LAUSR

Thrombotic microangiopathy (TMA) is a pathologic condition characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ injury due to microvascular endothelial lesions and thrombosis. It occurs in a variety of diseases and, unless recognized and treated, leads to severe morbidity and mortality. We present the case of a 48-year-old woman who underwent lung transplantation, initially under tacrolimus, mycophenolate mofetil (MMF), and prednisolone. Several complications emerged in the following months, including abdominal aortic and left renal artery thrombosis and cutaneous infections, although her renal function remained normal. Six months after transplant, her renal function began to deteriorate, which was assumed to be due to elevated tacrolimus levels and doses were adjusted. Due to leukopenia, MMF was changed to everolimus. One year after, she was admitted with fatigue, anemia, and renal dysfunction. Complementary exams revealed only iron deficiency, leukopenia, normal platelets, and elevated lactate dehydrogenase; her renal ultrasound was normal. A renal biopsy was performed and thrombotic microangiopathy was subsequently identified as the main cause of the renal dysfunction. Tacrolimus was therefore discontinued and MMF restarted with slow improvement of renal function. Only when everolimus was stopped did the patient's renal function show incremental improvement. TMA may be a serious complication after lung transplantation and the risk is higher when a combination of tacrolimus and everolimus is used. Renal biopsy findings are essential to confirm the final diagnosis of TMA, allowing for a change in immunosuppression to prevent permanent and severe renal damage.