A recent report in the NEJM describes a case of recurrent FSGS. A patient with FSGS was given a kidney from his sister and developed recurrent FSGS. Recurrent FSGS occurred within days after transplantation with over 10 grams of proteinuria. That kidney was removed and then re transplanted in another individual with known diabetic nephropathy. The kidney functioned very well and months out had normal renal function and no proteinuria.
This single case can be very enlightening in terms of the pathophysiology of FSGS post transplant. This might suggest that sUPAR is a major player. It enlightens us to the fact that the problem lies in the environment the kidney is placed in and not the kidney itself.
The once challenged thought of permeability factor causing FSGS is becoming more and more a reality of this disease entity.
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