2nd most common in adults (FSGN being the most common)
2 peaks (mid-20s and 60s)
Presentation: proteinuria / nephrotic syndrome / chronic kidney disease
Causes: 85% are idiopahic (HLA-DQA1); could occur secondary to infections (hep B, hep C, malaria, syphilis), rheumatoid drugs (gold, penicillamine, and NSAIDs), and systemic diseases (DM, immunologic disorders such as SLE and malignancy*), sarcoidosis, amyloidosis
Idiopathic membranous nephropathy is associated with circulating lgG4 antibodies to the phospholipase A2 receptor (PLA2R), which might play a role in the development of the disease.
The M-type PLA2R is a transmembrane receptor found in high concentrations in glomerular podocytes and thought to be a major antigen in the pathogenesis of idiopathic membranous nephropathy. (not seen secondary cases)
Eg, PLA2R antibodies are not seen in class V lupus nephritis (membranous nephropathy) because SLE is a secondary cause
Anti-PLA2R autoantibody titers correlate with disease activity (proteinuria).
Biopsy:
uniform, diffuse thickening of the glomerular capillary wall on light microscopy ((without an increase in cellularity))
Immunofluorescence => granular IgG and complement (C3) deposition on the GBM;
EM => subepithelial immune complexes appear as "spikes" with methenamine silver stain
Complication:
Renal vein thrombosis in 5%; greatest risk if serum albumin <20g/L (due to hypercoagulable state)
may presents with flank pain and hematuria; and diagnosis can be established by an MRI of renal arteries and veins