title: [De novo hemolytic uremic syndrome in a kidney-pancreas recipient in the postoperative period].
abstract: Among the numeruos adverse side effects of tacrolimus (TAC), de novo thrombotic microangiopathy stands out as an infrecuente but severe complication. Renal dysfunction is the only alteration that should lead to suspicion of thrombotic microangiopathy, because the clinical features of intravascular hemolysis are not always found. The definitive diagnosis can usually be made with kidney biopsy. Patientes with TAC induced thrombotic microangiopathy usually promptly recover after treatment withdrawal or reduction in the dose of TAC and a short course of plasma therapy, but the risk of rejection increases. Switching from TAC to cyclosporine has also been tried with resolution of the hemolysis but thrombotic microangiopathy has been noted with both and this condition may later recur. We present a 29-year-old man who received a kidney-pancreas transplant for end-stage diabetic nephropathy. After initial induction with basiliximab, the immunosuppression consisted of prednisone, tacrolimus and mycophenolate mofetil. Twenty four days posttransplantation his renal function declined with a peak creatine level of 2.35 mg/dl. Laboratory studies showed thrombocytopenia and features of intravascular hemolysis. TAC associated hemolytic uremic syndrome was suspected and drug was immediately stopped and converted to sirolimus. Also he was treated with plasma infusion. The allograft biopsy showed focal glomerular and arteriolar acute thrombosis without evidence of rejection. Our experience demostrate that switching from tacrolimus to sirolimus could be an adecuate strategy for patients who develop FK506-associated de novo thrombotic microangiopathy without increase risk of acute rejection.
authors.affiliation: Servicio de Nefrología, Hospital Carlos Haya, Málaga. crisgutierrez50@hotmail.com
authors.forename: C
authors.initials: C
authors.lastname: Gutiérrez de la Fuente
authors.forename: E
authors.initials: E
authors.lastname: Sola
authors.forename: M J
authors.initials: MJ
authors.lastname: Alférez
authors.forename: A
authors.initials: A
authors.lastname: Navarro
authors.forename: M
authors.initials: M
authors.lastname: Cabello
authors.forename: D
authors.initials: D
authors.lastname: Burgos
authors.forename: M
authors.initials: M
authors.lastname: González Molina
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000077552:Basiliximab; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000601:surgery; D003928:Diabetic Nephropathies / Q000150:complications; D004359:Drug Therapy, Combination; D004385:Duodenostomy; D006463:Hemolytic-Uremic Syndrome / Q000139:chemically induced* / Q000473:pathology / Q000628:therapy; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D007582:Jejunostomy; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000601:surgery; D016030:Kidney Transplantation; D007683:Kidney Tubular Necrosis, Acute / Q000209:etiology; D008297:Male; D009173:Mycophenolic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016035:Pancreas Transplantation; D010185:Pancreatic Fistula / Q000209:etiology; D010949:Plasma; D011183:Postoperative Complications / Q000139:chemically induced* / Q000473:pathology / Q000628:therapy; D011241:Prednisone / Q000627:therapeutic use; D011993:Recombinant Fusion Proteins; D020123:Sirolimus / Q000627:therapeutic use; D016559:Tacrolimus / Q000009:adverse effects*
chemical_list: D000911:Antibodies, Monoclonal; D007166:Immunosuppressive Agents; D011993:Recombinant Fusion Proteins; D000077552:Basiliximab; D009173:Mycophenolic Acid; D011241:Prednisone; D020123:Sirolimus; D016559:Tacrolimus