagnosis]
diffuse global hypercellularity, swelling of endothelial cells, obliterates capillary lumina, tubulointerstitial edema and inflammation, with RBC casts
EM: subepithelial humps on GBM
IF: granular deposits of IgG, C3, and Ig within the wall and mesangium
PSAGN
[diagnosis]
prototype renal disease of type III hypersensitivity reactions
PSGN
laboratory finding elevated in PSGN after pyoderma
Anti DNAse B
[diagnosis]
progressive loss of renal function characterized by nephritic syndrome with severe oliguria
proliferation of parietal epithelial cells admixed with leukocytes infiltrating the glomerulus (“crescents”)
EM: rupture in GBM
IF: linear IgG and C3 deposits along GBM
RPGN TYPE I
AntiGBM Disease
Goodpasture Syndrome
[diagnosis]
progressive loss of renal function characterized by nephritic syndrome with severe oliguria
proliferation of parietal epithelial cells admixed with leukocytes infiltrating the glomerulus (“crescents”)
EM: lumpy bumpy appearance of GBM
IF: granular IgG and C3 deposits in GBM
RPGN type II
PSAGN, Lupus Nephritis, HSP, Buerger disease
[diagnosis]
progressive loss of renal function characterized by nephritic syndrome with severe oliguria
proliferation of parietal epithelial cells admixed with leukocytes infiltrating the glomerulus (“crescents”)
EM: no detectable deposits
IF: negative IgG and C3 deposits along GBM
RPGN type III
ANCA vasculitides
[diagnosis]
20 y/o male, active smoker with hemoptysis AND renal failure
necrotizing hemorrhagic interstitial pneumonitis + RPGN
RPGN Type I
Goodpasture Syndrome
20 y/o male, active smoker with hemoptysis AND renal failure
necrotizing hemorrhagic interstitial pneumonitis + RPGN LIMITED to kidneyonly
RPGN Type I
Anti-GBM disease
[diagnosis]
children, no azotemia, on recent prophylactic immunization, with nephrotic syndrome
LM: no changes
EM: uniform and diffuse effacement of foot processes of the podocyte
IF: no changes
Minimal Change Disease
[diagnosis]
adult, with SLE and EBV infection, taking NSAIDs
LM: diffuse thickening of capillary wall
EM: subepithelial deposits along GBM (spike and dome appearance); effacement of foot processes
IF: granular deposit of immunoglobulin and complement along the GBM
Membranous Glomerulonephropathy
[diagnosis]
adult, with HIV on heroin
LM: deposition of hyalin masses, increased mesangial matrix in nonaffected segments
EM: effaced foot process
IF: non-specific trapping of IgM and C3 in areas of hyalinosis
FSGS
[diagnosis]
patient with schistosomiasis
LM: thickened split GBM (tram track)
EM: subENDOthelial electron-dense deposits
IF: irregular, granular C3 deposit WITH IgG and C1q and C4
MPGN Type I
Both classical and alternative pathways are active
[diagnosis]
patient with Factor H mutation, with ESRD
LM: thickened split GBM (tram track)
EM: lamina densa and glomerular capillary transformed into irregular, ribbon-like, dense structure
IF: irregular, chunky, segmental linear foci of C3 deposits in GBM and mesangium WITHOUT IgG and complement
MPGN Type II
Alternative pathway is active
Also called Dense Deposit Disease
[diagnosis]
Young adult with previous GIT infection
LM: mesangial widening and endocapillary proliferation
EM: mesangial electron dense deposits
IF: mesangial deposition of IgA, often with C3 and properdin
localized to kidneys
IgA nephropathy (Berger Disease)
most common type of GN worldwide
IgA nephropathy
[diagnosis]
6 year old child with purpuric lesion, abdominal pain, intestinal bleeding, arthralgial with renal abnormalities
LM: mesangial widening and endocapillary proliferation
EM: mesangial electron dense deposits
IF: mesangial deposition of IgA, often with C3 and properdin
systemic deposition of IgA
HSP
