Thrombotic microangiopathy (TMA) is a well known complication in renal allograft recipients particularly those treated with cyclosporine or tacrolimus, the author reports two cases, those immediate post transplantation courses, albeit they weren't received cyclosporine were deteriorated with this complication.
Case 1: 32 years old male with primary renal failure due to gentamycin nephrotoxicity, and two years on dialysis get cadaveric kidney transplantation (TX) his immunosuppressive regimens were, antilymphocyte globulin (ALG)/Mycophenolate mophetil, prednisolone, after transplantation he had delayed graft function (DGF) course. On the3th post transplantation day platelet (PLT) count reached 50000/mm3 then to14000 at the 5th day, (LDH>1500u,and schistocyte on peripheral blood smear) we started plasma exchange 2 litter daily platelet count raised and reached to 70000,and LDH dropped to< 900 after 3 days, but unfortunately at this time of glory , invasive pulmonary aspergillus's as an apocalypse devastated the course and despite of marked improvement in renal function and vigorous antifungal treatment he died due to apoplexy of a fungal mass in his brain.
Case 2: 47 years old female with ESRD (pyelonephritis) and 3 years on hemodialysis and also a previous history of hydatid cyst (echinococcosis) who got the complete treatment, she underwent living unrelated kidney transplantation, just after transplantation patients she had DGF, patients’ immunosuppressives; were prednisolone, Mycophenolate mophetil, ALG, the day after PLT counts reached 50000, and it was 20000at the 3rd post TX day, then we started plasma exchange, but thrombocytopenia continued, graft nephrectomy performed at the 7th day after TX but hers TMA continued in a relentless course and patient died in a complete brain death picture. Thrombotic microangiopathy is a potentially serious complication in patients with renal transplantation, cyclosporine and less frequently tacrolimus have been implicated in most cases of post transplantation TMA but our patients didn't received either, it will be postulated that our patients TMA is due to the recently known von willebrand cleaving protease deficiency, either inherited or secondary to hydatid cyst or aspergillus's as infectious triggers.