ArticleJournal of the American Society of Nephrology : JASN2013
Cyclosporine induces endothelial cell release of complement-activating microparticles.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Unveiling the Incidence and Graft Survival Rate in Kidney Transplant Recipients WithTransplant international : official journal of the European Society for Organ Transplantation · 2024Pooled it
- Thrombotic microangiopathy after kidney transplantation: diagnosis and management strategies.Clinical kidney journal · 2026Review
- Abatacept improves posttransplant survival and reduces endothelial injury syndromes in β-thalassemia major.Blood advances · 2025Article
- Critical role of complement in antibody mediated rejection in kidney transplantation.World journal of transplantation · 2025Review
- Chronic kidney disease enhances alternative pathway activity: a new paradigm.The Journal of clinical investigation · 2025Review
- Extracellular Vesicles and Immune Activation in Solid Organ Transplantation: The Impact of Immunosuppression.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025Review
- Thrombotic Microangiopathy After Kidney Transplantation: Insights Into Genetic Etiology and Clinical Outcomes.Kidney international reports · 2025Article
- Endothelial dysfunction in the kidney transplant population: Current evidence and management strategies.World journal of transplantation · 2025Review
- Review
- Effect of COVID-19 on Thrombosis Incidence and Patient Prognosis in Kidney Transplant Recipients.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- "Eculizumab First" in the Management of Posttransplant Thrombotic Microangiopathy.Kidney international reports · 2024Article
- Vascular injury in glomerulopathies: the role of the endothelium.Frontiers in nephrology · 2024Review
- Immunosuppressive Agents-Effects on the Cardiovascular System and Selected Metabolic Aspects: A Review.Journal of clinical medicine · 2023Review
- Thrombotic microangiopathies after kidney transplantation in modern era: nosology based on chronology.BMC nephrology · 2023Article
- Characteristics and management of thrombotic microangiopathy in kidney transplantation.Korean journal of transplantation · 2023Review
- The loss of glycocalyx integrity impairs complement factor H binding and contributes to cyclosporine-induced endothelial cell injury.Frontiers in medicine · 2023Article
- Alternative pathway diagnostics.Immunological reviews · 2023Review
- Complement Factor H and Related Proteins as Markers of Cardiovascular Risk in Pediatric Chronic Kidney Disease.Biomedicines · 2022Article
- Complement Mediated Endothelial Damage in Thrombotic Microangiopathies.Frontiers in medicine · 2022Review
- Kidney disease in children with heart or liver transplant.Pediatric nephrology (Berlin, Germany) · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Defective control of the alternative pathway of complement is an important risk factor for several renal diseases, including atypical hemolytic uremic syndrome. Infections, drugs, pregnancy, and hemodynamic insults can trigger episodes of atypical hemolytic uremic syndrome in susceptible patients. Although the mechanisms linking these clinical events with disease flares are unknown, recent work has revealed that each of these clinical conditions causes cells to release microparticles. We hypothesized that microparticles released from injured endothelial cells promote intrarenal complement activation. Calcineurin inhibitors cause vascular and renal injury and can trigger hemolytic uremic syndrome. Here, we show that endothelial cells exposed to cyclosporine in vitro and in vivo release microparticles that activate the alternative pathway of complement. Cyclosporine-induced microparticles caused injury to bystander endothelial cells and are associated with complement-mediated injury of the kidneys and vasculature in cyclosporine-treated mice. Cyclosporine-induced microparticles did not bind factor H, an alternative pathway regulatory protein present in plasma, explaining their complement-activating phenotype. Finally, we found that in renal transplant patients, the number of endothelial microparticles in plasma increases 2 weeks after starting tacrolimus, and treatment with tacrolimus associated with increased C3 deposition on endothelial microparticles in the plasma of some patients. These results suggest that injury-associated release of endothelial microparticles is an important mechanism by which systemic insults trigger intravascular complement activation and complement-dependent renal diseases.
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Registered trials
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.