title: Homocysteine and atheromatous renal artery stenosis.
abstract: Hyperhomocysteinemia is an independent risk factor for vascular disease, frequently observed in patients with severe renal impairment. Hyperhomocysteinemia has never been considered as a possible risk factor in renal artery stenosis. We investigated plasma folate and vitamin B12, methylenetetrahydrofolate reductase (MTHFR) C677T and cystathionine beta-synthase (CBS) 844ins68 polymorphisms, and homocysteine levels before and after methionine (100 mg/kg) loading in 58 patients with angiographically documented renal artery stenosis and mildly impaired renal function. One hundred and two normotensive subjects with angiographically normal coronary arteries and no history or clinical or angiographic evidence of atherosclerosis in other vascular districts, were considered as a control group. Mean total homocysteine levels were significantly higher in patients than in controls (P<0.01), as was the prevalence of hyperhomocysteinemia (51.7% vs. 32.3%, P<0.05). However, MTHFR alleles and genotypes as well as CBS 844ins68 mutation frequencies were similar in the two groups, whereas a lower folate level was observed in the patients. Moreover, patients with MTHFR A/A genotype showed a poorer folate status than control subjects, suggesting that a subclinical folate deficiency may be very frequent in renal artery stenosis, regardless of C677T mutation. In conclusions, hyperhomocysteinemia is common in patients with atheromatous renal artery stenosis; a subclinical folate deficiency seems to be involved, regardless of MTHFR thermolabile or CBS insertion genotypes. Folate supplementation might be useful in the management of overall vascular risk of these patients.
authors.affiliation: Department of Clinical and Experimental Medicine, University of Verona, Italy. oliviero.olivieri@univr.it
authors.forename: O
authors.initials: O
authors.lastname: Olivieri
authors.forename: S
authors.initials: S
authors.lastname: Friso
authors.forename: E
authors.initials: E
authors.lastname: Trabetti
authors.forename: D
authors.initials: D
authors.lastname: Girelli
authors.forename: F
authors.initials: F
authors.lastname: Pizzolo
authors.forename: G
authors.initials: G
authors.lastname: Faccini
authors.forename: C
authors.initials: C
authors.lastname: Stranieri
authors.forename: P F
authors.initials: PF
authors.lastname: Pignatti
authors.forename: R
authors.initials: R
authors.lastname: Corrocher
mesh_terms: D000368:Aged; D000483:Alleles; D001161:Arteriosclerosis / Q000097:blood* / Q000150:complications* / Q000235:genetics; D016022:Case-Control Studies; D003541:Cystathionine beta-Synthase / Q000235:genetics; D005260:Female; D005492:Folic Acid / Q000097:blood; D005838:Genotype; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D008875:Middle Aged; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000235:genetics; D011110:Polymorphism, Genetic; D012078:Renal Artery Obstruction / Q000097:blood* / Q000150:complications* / Q000235:genetics; D012307:Risk Factors; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D006710:Homocysteine; D005492:Folic Acid; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D003541:Cystathionine beta-Synthase; D014805:Vitamin B 12