TACROLIMUS-ASSOCIATED THROMBOTIC MICROANGIOPATHY PRESENTING WITH ISCHEMİC COLITIS AFTER KIDNEY TRANSPLANTATION

Abstract

Calcineurin inhibitors (CNIs) are a significant component of the immunosuppressive regimen after kidney transplantation. By inhibiting cytokine gene transcription, CNIs suppress T cell and T cell-dependent B cell activation. Tacrolimus is preferred in most patients undergoing kidney transplantation. Thrombotic microangiopathy (TMA) is a severe but rare complication of CNIs therapy. TMA defines a specific pathologic lesion of arterioles and capillaries that leads to microvascular thrombosis. A 45-year-old male underwent kidney transplantation five months ago due to autosomal dominant polycystic kidney disease (ADPKD). His triple-maintenance immunosuppressive therapy includes tacrolimus. Abdominal pain and bloody diarrhea occurred in the fifth month of posttransplant. The edematous and erythematous mucosa of the ascending colon was detected on the colonoscopy. The foci of microthrombi inside the vessel lumen in the lamina propria were shown biopsy. The thrombosis or occlusion was excluded with computerized tomography (CT) angiography in abdominal vessels. The fragmented red blood cells and moderate thrombocytopenia were detected on the peripheral blood smear. Eventually, TMA diagnosis was established through laboratory and histological findings. Tacrolimus was suspected as the trigger of the pathological process and promptly switched to the everolimus. Afterward, laboratory abnormalities and clinical symptoms were improved. In this case, we intend to emphasize drug-associated TMA and atypical presentations, such as colonic microvasculature involvement.