Related Experiment Video
Updated: Jun 6, 2025

Mouse Kidney Transplantation: Models of Allograft Rejection
Published on: October 11, 2014
The outcome of thrombotic microangiopathy in kidney transplant recipients
Kanza Haq1, Shanshan Lin2, Alana Dasgupta3
1Department of Medicine, Johns Hopkins Hospital, The Johns Hopkins University School of Medicine, 600 Wolfe St. Carnegie 344B, Baltimore, MD, 21287, USA.
Insights
Kidney transplant recipients with complement-mediated thrombotic microangiopathy (cTMA) face higher early transplant failure risk. Long-term outcomes are similar, but more research is needed for better management of post-transplant TMA.
Area of Science:
- Nephrology
- Transplantation immunology
- Vascular biology
Background:
- Outcomes for kidney transplant recipients with prior or de novo thrombotic microangiopathy (TMA) are not well understood.
- Complement-mediated TMA (cTMA) and de novo TMA (dnTMA) are distinct entities affecting kidney allografts.
Purpose of the Study:
- To compare the outcomes of kidney transplant recipients with a history of cTMA versus those who develop dnTMA.
- To identify risk factors and prognostic indicators for allograft survival in these patient groups.
Main Methods:
- Retrospective study of kidney transplant recipients with end-stage kidney disease due to cTMA or dnTMA.
- Analysis of patient demographics, transplant history, biopsy findings, and allograft survival over a 20-year period.
Main Results:
- 134 patients identified: 22 with cTMA and 112 with dnTMA.
- cTMA patients were younger at diagnosis. Rejection and toxicity were more common in dnTMA.
- cTMA significantly increased early (first-year) transplant failure risk (aHR: 6.37), with risk decreasing over time. Long-term survival was similar.
Conclusions:
- Post-transplant TMA is a significant factor in poor kidney allograft survival.
- While early risk is higher with cTMA, long-term outcomes may converge.
- Further research is essential to improve understanding and management strategies for TMA post-kidney transplantation.
Background:
The outcome of kidney transplant recipients with a history of complement-mediated thrombotic microangiopathy (cTMA) and those who develop post-transplant de novo TMA (dnTMA) is largely unknown.
Methods:
We retrospectively studied all kidney transplant recipients with end-stage kidney disease secondary to cTMA and those who developed dnTMA, between Jan 2000 and Dec 2020 in our center.
Results:
We identified 134 patients, 22 with cTMA and 112 had dnTMA. Patients with cTMA were younger at the time of TMA diagnosis (age at diagnosis, 28.9 ± 16.3. vs 46.5 ± 16.0 years; P < 0.001). T-cell mediated rejection, borderline rejection, and calcineurin inhibitor toxicity were more prevalent in the first kidney transplant biopsy (P < 0.05) in the dnTMA group, and antibody-mediated rejection was more prevalent in anytime-biopsy (P = 0.027). After adjusting for potential confounders, cTMA was associated with a sixfold increase in the hazard of transplant failure during the first-year post-transplant (adjusted hazard ratio (aHR): 6.37 [95%CI: 2.17 to18.68; P = 0.001]; the aHR decreased by 0.87 (95% CI: 0.76 to 0.99: P = 0.033) per year elapsed since transplantation. Long-term allograft survival was similar in both groups.
Conclusion:
Post kidney transplant TMA is an important cause of poor allograft survival. More studies are needed to enhance our understanding and management of this disorder.

