This study was undertaken to evaluate two different doses of folic acid and their effects on the control of hyperhomocysteinemia, and on pro-oxidant and antioxidant changes in a group of 32 hemodialysis (HD) patients. Blood samples were collected in a group of patients at three different times: before (basal; B), after the first (S1), and after the second (S2) three-month supplementation periods, and compared to samples from a group of healthy individuals. Analysis of vitamins (C, E, folate, and B12), oxidant parameters (lipid and protein oxidation), and homocysteine were performed. Hyperhomocysteinemia of different degrees was observed in all patients on HD (45.30 +/- 24.89 microM). Oxidative stress was also detected, with lipoperoxidation and protein oxidation being associated with lower concentrations of antioxidant substances (vitamins E and C). The first folate dose (2.5 mg after each dialysis session) reduced by half the initial concentrations of homocysteine (44.92 +/- 22.05 to 20.56 +/- 6.79 microM; p < 0.05) but did not normalize its values. The second dose (15 mg) did not show an additional effect, but it was at this time that lipoperoxidation was significantly reduced, although the protein oxidation showed no change. It was concluded that the first dose of folic acid was efficient in reducing homocysteine concentrations, without normalization of values. The participation of hyperhomocysteinemia in oxidative stress appeared to be partial, but in combination with dialysis treatment, may contribute to the induction of an oxidative environment in this group. The possible antioxidant action of folate must also be considered in this case, acting directly against lipoperoxidation or through hyperhomocysteinemia control. Routine supplementations of folic acid and other antioxidant vitamins should be considered in hemodialysis in order to reduce homocysteine levels to lower values, that although not normal, may be more beneficial in minimizing the cardiovascular risk in this group.
Glucose intolerance has been shown in patients with chronic renal failure (CRF), probably associated with insulin resistance in peripheral tissues. The present study was thus designed to investigate the effect of hemodialysis on peripheral muscle glucose metabolism of patients with CRF. Nine normal subjects and 6 patients with CRF were studied after an overnight fast (12-14 h) and during 3 h after ingestion of 75 g of glucose. Peripheral glucose metabolism was analyzed by the forearm technique to estimate the muscle exchange of substrates combined with indirect calorimetry. The CRF patients were studied before and after at least 1 month of hemodialysis treatment. Plasma glucose levels (arterial and venous) were higher in uremic patients before dialysis than in normal controls. After the dialysis therapy there was improvement in the glycemic profile of the CRF patients. Decreased forearm muscle glucose uptake was observed in the uremic patients before dialysis compared to the normal subjects (234 ± 71 vs. 858 ± 52 μmol/100 ml forearm-3 h, p < 0.05) with diminished nonoxidative glucose metabolism (128 ± 78vs.686 ± 58 μmol/100 ml forearm-3 hp < 0.05). After the hemodialysis treatment of the CRF patients, the forearm glucose uptake and the nonoxidative glucose metabolism increased significantly to values of 527 ± 64 and 384 ± 87 μmol/100 ml forearm · 3 h, respectively. Muscle glucose oxidation did not differ significantly between normals and CRF patients before and after dialysis, as well as the serum insulin levels. These data demonstrate that insulin resistance in the presence of chronic uremia is accompanied by impaired muscle glucose uptake and nonoxidative glucose metabolism, which are significantly improved by the hemodialysis treatment.
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