Membranous Glomerulopathy



Membranous GN is the most common cause of nephrotic syndrome in adults, accounting for about 50 per cent of adult cases. Most patients with membranous nephropathy are over 35 years of age, with the peak incidence in the fifth decade; it is not common in children. The disease may be detected as asymptomatic proteinuria, but as many as 80 per cent of patients present with mas­sive proteinuria and the nephrotic syndrome. The majority of cases of membranous GN are idi­opathic. However, the membranous lesion is also seen in association with multiple unrelated dis­orders, including hepatitis B, systemic lupus er­ythematosus, organic gold exposure, and neopla­sia (especially carcinoma).

Proteinuria in excess of 15 to 20 gm/day is not uncommon in membranous GN and is usually nonselective. Microscopic hematuria occurs in a substantial number of patients. Serum comple­ment levels are normal in the idiopathic disease. Renal vein thrombosis is a complication recog­nized with increasing frequency. A progressive fall in GFR occurs in a majority of patients, and hypertension and azotemia develop late in the disease.

The classic finding on light microscopy is that of uniform basement membrane thickening throughout the glomerulus. Cellular proliferation and infiltration are strikingly absent. Silver stains demonstrate distinctive “spikes” within the base­ment membrane, causing it to resemble a picket fence. The darkly stained spikes are basement membrane projections between immune deposits. IgG and C3 are prominent on immunofluorescent microscopy and show a uniform, finely granular pattern outlining the capillary loops (Fig. 34-lE). The extent and progression of the lesion can be classified by electron microscopy. The patterns range from Stage 1 (minimal basement membrane thickening with small subepithelial deposits) to Stage IV (very thick, irregular basement mem­brane with lucent zones representing former sites of deposits).