Mesangiocapillary glomerulonephritis

Mesangiocapillary glomerulonephritis (MCGN)—which is synonymous with membranoproliferative glomerulonephritis—is diagnosed when renal biopsy reveals glomeruli with a characteristic lobular appearance. Immunohistology and electron microscopy allow further subdivision into three patterns, types I, II (also called dense deposit disease), and III. Clinical presentation is with proteinuria (sometimes nephrotic syndrome) and/or haematuria; hypertension and/or impairment of excretory kidney function may be associated.

Aetiology and pathogenesis—MCGN can be a primary idiopathic form of glomerulonephritis, but also (especially type I) occurs as a secondary complication, especially of infections, e.g. hepatitis C virus, or of systemic diseases, e.g. systemic lupus erythematosus. All forms are characterized by activation of the complement system, with the pattern of activation differing in the three types. There is good evidence that complement activation is of pathogenetic importance, at least in type II MCGN, which is closely associated with the presence of an IgG autoantibody called nephritic factor that activates the alternative pathway of complement. Such activation may also directly injure fat cells (leading to association with partial lipodystrophy), and possibly be responsible for drusen in the eye, which is associated with age-related macular degeneration.

Management and prognosis—the prognosis may be good if an underlying cause can be identified and eradicated, but there is no proven form of therapy for the ‘primary’ forms of the disease, although all patients should have their blood pressure aggressively managed. Overall, renal survival in MCGN is about 50% at 10 years from diagnosis. There is a high rate of recurrence of the disease in renal transplants.