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. 2024 Nov 28;25(1):433.
doi: 10.1186/s12882-024-03846-x.

The outcome of thrombotic microangiopathy in kidney transplant recipients

Affiliations

The outcome of thrombotic microangiopathy in kidney transplant recipients

Kanza Haq et al. BMC Nephrol. .

Abstract

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.

Keywords: Complement-mediated TMA; De novo TMA; Kidney; Thrombotic Microangiopathy; Transplant.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: The ethics committee is the Johns Hopkins Hospital’s Institutional Review Board. This is a retrospective study, data were collected from the electronic medical records, consents were waived by Johns Hopkins Hospital’s Institutional Review Board. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Kaplan–Meier plot of transplant survival (death or end-stage kidney disease, ESKD) of primary cTMA vs dnTMA. Time at risk starts from transplantation and includes patients with available follow-up. The population is divided into those who had known cTMA before transplantation (red) and those who had dnTMA (blue). There was a sudden drop by 10% in cTMA patients shortly after follow-up, but survival was similar between the groups in the long term; cTMA
Fig. 2
Fig. 2
Time-varying adjusted hazard ratio (HR) of transplant failure (death or end-stage kidney disease, ESKD) of patients with cTMA compared to dnTMA. The hazard ratio is highest shortly after transplantation, and then decreases with time. The model is adjusted for age, gender, ethnicity, donor type, induction with lymphodepleting agents, DGF, eculizumab use (any time), and biopsy diagnosis (time-varying cumulative sum). The line represents the hazard ratio estimates, the blue shaded area represents the 95 percent confidence interval; cTMA, complement-mediated thrombotic microangiopathy
Fig. 3
Fig. 3
Kaplan–Meier patient survival estimates in cTMA and dnTMA. Time at risk started from transplantation and included patients with available follow-up. Patients starting dialysis were censored
Fig. 4
Fig. 4
Kaplan–Meier allograft survival estimates according to the use of eculizumab

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