Pathophysiology
This kidney condition typically develops 2–3 weeks after a streptococcal throat or skin infection due to immune complex deposition in the glomeruli.
Post-streptococcal glomerulonephritis
This genetic kidney disorder often presents in children or young adults with persistent hematuria and may include hearing loss or eye abnormalities.
Alport Syndrome
"Can't see, can't pee, and hear a bee"
In this kidney disease, abnormally glycosylated immunoglobulins form immune complexes that deposit in the mesangium, activating complement and causing mesangial proliferation, often after upper respiratory or gastrointestinal infections.
IgA Nephropathy
On light microscopy, this type of glomerulonephritis shows a “tram-track” appearance due to mesangial cell interposition and thickened capillary walls, often associated with hepatitis C
Membranoproliferative glomerulonephritis (MPGN)
IF shows mesangial IgA and C3 deposits with a granular pattern
IgA nephropathy
On electron microscopy, there are “subepithelial humps” that represent immune complex deposits.
Post-strep glomerulonephritis (subendothelial humps are due to deposition of immune complexes in a limited space, causing an expansion of the GBM)
Patients with this autoimmune disease may present with hematuria, proteinuria, edema, and hypertension, often alongside systemic symptoms such as malar rash, arthritis, and cytopenias, reflecting its role as a secondary cause of nephritic or mixed glomerular syndrome.
Systemic lupus erythematosus (SLE) (Lupus commonly leads to type II Rapidly Progressive/Crescentic Glomerulonephritis)
This hereditary kidney disease results from mutations in type IV collagen genes, leading to defective glomerular basement membrane structure, thinning and splitting of the GBM, progressive hematuria, and eventual renal failure.
Alport syndrome
Secondary rapidly progressive nephritic syndrome (RPGN) that has linear pattern on IF
Anti-GBM Disease (Goodpasture Syndrome)
Basket-weave appearance due to irregular thickening and longitudinal splitting of the GBM
Alport syndrome
This kidney disease often presents with recurrent episodes of painless hematuria, typically coinciding with mucosal infections like a sore throat or gastrointestinal illness, and may slowly progress to proteinuria and chronic kidney disease in some patients.
IgA nephropathy (Berger disease)
This rare form of membranoproliferative glomerulonephritis is caused by dysregulation of the alternative complement pathway, often due to C3 nephritic factor stabilizing C3 convertase,
Dense Deposit Disease (MPGN Type II)
This secondary cause of nephritic syndrome is a type of rapidly progressive glomerulonephritis. On light microscopy, glomeruli show crescent formation in Bowman's space due to severe glomerular injury, and it is typically pauci-immune on immunofluorescence
ANCA-associated vasculitis (leads to type III Rapidly Progressive/Crescentic Glomerulonephritis, also known as "pauci-immune")
IF shows a granular, starry-sky appearance due to IgG, IgM, and C3 deposition along the GBM
Post-streptococcal glomerulonephritis
Ribbon-like deposits on EM
Type II MPGN: Dense Deposit Disease
Chronic infection with this virus can lead to circulating immune complexes that deposit in the subendothelial space of glomerular capillaries, activating the classical complement pathway, causing mesangial proliferation, capillary wall remodeling, and the “tram-track” appearance on light microscopy, characteristic of Type I MPGN.
Hepatitis C virus (HCV)