RESUMO
Tacrolimus, widely known as Prograf, has become the preferred immunosuppressant for preventing graft rejection in solid organ transplant recipients, particularly in steroid-sparing regimens. Its efficacy and reduced risk of acute and chronic rejection compared to cyclosporine have made it the preferred treatment option for transplant patients. However, tacrolimus has drawbacks as it is associated with adverse effects, such as renal tubular necrosis, kidney failure, hypertension, metabolic acidosis, and new-onset diabetes mellitus. Among the less common but potentially severe complications is thrombotic microangiopathy linked to tacrolimus usage. Identifying and addressing this condition early on is crucial given its severity and potential complications. Manifestations of this microangiopathy can vary, encompassing renal, neurological, cardiac, and respiratory symptoms, and, in some cases, presenting as pancreatitis, intestinal ischemia, or skin abnormalities. Although conventional management often involves plasma exchange as the primary therapeutic option, recent insights into the pathophysiology have led to newer drugs, such as eculizumab and belatacept, offering promising outcomes. In this narrative review, we delve deeper into the underlying pathophysiological mechanisms of tacrolimus-induced thrombotic microangiopathy and aim to provide clinicians with valuable recommendations for efficient and timely treatment strategies. By understanding the complexities of this condition and staying abreast of the latest advancements in therapeutic options, healthcare providers can optimize patient outcomes and ensure safer tacrolimus administration in solid organ transplant recipients.
