title: Hyperhomocyst(e)inemia in renal transplant recipients with and without cyclosporine.
abstract: Studies have demonstrated that hyperhomocyst(e)inemia is present in renal transplant recipients and is correlated with cardiovascular disease. It is still unclear whether hyperhomocyst(e)inemia observed in renal transplant recipients solely depends on the moderate reduction of renal function in these patients or if additional mechanisms are operative in this patient category. A recent study suggested that cyclosporine (CsA) increased plasma homocyst(e)ine concentration in interfering with folate-assisted remethylation of homocysteine. To confirm this hypothesis, we studied plasma homocyst(e)ine folic acid and cobalamin concentrations in 122 renal transplant recipients (104 on CsA and 18 not receiving CsA). After adjusting for age, gender, transplant duration and serum creatinine concentration, patients with and without CsA had similar plasma homocyst(e)ine concentrations (17.9 +/- 6.1 mumol/l in CsA(+)patients vs 17.1 +/- 5.6 mumol/l in CsA(-)patients; p = 0.3). Moreover, we found a significant inverse relationship between plasma homocyst(e)ine and folic acid concentrations in both CsA(+) (r = 0.218; p < 0.01) and CsA(-) (r = -0.678; p < 0.05) patients. Patients with a past history of cardiovascular incidents had higher plasma homocyst(e)ine concentrations than those without cardiovascular antecedent (20.5 +/- 7.8 mumol/l vs. 18.01 +/- 9.9 mumol/l; p < 0.05. To conclude: 1, We did not find any influence of CsA on plasma homocyst(e)ine concentrations. 2. We demonstrated that as in other patient category, plasma folic acid and homocyst(e)ine concentrations are significantly correlated in CsA(+) patients. 3. Homocyst(e)ine-lowering therapy would be prescribed in CsA(+) patients to allow correction of hyperhomocyst(e)inemia.
authors.affiliation: Department of Nephrology and Renal Transplantation, Hôpital Saint Jacques, Besançon, France.
authors.forename: D
authors.initials: D
authors.lastname: Ducloux
authors.forename: V
authors.initials: V
authors.lastname: Fournier
authors.forename: J M
authors.initials: JM
authors.lastname: Rebibou
authors.forename: C
authors.initials: C
authors.lastname: Bresson-Vautrin
authors.forename: R
authors.initials: R
authors.lastname: Gibey
authors.forename: J M
authors.initials: JM
authors.lastname: Chalopin
mesh_terms: D001161:Arteriosclerosis / Q000097:blood / Q000453:epidemiology; D016022:Case-Control Studies; D003404:Creatinine / Q000097:blood; D016572:Cyclosporine / Q000627:therapeutic use*; D005260:Female; D005492:Folic Acid / Q000097:blood; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007165:Immunosuppression Therapy; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D007166:Immunosuppressive Agents; D006710:Homocysteine; D016572:Cyclosporine; D005492:Folic Acid; D003404:Creatinine; D014805:Vitamin B 12