Membranous nephropathy (MN) is among the most common causes of the nephrotic syndrome in nondiabetic adults, accounting for up to one-third of biopsy diagnoses in some regions. (See "Overview of heavy proteinuria and the nephrotic syndrome", section on 'Etiology'.)
The term MN reflects the primary histologic change noted on light microscopy: glomerular basement membrane thickening with little or no cellular proliferation or infiltration [1,2]. MN is most often primary (idiopathic), although it has been associated with hepatitis B antigenemia, autoimmune diseases, thyroiditis, malignancies, and the use of certain drugs such as gold, penicillamine, captopril, and nonsteroidal anti-inflammatory drugs. In the majority of cases of tumor-associated MN, the malignancy has been diagnosed or is clinically apparent at the time that proteinuria is discovered.
The pathogenesis, causes, and diagnosis of MN will be reviewed here. The treatment and prognosis of MN are presented separately. (See "Treatment of idiopathic membranous nephropathy" and "Alternative agents in the treatment of idiopathic membranous nephropathy".)
At one time, membranous nephropathy (MN) was the most common biopsy diagnosis in adults (particularly over age 40 years) with the nephrotic syndrome, but the relative frequency of MN on kidney biopsy has declined to between 15 and 33 percent since 1990 [3-6]. This reflects at least in part an increase in the relative frequency with which focal segmental glomerulosclerosis is identified in black and Hispanic patients with nephrotic syndrome [3-5]. (See "Overview of heavy proteinuria and the nephrotic syndrome", section on 'Etiology'.)
MN is seen in all ethnic and racial groups and in both sexes, but idiopathic MN is more common in white males over the age of 40 years. MN in young women should raise the suspicion of lupus. MN is less commonly seen in children, in whom it is often associated with hepatitis B, or less commonly autoimmune or thyroid disease .