3.7.3 Path: Nephritic Syndrome Flashcards
Acute renal failure
Pre-renal: Shock or HF caused by MI
Renal: Glomerular destruction, Glomerulonephritis
Post renal: Sudden obstruction to urine outflow
EM findings of Acute Post-Infectious Glomerulonephritis
Subepithelial dense deposits that are shaped like humps on the epithelial side of the BM that are deposits of immune complexes
IF findings of Acute post infectious glomerulonephritis
Granular or “Lumpy-bumpy”deposits are both IgG and complement along the BM
Rapidly Progressive (Crescentic) GMN
Severe glomerular injury accompanied by formation of epithelial crescents in urinary space.
Inflammatory cells surround the compressed capillary loops in the form of crescent moon
Happens after focal necrosis of the glomerular capillaries in diseases such as goodpastures syndrome
Goodpasture syndrome
AI disease. Antibodies formed against collagen type 4.
Hallmark of Goodpasture syndrome
Diffuse linear staining of GBM for IgG–>Autoantibodies bound to BM
Goodpasture AKA
Antiglomerular basement membrane disease or anti-GBM disease
Renal characteristics associated with goodpasture
Involves glomeruli
Explosive acceleration of disease–>Rapidly progressive glomerulonephritis or crescentic glomerulonephritis
Urine output declines with hematuria and fluid retention with edema. Build up of urea and other wastes in blood
What is the most common glomerulonephritis?
IgA nephropathy (Berger diseasE)
Pathogenesis of IgA nephropathy?
Mucosal exposure to viral or bacterial antigens. Stimulates nephritogenic IgA dominant immune complexes within the glomeruli and mesangium which activate complement
IF dx for IgA nephropathy?
Essential for dx. Mesangial staining for IgA and C3 needed for dx. Severe–>staining of glomerular capillar wall suggests less favorable prognosis
EM of IgA nephropathy
Mesangial electron dense deposits under GBM, severe cases, deposits in capillary walls
Alport syndrome
X-linked; Abnormal Type IV collagen;
EM of alport syndrome
Most diagnostic
Irregularly thickened glomerular BM with splitting of lamina densa into interlacing string like lamina that surround electron lucent areas
Sx of alport
Hematuria, proteinuria, progressif renal failure and HTN
Hearing impariement, defect to lens
Thin glomerular BM disease
Hematuira due to thinning and rupure of the GBM
Dx: Biopsy and EM not Light micro
AD inheritance
Type I Membranoproliferative Glomerulonephritis AKA
Mesangiocapillary glomerulonephritis
Secondary causes of Type I Membranoproliferative Glomerulonephritis
Subacute bacterial endocarditis
Osteomylitis
Hep B virus infection
Neoplasia
Silver stain of Type I Membranoproliferative Glomerulonephritis
Doubling or tram track replication of GBMs from thickened capillary walls
AKA for Type II Membranoproliferative Glomerulonephritis
Dense deposit disease
IF of Type II Membranoproliferative Glomerulonephritis
Linear staining of capillary walls and mesangial nodules for Complement C3 little or no staining for immunoglobulins
Lupus nephritis
AI and immune complexes deposited in glomerular capillary loops–>complement–>Tissue injury
Histo classification of Lupus nephritis- most severe
IV diffuse proliferative: Most serious; mesangial and subendothelial deposits; Moderate nephritis
Class I and Class I Lupus nephritis on EM
Mesangial deposits
Class V Lupus nephritis on EM
Several subepithelial dense deposits
IF of Lupus nephritis
Subepithelial and subendothelial complexes are granular
Lab findings of Lupus nephritis
Elevated BUN/Creatinine Ua proteinuria Leukocytes and casts Autoab: AntidsDNA and Anti smith Serum complement decreased-->Active renal disease
