Secondary Membranous Nephropathy. A Narrative Review

Abstract

Membranous nephropathy (MN) is a common cause of proteinuria and nephrotic syndrome all over the world. It can be subdivided into primary and secondary forms. Primary form is an autoimmune disease clinically characterized by nephrotic syndrome and slow progression. It accounts for ~70% cases of MN. In the remaining cases MN may be secondary to well-defined causes, including infections, drugs, cancer, or autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), urticarial vasculitis, sarcoidosis, thyroiditis, Sjogren syndrome, systemic sclerosis, or ankylosing spondylitis. The clinical presentation is similar in primary and secondary MN. However, the outcome may be different, being often related to that of the original disease in secondary MN. Also, the treatment may be different, being targeted to the etiologic cause in secondary MN. Thus, the differential diagnosis between primary and secondary MN is critical and should be based not only on history and clinical features of the patient but also on immunofluorescence and electron microscopy analysis of renal biopsy as well as on the research of circulating antibodies. The identification of the pathologic events underlying a secondary MN is of paramount importance, since the eradication of the etiologic factors may be followed by remission or definitive cure of MN. In this review we report the main diseases and drugs responsible of secondary MN, the outcome and the pathogenesis of renal disease in different settings and the possible treatments.

Keywords: HBV infections; NSAIDs; cancer; membranous lupus nephropathy; primary membranous nephropathy; secondary membranous nephropathy.

Figure 1

Primary membranous nephropathy. A light microscopy there is diffuse thickening of glomerular capillary walls due to the presence of many immunedeposits in subepithelial position.

Figure 2

Membranous nephropathy in a patient with lung cancer. At light microscopy together with the diffuse thickening of glomerular capillary walls, some infiltration of leukocytes is present in capillary lumens.

Figure 3

Lupus membranous nephropathy. At electron microscopy, sub-endothelial immune complexes deposits, structured in aggregates of concentric lamellae to form “finger prints” images; a tubulo-reticular inclusion (TRI) is observed in the endothelial cell. Bars: 500 nm.