Sunday, July 15, 2018

Primary Membranous Nephropathy

The landscape of Primary Membranous Nephropathy (PMN) has significantly changed over the last decade. Most of what we now understand about the pathogenesis of PMN is derived from the Heymann Nephritis model in rats. In 1959, Dr. Walter Heymann published this landmark article, which established the autoimmune nature of the disease. In the late 1970s, two groups (Dr. Couser et al in Boston and Dr. Van Damme et al in the Netherlands) established that the deposits of Heymann Nephritis were not from circulating immune complex trapping, but due to in situ formation. The rat antigen was eventually identified as megalin. The human antigen equivalent remained unknown until much later. Finally, 2009, Salant, Beck et al found that 70% of adult patients with “idiopathic” membranous nephropathy had antibodies against M-type phospholipase A2 receptor (PLA2R), a transmembrane glycoprotein found on podocytes. Soon after, another podocyte transmembrane glycoprotein called thrombospondin type-1 domain-containing 7A (THSD7A) was discovered (See NEJM 2014; 371(24):2277-2287).

Now, approximately 85% of PMN is found to be mediated by anti-PLA2R or anti-THSD7A, with still 15% of PMN “idiopathic”. With a serologic test for anti-PLA2R now commercially available as well as a biopsy immunofluorescent stain, the diagnosis and management of patients with PMN has been completely revamped.

For more on this discussion, please join us in the next GlomCon Interactive Fellows’ Curriculum on Tuesday, July 17th at 11 am eastern time. We will be walking through a case scenario as we review several different aspects of PMN.

To join the meeting go to: and select 'Join a Meeting'. Enter the Meeting ID into the web site (or connect directly from your Zoom app).
Meeting ID: 394-801-817
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