Thrombotic microangiopathy after kidney transplantation: diagnosis and management strategies - PubMed
5 hours ago
- #kidney transplantation
- #thrombotic microangiopathy
- #complement inhibitors
- Thrombotic microangiopathy (TMA) affects 0.8%-14% of kidney transplant recipients, manifesting as recurrent or de novo disease.
- TMA is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and ischemic organ dysfunction due to endothelial damage.
- Kidney-limited TMA is not rare, with histopathologic features showing endothelial injury and possible coexisting acute/chronic lesions.
- Triggers include ischemia-reperfusion injury, antibody-mediated rejection, immunosuppressive agents (calcineurin/mTOR inhibitors), and infections.
- Genetic predisposition (alternative complement pathway dysregulation) plays a key role in recurrent TMA, while environmental/transplant stressors drive de novo cases.
- Recurrent atypical hemolytic uremic syndrome is managed with terminal complement inhibitors (e.g., eculizumab), reducing recurrence rates prophylactically.
- De novo TMA management involves identifying/removing triggers; refractory cases may benefit from complement inhibition.
- Prognosis has improved with complement-targeting therapies, but research is needed to optimize strategies.