Recurrent GN after transplant can be difficult to deal with. I mean if someone is already going to be on a CNI, mycophenolate mofetil, and prednisone what more can you do? During today’s session there were a number of abstracts aimed at predicting post transplant recurrence and treatment of GN.
1. SuPAR in recurrent FSGS.
We have all read the seminal Nature paper by Wei which determined that urokinase plasminogen activation receptor (suPAR) was the factor responsible for primary FSGS and recurrent FSGS. Two papers today aimed to study and confirm the association post-transplantation. Dr. Vincenti looked at pre-transplant and post-transplant suPAR as well as suPAR fragments that may have a role in recurrance. Unfortunately he did not find a correlation with suPAR/fragment levels and recurrence, nor did he find a correlation with suPAR and FSGS at all.
The second study to evaluate this association was presented by Dr. Halleck from Germany. In the 16 patients they studied with pre-transplant FSGS they found that suPAR levels were high pre-transplant but quickly fell post-transplantation. There were 7 patients with recurrence of FSGS. Patients with higher suPAR levels pre-transplant tended towards a higher incidence of recurrent FSGS. Post-transplant suPAR levels did not correlate with recurrent FSGS. What suPAR did correlate with was creatinine and negatively correlated with eGFR.
The bottom line? Currently suPAR cannot be used as a biomarker for recurrent FSGS but it definitely has a correlation with eGFR. It may still be implicated in the pathophysiology of FSGS although the relationship may be more complicated then previously thought. Of note FSGS is a very heterogeneous diagnosis post-transplant and it is possible that some of the cases of “recurrence” may not actually be primary FSGS. Looks like the mystery of the elusive circulation factor may not be solved yet…
Post written by Dr. Vinay Nair, eAJKD Advisory Board member.