Glomerular Disease 1 Flashcards
how does glomerular disease present?
Hematuria (quality)
Loss of GFR (temporal change)
Proteinuria (quantity)
factors of nephrotic syndrome
Proteinuria >3.5 g/day
Hypoalbuminemia
Edema
Hyperlipidemia (increased hepatic production)
Lipiduria
Hypercaogulabiltiy (loss of anticoag C and S)
nephrtitis
mild proteinuria
**Hematuria **(RBCs, RBC casts, dysmorphic RBCs)
HTN
Edema
causes of acute glomerulonephritis
IgA nephropathy
Post-infectious GN
Anti-GMB disease / good pastures
small vessel vasculitis
lupus nephritis
membranproliferative GN
(I poop good, small, little, marbels)
most common Gn
IgA nephropahty
most prominent feature IgA nephropathy
hematuria (50-60% episodic, 30% persistent, 10% acute Gn or nerphtoic syndrome)
presentation IgA nephropathy
Dysuria
Loin Pain
Hematuria
co-present w/ URI (synpharrngitic hematuria)
pos HTN
Histology IgA nephopathy
LM - messangianl hypercellularity, scelorosis+necrosis with crescents
IF: **Msangial IgA deposition **
EM- mesangional paramesangial elctron dense deposits
treatment IgA nephropathy
fish oil may slow
ACE
corticosteroids or other immunosuppresants
presentation Henoch-Schonlein Purpura
skin non blanching pupura on legs+buttucks
transient arthraligias
GI (hematochezia)
kidney - hematuria, proteinuria
infection presentation post infectious GN
7-14 days post pahryngitis, 14-28 post skin infection (esp A beta hemolytic strep)
clinical presentatiion Post strep GN
sudden onset HTN
azotemia
oliguria
edema
tea-colored urine
**Labs: **low C3 comp, ASO elevated, RBC casts in urine, proteinuria
histo post strep GN
LM - enlarged hypercell. glomeruli
diffuse mesangial+endocapilary proliferation with PMNs
crescents
**IF **granular capillary wall, mesangial IgG and C3
EM: Mesangial and large subepithelial humb-like deposits
causes of rapidly progressive GN
description
classic nephritic syndrome with rapid progression to renal failure
anti GBM / Goodpastures
ANCA asssociated GN (Pauci Immune)
histo rapidily progressive GN
crescentic
early segmental necrosis early
cause of Anti GBM / goodpastures
circulating anti GBM antibody (antigen is a3chain of type IV collagen)
posible presentation of Anti-GBM ./ goodpastures
Males>femailes
pulmonary renal syndome: hemoptysis, pulmonary infiltrates, glomerulonephritis
diagnosis/ treatment anti-GBM / goodpastures
antiGBM in blood
Linear IgG and C3 on kidney biospy IF
plasmapheresis, prednisone, cytoxan
crescenteric GN with little deposition of immune reactants
Pauci-immune
pauci - immune GN possibly associated with
ANCA vasculititis
differentiation
microscopic polyangiitis
wegner’s granulomatosis
churg straus
**microscopic polyangiitis: **no granulomatous inflam, no asthma
wegner’s granulomatosis: necrtizing granulomatous inflam, no asthma
**churg strauss: **necrotizing granulomatous inflam, asthma, eosinophilia
renal biopsy wegenrs
cresenteric GN without immune deposits
treatment for all causes of nephrotic syndrome
ACE/ARBs to lower pressure+reduce proteinuria
Statins reduce lipids
diuretics+salt restriction to improve edema
most common cause of nephrotic syndrome in children
minimal change disease
adult associations minimal change disease
NSAIDs
neoplasms esp Hodgkins Lymphoma
Syphilis, HIV
histo Minimal change disease
LM: glmeruli intersitium and tubules normal
IF negative or mesangial IgM
EM: podocyte foot process effacement (fusion)
treatment minimal change disease
corticosteroids (adults take longer, more remission)
most common cause of nephrotic syndrome in cuacasian adults
membranous nephropathy
secondary causes membranous nephrpathy
infection (HBV)
Connective tissue disease (SLE)
Neoplasms: carcinoma of lung, colon, stomach or breast, Non hodkin’s lymphoma
Drugs
presentation membranous nephropathy
heavy proteinuria and nephrotic syndrome
HTN and azotemia later
renal vein thrombosis in 20%
histo membranous nephropathy
LM: diffuse thickening of GBM, GBM spikes on silver stain
IF: granular GBM deposits of IgG
EM: subepithelial depsoits
membranous nephropathy outcome
1/3 spontaneous remission
1/3 partial remissions + stable
1/3 slow progressive loss of renal function
treatment Membranous neropathy
ok prognosis : ACE or ARB
poor prognosis : steroids or other immunosuprresion
most common casue of nephrotic syndrome in African americans
focal segmental glomerulosclerosis
presentation focal segmental glomerulosclerosis
HTN
Hematuria
end stage renal disease in 5 years
primary = acute onset nephrotic syndrome
secondary: slow renal insufficiency+ proteinuria
cauases secondary FSGS
Drugs - NSAIDs, heroin
infections HIV
obesity
past glomerular injury
loss of renal mass
histology focal segmental glomerular sclerosis
LM: glomerular scloeriss with capilalry colapse, hyaline and lipid deposits in bowman’s capsule
IF: negative or IgM and c3 in mesangium or in segmental scars
EM: podocyte foot process effacemen,t segmental sclerosis
treatment FSGS
ACE, corticosteroids,
presentation membranoproliferative glomerulonephrtiis
proteinuria+hematuria
HTN
low C3 complement
variable (nephrotic/asympotomatic preteinuria+hematuria/acute GN)
secondary causss PRGN
connective tissue disease (SLE)
Cryoglobulinemia
Infection: **Hep C, **Hep B, endocarditis, abscesses
neoplasm
histo MPGN
LM: hypercellular glomeruli, endocapillary prlif, lobular apparing glomeruli
IF: granular C3 depotsits
EM: subendothelial deposits
