De novo thrombotic microangiopathy. An underrated complication of renal transplantation

Area of Science:

• Nephrology
• Transplantation Immunology
• Pathology

Background:

• Thrombotic microangiopathy (TMA) can occur after kidney transplantation, either as a recurrence in patients with prior hemolytic uremic syndrome or as a de novo event.
• While large registries report low incidence (<1%), single centers indicate higher rates (14-20%) for de novo TMA post-renal transplant.
• Several factors, including ischemia-reperfusion injury, acute rejection, viral infections, and immunosuppressive drugs, can predispose to post-transplant TMA.

Purpose of the Study:

• To review the incidence, predisposing factors, clinical presentation, histological findings, and treatment strategies for de novo thrombotic microangiopathy following kidney transplantation.

Main Methods:

• Review of existing literature and registry data on post-transplant thrombotic microangiopathy.
• Analysis of clinical and histological characteristics of de novo TMA.
• Evaluation of treatment outcomes, including plasmapheresis, intravenous immunoglobulins, and rituximab.

Main Results:

• De novo TMA incidence varies significantly between large registries and single-center reports.
• Calcineurin inhibitors and anti-mTOR agents are implicated immunosuppressive treatments contributing to TMA.
• Clinical features include progressive renal failure and hypertension; hematologic abnormalities are present in ~60% of cases.
• Histological findings can involve glomeruli, arteries, or both.

Conclusions:

• Timely diagnosis and appropriate histological assessment are critical for managing post-transplant TMA.
• Treatment focuses on removing inciting factors, with early plasmapheresis showing potential to improve outcomes.
• Further research is needed to optimize management strategies for this rare but serious complication.