A case of late onset cyclosporine-induced hemolytic uremic syndrome resulting in renal graft loss

Citation
R. Katafuchi et al., A case of late onset cyclosporine-induced hemolytic uremic syndrome resulting in renal graft loss, CLIN TRANSP, 13, 1999, pp. 54-58
Citations number
14
Categorie Soggetti
Surgery
Journal title
CLINICAL TRANSPLANTATION
ISSN journal
09020063 → ACNP
Volume
13
Year of publication
1999
Supplement
1
Pages
54 - 58
Database
ISI
SICI code
0902-0063(1999)13:<54:ACOLOC>2.0.ZU;2-N
Abstract
A case of late onset hemolytic uremic syndrome (HUS) associated with cyclos porine (CYA) is described in this report. A 50-yr-old man with end-stage re nal failure due to immunoglobulin A (IgA) nephropathy received a renal tran splant from his wife. Human leucocyte antigen was completely unmatched. Imm unosuppressant was a combination of prednisolone. azathioprine. and CYA. We was discharged 1 month after transplantation. with no episode: of acute re jection. Twenty-one months after transplantation. his platelet count and he matocrit began to decrease and lactate dehydrogenase began to increase. Gra ft biopsy showed thrombotic microangiopathy and recurrent lgA nephropathy. Graft function was rapidly deteriorated and methylprednisolone pulse therap y was not effective. Twenty-five months after transplantation. he returned to a regular hemodialysis. Hemolysis was immediately improved after a reduc tion of the dose of CYA to 50 mg/d. The trough level of CYA was less than 2 00 ng/mL in most periods of his clinical course. Blood pressure was high th roughout the clinical course. Although acute vascular rejection or malignan t hypertension could also cause a thrombotic microangiopathy. CYA was most likely a cause of HUS in the present case because of the following reasons: neither anti-acute rejection therapy nor an adequate control of his blood pressure was effective in improving clinical features of HUS; hemolysis and thrombocytepenia disappeared immediately after the reduction of the dose o f CYA to 50 mg/d. It has been reported that HUS carried poor prognosis only when occurring shortly after transplantation in cadaver kidney recipients. The present transplant was from a living donor and HUS occurred 21 months after transplantation and was severe enough to result in graft loss. nigh b lood pressure might be one of the predisposing factors of HUS associated wi th CYA in the present case. CYA should be stopped and other alternative imm unosuppressants should be given in cases of acute graft deterioration with hemolysis and thrombocytopenia. irrespective of the interval fi om transpla ntation. CYA dose. or CYA trough level.