Introduction

Membranoproliferative glomerulonephritis (MPGN) is a histopathologic pattern of glomerular injury with a wide range of clinical manifestations, including nephrotic syndrome (heavy proteinuria, hypoalbuminemia, edema), nephritic syndrome (hematuria, hypertension, renal dysfunction), or mixed nephrotic-nephritic syndrome.  Historically categorized into types I, II, and III based on electron microscopy findings, MPGN's contemporary classification emphasizes etiology, distinguishing between immune complex–mediated and complement-mediated MPGN.

Etiologies and pathophysiology

MPGN accounts for roughly 5%-10% of biopsy-confirmed glomerulonephritis cases.  It can arise from 2 distinct pathways:  immune complex deposition or dysregulated complement activation.

Immune complex–mediated MPGN

MPGN mediated by immune complexes (antigen-antibody complexes) constitutes 70%-80% of cases, predominantly affecting adolescents and young adults.  It is associated with:

  • Chronic infection:  Hepatitis C virus (HCV) is the most common cause; the mechanism involves cryoglobulin formation (discussed in a separate article).  Additional causes include hepatitis B virus (HBV) and endocarditis.

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