Evidence map›Paper›PMID 39609684›Full record

ArticleBMC nephrology2024

The outcome of thrombotic microangiopathy in kidney transplant recipients.

Kanza Haq, Shanshan Lin, Alana Dasgupta, Zainab Obaidi, Serena Bagnasco, Umberto Maggiore, Nada Alachkar

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Article in BMC nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Kanza HaqDepartment of Medicine, Johns Hopkins Hospital, The Johns Hopkins University School of Medicine, 600 Wolfe St. Carnegie 344B, Baltimore, MD, 21287, USA.
Shanshan LinDepartment of Epidemiology, The Johns Hopkins University School of Public Health, Baltimore, MD, USA.
Alana DasguptaDepartment of Renal Pathology, The Ohio State University School of Medicine, OH, Columbus, USA.
Zainab ObaidiDepartment of Medicine, University of Chicago, Chicago, IL, USA.
Serena BagnascoDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Umberto MaggioreDepartment of Medicine and Surgery, University of Parma, Parma, Italy.
Nada AlachkarDepartment of Medicine, Johns Hopkins Hospital, The Johns Hopkins University School of Medicine, 600 Wolfe St. Carnegie 344B, Baltimore, MD, 21287, USA. nalachk1@jhmi.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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.

methodsWe 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.

resultsWe 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.

conclusionPost kidney transplant TMA is an important cause of poor allograft survival. More studies are needed to enhance our understanding and management of this disorder.

Indexed as

Graft RejectionKidney TransplantationThrombotic MicroangiopathiesAdultFemaleHumansKidney Failure, ChronicMaleMiddle AgedPostoperative ComplicationsRetrospective StudiesYoung AdultComplement-mediated TMADe novo TMAKidneyThrombotic MicroangiopathyTransplant

Identifiers

PMID39609684
PMCPMC11606107

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.