Rapidly Progressive Glomerulonephritis (RPGN) (Study Outline…
Rapidly Progressive Glomerulonephritis (RPGN) (Study Outline) 1. Background Definition: A clinical syndrome of glomerular injury characterized by rapid loss of kidney function over days to weeks, often leading to ESRD if untreated. Pathophysiology: Severe glomerular inflammation → crescent formation in Bowman’s space (proliferation of parietal epithelial cells + macrophages). Loss of filtration barrier → hematuria, proteinuria, rapid GFR decline. Major etiologic categories (exam-high yield): Type I: Anti-GBM disease (Goodpasture syndrome) Anti–glomerular basement membrane antibodies; lung involvement common. Type II: Immune Complex–mediated PSGN, IgA nephropathy, lupus nephritis. Type III: Pauci-immune (ANCA-associated vasculitis) Granulomatosis with polyangiitis (c-ANCA), microscopic polyangiitis (p-ANCA), eosinophilic granulomatosis with polyangiitis. 2. History Rapid onset hematuria (tea/cola-colored). Oliguria or anuria—strong warning sign. Systemic symptoms depending on cause: Goodpasture: cough, hemoptysis. ANCA vasculitis: sinusitis, pulmonary symptoms, constitutional complaints. Immune complex diseases: rash (SLE), recent infection (PSGN), arthralgias. Hypertension from fluid retention. Edema (periorbital, peripheral). 3. Exam Findings Vital signs: hypertension common; may see tachypnea if acidosis. Edema: periorbital, dependent. Pulmonary involvement: crackles, hemoptysis (Goodpasture, GPA). Skin findings: purpura (vasculitis), malar rash (SLE). Signs of severe kidney failure: asterixis, uremic symptoms in advanced cases. 4. Making the Diagnosis Urinalysis: Hematuria with RBC casts (nephritic). Proteinuria (usually