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现代时代肾移植后的血栓性微血管病:基于时间顺序的分类学。

Thrombotic microangiopathies after kidney transplantation in modern era: nosology based on chronology.

机构信息

Service de Néphrologie-HTA, Dialyses, Transplantation Rénale, Hôpital Bretonneau Et Hôpital Clôcheville, CHU Tours, 2 Bd Tonnellé, 37044, Tours, Tours Cedex, France.

EA4245, François-Rabelais University, Tours, France.

出版信息

BMC Nephrol. 2023 Sep 20;24(1):278. doi: 10.1186/s12882-023-03326-8.


DOI:10.1186/s12882-023-03326-8
PMID:37730583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10512637/
Abstract

BACKGROUND: Thrombotic microangiopathies (TMAs) are rare but can be severe in kidney transplant. recipients (KTR). METHODS: We analysed the epidemiology of adjudicated TMA in consecutive KTR during the. 2009-2021 period. RESULTS: TMA was found in 77/1644 (4.7%) KTR. Early TMA (n = 24/77 (31.2%); 1.5% of all KTR) occurred during the first two weeks ((median, IQR) 3 [1-8] days). Triggers included acute antibody-mediated rejection (ABMR, n = 4) and bacterial infections (n = 6). Graft survival (GS) was 100% and recurrence rate (RR) was 8%. Unexpected TMA (n = 31/77 (40.2%); 1.5/1000 patient-years) occurred anytime during follow-up (3.0 (0.5-6.2) years). Triggers included infections (EBV/CMV: n = 10; bacterial: n = 6) and chronic active ABMR (n = 5). GS was 81% and RR was 16%. Graft-failure associated TMA (n = 22/77 (28.6%); 2.2% of graft losses) occurred after 8.8 (4.9-15.5) years). Triggers included acute (n = 4) or chronic active (n = 14) ABMR, infections (viral: n = 6; bacterial: n = 5) and cancer (n = 6). 15 patients underwent transplantectomy. RR was 27%. Atypical (n = 6) and typical (n = 2) haemolytic and uremic syndrome, and isolated CNI toxicity (n = 4) were rare. Two-third of biopsies presented TMA features. CONCLUSIONS: TMA are mostly due to ABMR and infections; causes of TMA are frequently combined. Management often is heterogenous. Our nosology based on TMA timing identifies situations with distinct incidence, causes and prognosis.

摘要

背景:血栓性微血管病(TMA)在肾移植受者(KTR)中虽罕见,但可能很严重。

方法:我们分析了 2009-2021 年期间连续 KTR 中经裁决的 TMA 流行病学。

结果:77/1644(4.7%)例 KTR 发现 TMA。早期 TMA(n=24/77(31.2%);所有 KTR 的 1.5%)发生在头两周内(中位数,IQR 3[1-8]天)。触发因素包括急性抗体介导的排斥反应(ABMR,n=4)和细菌感染(n=6)。移植物存活率(GS)为 100%,复发率(RR)为 8%。意外 TMA(n=31/77(40.2%);1.5/1000 患者年)在随访期间的任何时间发生(3.0(0.5-6.2)年)。触发因素包括感染(EBV/CMV:n=10;细菌:n=6)和慢性活跃性 ABMR(n=5)。GS 为 81%,RR 为 16%。与移植物衰竭相关的 TMA(n=22/77(28.6%);2.2%的移植物丢失)发生在 8.8(4.9-15.5)年后。触发因素包括急性(n=4)或慢性活跃性(n=14)ABMR、感染(病毒:n=6;细菌:n=5)和癌症(n=6)。15 例患者接受了移植切除术。RR 为 27%。罕见的有不典型(n=6)和典型(n=2)溶血尿毒综合征和孤立的钙调神经磷酸酶抑制剂毒性(n=4)。三分之二的活检呈现 TMA 特征。

结论:TMA 主要由 ABMR 和感染引起;TMA 的原因经常是组合的。治疗往往是多样的。我们基于 TMA 时间的分类法确定了具有不同发病率、病因和预后的情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7292/10512637/054117e47198/12882_2023_3326_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7292/10512637/15cbcd436167/12882_2023_3326_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7292/10512637/054117e47198/12882_2023_3326_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7292/10512637/15cbcd436167/12882_2023_3326_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7292/10512637/054117e47198/12882_2023_3326_Fig2_HTML.jpg

相似文献

[1]
Thrombotic microangiopathies after kidney transplantation in modern era: nosology based on chronology.

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[4]
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[5]
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[6]
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[7]
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[9]
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引用本文的文献

[1]
Thrombotic Microangiopathy After Kidney Transplantation: Insights Into Genetic Etiology and Clinical Outcomes.

Kidney Int Rep. 2025-1-30

[2]
Conservative Management of Thrombotic Microangiopathy in a Renal Transplant Recipient: The Importance of Early Recognition.

Clin Case Rep. 2025-3-27

[3]
Atypical Hemolytic Uremic Syndrome Associated with BNT162b2 mRNA COVID-19 Vaccine in a Kidney Transplant Recipient: A Case Report and Literature Review.

Infect Dis Rep. 2025-2-11

[4]
Paraneoplastic Syndrome After Kidney Transplantation: Frequency, Risk Factors, Differences to Paraneoplastic Occurrence of Glomerulonephritis in the Native Kidney, and Implications on Long-Term Kidney Graft Function.

Transpl Int. 2024

本文引用的文献

[1]
Clinical characteristics and outcomes of a patient population with atypical hemolytic uremic syndrome and malignant hypertension: analysis from the Global aHUS registry.

J Nephrol. 2023-4

[2]
What is the impact of blood pressure on neurological symptoms and the risk of ESKD in primary and secondary thrombotic microangiopathies based on clinical presentation: a retrospective study.

BMC Nephrol. 2022-1-20

[3]
Complications after native kidney biopsy: definitive data.

Curr Opin Nephrol Hypertens. 2021-11-1

[4]
Major Bleeding and Risk of Death after Percutaneous Native Kidney Biopsies: A French Nationwide Cohort Study.

Clin J Am Soc Nephrol. 2020-11-6

[5]
Etiology and Outcomes of Thrombotic Microangiopathies.

Clin J Am Soc Nephrol. 2019-3-12

[6]
HLA class II antibodies induce necrotic cell death in human endothelial cells via a lysosomal membrane permeabilization-mediated pathway.

Cell Death Dis. 2019-3-8

[7]
Thrombotic microangiopathy after renal transplantation: Current insights in and recurrent disease.

World J Transplant. 2018-9-10

[8]
AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy.

Am J Kidney Dis. 2016-12

[9]
Cyclosporine induces endothelial cell release of complement-activating microparticles.

J Am Soc Nephrol. 2013-10-3

[10]
De novo thrombotic microangiopathy after kidney transplantation: clinical features, treatment, and long-term patient and graft survival.

Transplant Proc. 2012-10

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