Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
On the basis of the electron microscopical findings, MPGN is traditionally classified as type I (idiopathic, most common), type II, or type III (rare). In another classification that is more useful and based on the pathogenetic process, MPGN can be classified as immune complex mediated, complement mediated, or MPGN without immunoglobulin or complement deposition.
Laboratory Findings
Variable degree of proteinuria, which can be marked or reach the nephrotic range.
Hematuria is present in patients with active disease.
Decreased serum levels of complement C3. C4 may be normal or decreased. Clinical course is not related to serum complement levels.
GFR <80 mL/minute/1.73/m
2
in two thirds of patients.
Relevant tests for the detection of secondary causes may be helpful (e.g., serologic testing and culture to detect infections, anti-GBM antibodies, cryoglobulins, serum protein electrophoresis and immunofixation, and antinuclear antibody testing).
Suggested Reading
Sethi S, Fervenza FC. Membranoproliferative glomerulonephritis—a new look at an old entity.
N Engl J Med.
2012;366(12):1119–1131.
GLOMERULONEPHRITIS, MEMBRANOUS
Definition
Membranous GN is an antibody-mediated disorder in which immune complexes localize between the outer aspect of glomerular basement membrane and epithelial cells. These complexes are formed by binding of antibodies to antigens that are part of the basement membrane, or deposited from elsewhere by the systemic circulation.
It usually occurs in adults and is the second most common cause of nephrotic syndrome.
It may be primary (≥75% of cases) or secondary. Secondary membranous GN may be due to autoimmune diseases (e.g., SLE), infections (e.g., HBV, syphilis, malaria, schistosomiasis, leprosy), drugs (e.g., NSAIDs, penicillamine), or neoplasms (e.g., non-Hodgkin lymphoma, leukemia, carcinomas, melanoma).
Approximately 20% of patients will progress to ESRD in 20–30 years.