Studies have demonstrated that hyperhomocyst(e)inemia is present in re
nal transplant recipients and is correlated with cardiovascular diseas
e. It is still unclear whether hyperhomocyst(e)inemia observed in rena
l transplant recipients solely depends on the moderate reduction of re
nal function in these patients or if additional mechanisms are operati
ve in this patient category. A recent study suggested that cyclosporin
e (CsA) increased plasma homocyst(e)ine concentration in interfering w
ith folate-assisted remethylation of homocysteine. To confirm this hyp
othesis, we studied plasma homocyst(e)ine, folic acid and cobalamin co
ncentrations in 122 renal transplant recipients (104 on CsA and 18 not
receiving CsA). After adjusting for age, gender transplant duration a
nd serum creatinine concentration, patients with and without CsA had s
imilar plasma homocyst(e)ine concentrations (17.9 +/- 6.1 mu mol/l in
CsA(+) patients vs 17.1 +/- 5.6 mu mol/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 = -0.2
18; 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 mmol/l vs 18.01 +/- 9.9 mmol/l; p <0.05). To conclude: 1. W
e did not fmd any influence of CsA on plasma homocyst(e)ine concentrat
ions. 2. We demonstrated that as in other patient category, plasma fol
ic acid and homocyst(e)ine concentrations are significantly correlated
in CsA (+) patients. 3. Homocyst(e)ine-lowering therapy would be pres
cribed in CsA (+) patients to allow correction of hyperhomocyst(e)inem
ia.