Correction of metabolic acidosis in hemodialysis: consequences on serum leptin and mineral metabolism

Hyperleptinemia and metabolic acidosis (MA) are frequently observed in patients on hemodialysis (HD). While the role of leptin in patients on HD is not completely understood, HD only partially corrects MA. Both leptin and acidosis have effect on bone disease. The goal of the present study was to evaluate the effects of MA correction on chronic kidney disease-mineral and bone disorder laboratory parameters and leptin levels. Forty-eight patients on HD, aged 43 +/- A 19 years, were prospectively studied. Individual adjustments in the bicarbonate dialysate concentration were made to maintain pre-dialysis concentration a parts per thousand yen22 mEq/l. Blood gas analysis was done monthly for 4 months (M1-M4). From M0 to M4, serum albumin increased (from 3.5 +/- A 0.3 to 4.0 +/- A 0.3 g/l, p < 0.0001) while beta(2) microglobulin decreased (from 27.6 +/- A 8.3 to 25.8 +/- A 6.8 A mu g/ml, p = 0.025). Serum leptin decreased in all but three patients, as well as leptin/adiponectin ratio (p < 0.0001). There was a decrease in ionized serum calcium (from 5.0 +/- A 0.5 to 4.7 +/- A 0.5 mg/dl, p = 0.002) and an increase in parathyroid hormone (PTH) [from 191 (85, 459) to 446 pg/ml (212, 983), p < 0.0001] and in serum phosphate (from 5.4 +/- A 1.4 to 5.8 +/- A 1.1 mg/dl, p = 0.048). MA correction in HD patients can decrease leptin, an atherogenic marker. The impact of such treatment extends to uremic bone disease, as decrease in serum calcium and increase in PTH. However, this could be an undesirable effect because it may aggravate a secondary hyperparathyroidism. Whether the reduction in leptin levels has impact on outcomes in patients on hemodialysis deserves further investigation.