De novo thrombotic microangiopathy after kidney transplantation

Garg, Neetika; Rennke, Helmut G.; Pavlakis, Martha; Zandi‐Nejad, Kambiz

doi:10.1016/j.trre.2017.10.001

Cited by 67 publications

(97 citation statements)

References 87 publications

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“…The major proportion of post‐transplant TMA is de novo TMA . A wide range of associated risk factors of de novo TMA are recognized after KTx, including immunosuppressive drugs, such as CNI and mTOR inhibitor, viral infection, ischemia‐reperfusion injuries and ABMR . In contrast to localized TMA in the graft, which is diagnosed later by biopsy in the post‐transplant course with slow progressing renal dysfunction, sdTMA could be diagnosed in the early postoperative period with laboratory findings indicative of thrombocytopenia and microangiopathic hemolytic anemia .…”

Section: Introductionmentioning

confidence: 99%

Analysis of the prevalence of systemic de novo thrombotic microangiopathy after ABO‐incompatible kidney transplantation and the associated risk factors

et al. 2019

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Objectives: To analyze the prevalence of systemic de novo thrombotic microangiopathy in ABO-incompatible kidney transplantation and risk factors associated with this condition. Methods: A total of 201 patients who received living-donor kidney transplantation (114 patients with ABO-identical kidney transplantation and 87 patients with ABO-incompatible kidney transplantation) were retrospectively analyzed. Systemic de novo thrombotic microangiopathy was diagnosed clinically according to the presence of thrombocytopenia with microangiopathic hemolytic anemia and pathological findings of thrombotic microangiopathy. Anti-A and anti-B antibodies were purified from human plasma, and these antibodies' bindings to human kidney were investigated in vitro. Results: ABO-incompatible kidney transplantation was a significant risk factor of systemic de novo thrombotic microangiopathy (odds ratio 55.9, 95% CI 1.8-8.9, P < 0.001) after transplantation. Multivariate logistic regression analysis showed that non-use of mycophenolate mofetil, pretreatment immunoglobulin G antibody titer ≥64fold and pretransplant immunoglobulin M antibody titer ≥16-fold were significant risk factors for systemic de novo thrombotic microangiopathy in ABO-incompatible kidney transplantation. Microvascular inflammation of 1-h post-transplant biopsy could be observed more frequently in thrombotic microangiopathy patients than in nonthrombotic microangiopathy patients. Anti-A and anti-B antibodies purified from human plasma showed a strong in vitro reaction against human kidney when the antibody titer was ≥16-fold. Conclusions: Antibody titer should be decreased to ≤16-fold until the day of ABOincompatible kidney transplantation by desensitization therapy including mycophenolate mofetil. The 1-h biopsy results might help to diagnose systemic de novo thrombotic microangiopathy.

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Section: Introductionmentioning

confidence: 99%

Analysis of the prevalence of systemic de novo thrombotic microangiopathy after ABO‐incompatible kidney transplantation and the associated risk factors

et al. 2019

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“…The vast majority of post-transplant TMAs are attributed to de novo disease [8]. The incidence of de novo TMA ranges between 4% and 15%, with 43% graft survival [11].…”

Section: Discussionmentioning

confidence: 99%

“…Post-transplantation TMA can occur either due to recurrence of primary TMA that caused initial kidney failure, or it may arise as a de novo clinical condition. Despite that patients with TTP are at high risk for recurrence, most of the posttransplant TMAs are attributed to de novo occurrence [6,8]. De novo post-transplant TMA usually occurs one week after transplantation when patients are treated with high doses of immunosuppressant, wherein the incidence of de novo TMA is 4-15% in renal transplant patients treated with Cyclosporine, with 43% graft survival [9].…”

Section: Introductionmentioning

confidence: 99%

“…De novo post-transplant TMA usually occurs one week after transplantation when patients are treated with high doses of immunosuppressant, wherein the incidence of de novo TMA is 4-15% in renal transplant patients treated with Cyclosporine, with 43% graft survival [9]. In fact, de novo TMA post-transplantation may occur due to several etiologies such as calcineurin inhibitors (CNIs) toxicity and AMR post-transplantation [8,10]. In the latter case, diagnostic features such as intraluminal thrombi,…”

Section: Introductionmentioning

confidence: 99%

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Concomitant Thrombotic Microangiopathy and Rejection in a Recent Kidney Transplant: A Case Study

Al-Thumali¹,

Yousif²,

Bukhari³

et al. 2020

TCR

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Thrombotic microangiopathy (TMA) is an uncommon, life-threatening complication that adversely affects kidney transplant recipient and allograft survival. Post-transplantation TMA can occur as recurrence of the primary TMA or as a de novo condition. The latter can be triggered by numerous factors post-transplantation including calcineurin inhibitors, certain infections and antibody-mediated rejection. Rejection-associated TMAs carry a significantly lower graft survival rate compared with post-transplant TMAs that are not associated with rejection. In this case report, we present a rare case of rejection-associated TMA in a recently transplanted renal allograft that was managed in Al-Hada Armed Forces Hospital. Despite the poor expected outcome of this condition; the patient was successfully treated after early initiation of medical interventions. Transplantation teams may face many challenges managing such a combination of medical conditions, which may halt pursuing appropriate diagnostic and therapeutic measures in a timely fashion. This article highlights some of these challenges for better understanding of such a complex condition.

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“…After kidney transplantation, TTP is very much less common than atypical hemolytic uremic syndrome. 12 Indeed, post-transplantation TTP is extremely rare, occurs at least 1 week after transplantation and is usually not related to ADAMTS13 antibodies. [1][2][3][4][5]11 The TTP observed in our two kidney recipients did not, therefore, fit the classical framework.…”

Section: Case Reportsmentioning

confidence: 99%

Transfer of ADAMTS13 antibody-mediated thrombotic thrombocytopenic purpura via kidney transplantation

et al. 2019

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De novo thrombotic microangiopathy after kidney transplantation

Cited by 67 publications

References 87 publications

Analysis of the prevalence of systemic de novo thrombotic microangiopathy after ABO‐incompatible kidney transplantation and the associated risk factors

Analysis of the prevalence of systemic de novo thrombotic microangiopathy after ABO‐incompatible kidney transplantation and the associated risk factors

Concomitant Thrombotic Microangiopathy and Rejection in a Recent Kidney Transplant: A Case Study

Transfer of ADAMTS13 antibody-mediated thrombotic thrombocytopenic purpura via kidney transplantation

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