This is a mechanism of disease map for glomerulonephritis, which includes the pathophysiology of glomerulonephritis, the clinical and lab manifestations, as well as an overview of the etiologies.
ADDITIONAL TAGS:
Diffuse proliferative glomerulonephritis
- Associated with lupus (most common) and also IgA nephropathy
- +/- nephrotic - low serum C3 levels -granular appearnce on IM
Glomerulonephritis
Etiology ( + distinguishing features)
Pathophysiology
Manifestation
Inflammation
↓ cytokine release
↓ glomerular capillary damage
Porous glomerular basement membrane
Proteinuria (3.5 g/24h)
Leakage of protein
Leakage of RBCs
Hematuria, sometimes gross (coca-cola urine)
RBCs stick together in the renal tubules
Core concepts
Electrolyte disruption
Inflammation / cell damage
Genetic / hereditary
Microbial pathogenesis
Cardiovascular pathology
Cellular physiology
Chronic inflammation pathology
Pharmacology / iatrogenic
Immune system dysfunction
Flow gradients physiology
Nervous system pathology
Respiratory gas regulation
Signs / symptoms
Labs / tests / imaging results
Inflammatory infiltrates reduce fluid movement across the membrane
↓ GFR
Insufficient filtering and excretion of urea
RBC casts
Oliguria
Salt retention
Intravascular fluid expansion
Hypertension
Azotemia
Edema (pitting)
Poststreptococcal glomerulonephritis
- children 3-12 yo
- weeks after group A β-hemolytic streptococcal infections (skin or throat)
- Dx: positive antistrep Ab; low serum C3 (consumed); depositions of IgG, IgM, C3 on immunofluorescence and humps on EM
- prognosis: typically self limiting
IgA nephropathy (Berger disease)
- most common idiopathic subtype - high IgA, normal C3 levels
- renal pathology findings of IgA vasculitis. LM: mesangial proliferation
IF + EM: mesangial IgA immune complex deposits
Granulomatosis with polyangiitis
- c-ANCA/PR3-ANCA antibodies
Microscopic polyangiitis
- p-ANCA/MPO-ANCA antibodies
Eosinophilic granulomatosis w polyangiitis
- p-ANCA; peripheral eosinophilia
Goodpasture syndrome
- anti-GBM (type IV collagen) IgG antibody visible on IF; type 2 hypersens
Thin basement membrane nephropathy (benign familial hematuria)
- EM: diffuse thinning of GBM
Alport syndrome
- hereditary (XLD) collagen mutation → SNHL; abnormal eye (anterior lenticonus, retinopathy)
Rapidly progressive glomerulonephritis
- Crescent formation on LM, EM, IF
- Poor prognosis → ESRD within weeks
Membranoproliferative glomerulonephritis
- typically children, +/- nephrotic syndrome
- low serum C3 - tram track appearance on LM
small vessel vasculitis
hereditary