For decades we have known that membranous nephropathy was an antibody induced glomerulonephritis, we just didn’t know what the antigen was. Then, in 2009, Beck et al. rocked nephrology by discovering the antigen, Phospholipase A2 antibodies were detracted in 70% of patients with membranous nephropathy and no patients with either secondary membranous, other proteinuric glomerulonephritis or normal controls. Since then there has been a steady stream of positive trials showing tight association with aPLA2R antibodies and disease activity in idiopathic membranous nephropathy.
 |
| Panel H illus trates the domain structure of PLA2R, which is composed of an N-terminal cysteinerich domain (CysR), a fibronectin type II domain (FNII), eight CTLDs, a transmembrane domain (TM), and a short intracellular C-terminal tail (IC). The blocking fragment used in the experiments consists of CTLDs 4, 5, and 6 of a recombinant rabbit PLA2R. |
This month both CJSAN’s eJC and #NephJC will be going deep with studies that examine the state of the art in aPLA2R research.
This month CJASN’s online journal club is doing an interesting article looking at aPLA2R status at the beginning and end of therapy and its ability to predict long-term outcomes. It is a unique study with multiple titers of aPLA2r over the course of time matched with 5 years of follow-up. Though it is not the biggest trial of aPLA2R in some ways it is the best and it is an important step in understanding how to use this new tool in the management of membranous nephropathy.
Every month eJC has a sponsor, this month that sponsor is my home institution St John Hospital and Medical Center in Detroit. My fellow and I reviewed most of the key studies in aPLA2r and provided a helpful summary of this study. Check out our background post at Medium and then participate in the forum.
#NephJC will be shortly announcing its article for discussion and then have a twitter discussion on August 12th at 9pm EDT.