[Frequency of hyperhomocysteinemia in hemodialysis patients with folic acid supplementation].
BACKGROUND
It is known that hyperhomocystinemia is an independent risk factor for development of atherosclerosis. In end stage renal disease the frequency of hyperhomocystinemia is much greater than in normal populations.


OBJECTIVE
In this study homocystein (Hcy), folic acid and vitamin B12 concentrations were determined in 125 chronic renal failure patients being on folic acid supplementation (3 mg/day). In 107 patients the frequency of C667T polymorphism of methylene tetrahyrofolate reductase (MTHFR) was also determined. The relationships between these parameters were also studied.


RESULTS
It was found that in these patients who are under continuous folic acid supplementation the mean level of homocysteine was 16.8 +/- 7.2 mumol/L, a value considerably lower than the homocysteine concentration reported for non-supplemented patients. The elevation of homocysteine concentrations was independent of gender, time spent in renal replacement therapy, and the type of renal replacement therapy (hemodialysis: 17.6 +/- 12.6; hemodiafiltration: 16.6 +/- 12.9 mumol/L). Data showed an inverse relation between plasma homocysteine concentrations and the concentrations of folic acid and vitamin B12. Moderately severe hyperhomocystinemia (Hcy > 20 mumol/L) was found in about 30% of patients. In those the frequency of patients for homozygous T677 allele of MTHFR was about 25-30%. However, in all ESRD patients the frequency of the homozygotes was the same then in the normal population. Homocysteine plasma levels correlated with MTHFR polymorphism: in the wild type group Hcy was 14 +/- 7 mumol/L, in the heterozygous group was 17.2 +/- 6.2 mumol/L, and in the homozygous group was 21 +/- 19 mumol/L.


CONCLUSIONS
Long-term folic acid supplementation decreased the homocysteine level in end stage renal disease patients. However, in folic acid resistant group, who were in 30% homozygotes for C667T of MTHFR (suggesting that homocysteine-methionine remethylation cycle is disturbed), instead of the administration of folic acid, methylene tetrahydrofolate supplementation might be considered.
Kárpáti
István
I
Debreceni Egyetem Orvos- és Egészségtudományi Centrum, I. sz. Belgyógyászati Klinika. karpati@ibel.dote.hu
Balla
József
J
Szóke
Gabriella
G
Bereczky
Zsuzsanna
Z
Páll
Dénes
D
Ben
Thomas
T
Toma
Kornél
K
Katona
Evelin
E
Mohácsi
Attila
A
Paragh
György
G
Varga
Zsuzsa
Z
Kakuk
György
G
Muszbek
László
L
D000328:Adult; D000367:Age Factors; D000368:Aged; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage* / Q000097:blood*; D017583:Hemodiafiltration; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000453:epidemiology*; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D008875:Middle Aged; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000378:metabolism; D011110:Polymorphism, Genetic; D006435:Renal Dialysis; D013997:Time Factors; D014805:Vitamin B 12 / Q000097:blood*
D006710:Homocysteine; D005492:Folic Acid; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D014805:Vitamin B 12