title: Follow-up of kidney graft recipients with cyclosporine-associated hemolytic-uremic syndrome and thrombotic microangiopathy.
abstract: The study was based on 462 patients who underwent kidney transplantation from 1986 through 2004. Cyclosporine (CsA)-related thrombotic microangiopathy (TMA) was observed in 15 (3.3%) patients. The donor ages ranged from 9 to 51 years and cold ischemia times from 12 to 31 hours. Hemolytic-uremic syndrome (HUS) developed 2 weeks after transplantation in 14 patients and later in 1 subject. Histopathologic examination demonstrated glomerular-type TMA in 3 patients, a mixed type (glomerular and vascular) in 11 patients, and a nonspecific mesangial widening with tubulointerstitial lesions in 1 patient. Follow-up biopsies revealed resolution of TMA in 4 patients and chronic vascular TMA in 1 patient. Six patients with mixed-type TMA needed transient hemodialysis. No patient with the glomerular-type TMA needed dialysis (P = .103), and 14 of 15 had good resolution of graft function after CsA dose reduction or temporary discontinuation or continuation of optimal dose. Only 1 graft with mixed-type TMA was lost due to irreversible HUS. The mean glomerular filtration rate (GFR), predicted by the Nankivell equation, was 76 +/- 13 mL/min and 80 +/- 27 mL/min at 1 month after discharge for glomerular- and mixed-type TMA, respectively (P > .05). GFRs 1 year after HUS were 82 +/- 12 and 87 +/- 21 mL/min for the glomerular and the mixed types, respectively (P > .05). We concluded that the mixed-type TMA was associated with a more severe early clinical course than the glomerular-type TMA. The 1-year prognosis was good in the majority of patients, with no significant differences between those with the glomerular- and mixed-type TMA.
authors.affiliation: Department of Nephrology, University Medical Center, Ljubljana, Slovenia.
authors.forename: A
authors.initials: A
authors.lastname: Bren
authors.forename: J
authors.initials: J
authors.lastname: Pajek
authors.forename: K
authors.initials: K
authors.lastname: Grego
authors.forename: J
authors.initials: J
authors.lastname: Buturovic
authors.forename: R
authors.initials: R
authors.lastname: Ponikvar
authors.forename: J
authors.initials: J
authors.lastname: Lindic
authors.forename: B
authors.initials: B
authors.lastname: Knap
authors.forename: A
authors.initials: A
authors.lastname: Vizjak
authors.forename: D
authors.initials: D
authors.lastname: Ferluga
authors.forename: A
authors.initials: A
authors.lastname: Kandus
mesh_terms: D000293:Adolescent; D000328:Adult; D000740:Anemia / Q000453:epidemiology; D002648:Child; D016572:Cyclosporine / Q000009:adverse effects* / Q000493:pharmacokinetics; D005260:Female; D006463:Hemolytic-Uremic Syndrome / Q000139:chemically induced*; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects* / Q000493:pharmacokinetics; D007518:Isoantibodies / Q000097:blood; D007676:Kidney Failure, Chronic / Q000601:surgery; D007678:Kidney Glomerulus / Q000098:blood supply / Q000473:pathology; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000276:immunology* / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications / Q000139:chemically induced / Q000453:epidemiology; D012189:Retrospective Studies; D013927:Thrombosis / Q000139:chemically induced* / Q000473:pathology; D014019:Tissue Donors
chemical_list: D007166:Immunosuppressive Agents; D007518:Isoantibodies; D016572:Cyclosporine; D007770:L-Lactate Dehydrogenase