Glomerular Disease 1 Flashcards
(41 cards)
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