A new
potential culprit might have been found for the recurrence of FSGS post
transplant. A recent article evaluated pathogenic antibodies in
141 serum samples over 64 patients and looked at many potential culprits such
as CD40, PTPRO, CGB5.etc and pre transplant elevation of anti CD40 alone was
the best predictor of FSGS recurrence after transplantation. Another study
highlight is the observation that patient-derived antibodies against CD40
functionally cooperate with a previously identified culprit of FSGS called
soluble urokinase plasminogen activator receptor (suPAR). Co-injection of
patient-derived CD40 anti-autobodies and suPAR caused enhanced kidney filter
failure more than each component did by itself.
This is
fascinating as can anti CD40 therapies then lead to preventing FSGS in kidney
transplantation?
Abatacept or belatacept
may have some role in FSGS treatment. A recent study showed
the success of using such agents in minimal change disease. It is interesting
to note that in presence of cd40 auto antibody, the wild type suPAR becomes pathogenic
to the podocyte. There seems to be an
on/off switch for suPAR perhaps with Cd40 and a trial of belatacept in FSGS
might be warranted.
Would co stimulating blockade agents be sufficient as their interaction as an anti CD40 is possible?-
as we use those in transplant anyway? Perhaps, looking at the recurrence of
FSGS in patients on belatacept might be a good start. Or are we specifically going to look at ant
CD40 agents( some of which are being studied as anti cancer agents in colon
cancer and others)
There is some
data of use of this agent in panc transplantation as well.
http://www.jimmunol.org/content/166/1/89.abstract
http://www.jimmunol.org/content/166/1/89.abstract
For full
paper look here
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