ArticleCase reports in medicine2013
Use of belatacept as alternative immunosuppression in three renal transplant patients with de novo drug-induced thrombotic microangiopathy.
Article in Case reports in medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Shiga Toxin-ProducingKidney international reports · 2025Article
- Thrombotic Microangiopathy After Kidney Pancreas Transplant Managed With Eculizumab and a Calcineurin Inhibitor-free Basiliximab/Belatacept Maintenance Regimen: Between a Rock and a Hard Place.Transplantation direct · 2025Article
- Endothelial dysfunction in the kidney transplant population: Current evidence and management strategies.World journal of transplantation · 2025Review
- "Eculizumab First" in the Management of Posttransplant Thrombotic Microangiopathy.Kidney international reports · 2024Article
- Three-Year Outcomes in Kidney Transplant Recipients Switched From Calcineurin Inhibitor-Based Regimens to Belatacept as a Rescue Therapy.Transplant international : official journal of the European Society for Organ Transplantation · 2022Article
- Review
- Thrombotic microangiopathy after renal transplantation: Current insights inWorld journal of transplantation · 2018Review
- Complement C5-inhibiting therapy for the thrombotic microangiopathies: accumulating evidence, but not a panacea.Clinical kidney journal · 2017Article
- Belatacept As an Alternative to Calcineurin Inhibitors in Patients with Solid Organ Transplants.Frontiers in medicine · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thrombotic microangiopathy (TMA), a severe complication of renal transplantation, is a pathological process involving microvascular occlusion, thrombocytopenia, and microangiopathic hemolytic anemia. It generally appears within the first weeks after transplantation, when immunosuppressive drugs are used at high doses. De novo TMA may also be drug-induced when calcineurin inhibitors or proliferation signal inhibitors are used. We report three cases of de novo drug-induced TMA in renal transplant patients who were managed by replacing calcineurin inhibitors or proliferation signal inhibitors with belatacept, a primary maintenance immunosuppressive drug, which blocks the CD28 costimulation pathway, preventing the activation of T lymphocytes. To identify the cause of TMA, we ruled out HUS, hepatitis C serology, HIV serology, parvovirus B19, cytomegalovirus, anti-HLA antibodies, and prolonged activated partial thromboplastin time. We suspect that the TMA was caused by the calcineurin inhibitors or proliferation signal inhibitors. Belatacept treatment was initiated at a dose of 10 mg/kg on days 1, 5, 14, 28, 60, and 90; maintenance treatment was 5 mg/kg once a month for 1 year. Belatacept, in combination with other agents, prevented graft rejection in three patients.
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Registered trials
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