Amino-acid-based dialysis solution changes leptinemia and leptin peritoneal clearance.

In continuous ambulatory peritoneal dialysis (CAPD) patients, nutritional parameters, appetite, and transperitoneal solute movement can be modified by treatment with amino-acid-based dialysis solution (AADS). Because leptin is involved in energy expenditure and appetite regulation, we decided to examine the influence of AADS on serum and dialysate leptin concentrations. We prospectively evaluated AADS influence on leptinemia and peritoneal transport indices in CAPD patients. Nine clinically stable patients (7 males, 2 females), mean age 55.4 +/- 10.5 years, who had been treated with CAPD for 6.1 +/- 5.8 months, were studied. Examinations were conducted before treatment with 1.1% AADS (period I), after 3 months of AADS administration (period II), after 6 months of AADS administration (period III), and at 3 months after AADS discontinuation (period IV). The primary outcome measure was concentration of leptin in serum and dialysate. Secondary measures included anorexia incidence, nutrient intake, and nutritional parameters. Dialysate-to-plasma ratio (D/P), peritoneal excretion, and clearance (PCl) of leptin were calculated. After 3 months of AADS administration (period II), leptinemia was transiently lower (9.8 +/- 6.2 ng/mL vs 17.1 +/- 14.2 ng/mL, p = 0.017), while D/P (0.51 +/- 0.44 vs 0.23 +/- 0.19, p = 0.012), peritoneal excretion (72.9 +/- 85.4 micrograms/day vs 37.2 +/- 32.3 micrograms/day, p = 0.015), and PCl (4.02 +/- 3.40 mL/min vs 1.75 +/- 1.32 mL/min, p = 0.008) of leptin were higher than measurements obtained at entry. Anorexia incidence and daily protein and energy intakes showed no significant changes during the study. Total body mass, body mass index, and plasma concentrations of total protein and of albumin increased significantly during AADS treatment. A significant positive relation of leptinemia to total fat mass was observed when AADS was not used (periods I and IV). We conclude that administration of AADS in CAPD patients causes a transient decrease in leptinemia and increases in peritoneal excretion and in PCl of leptin, as well as dissociation of the physiological relationship between serum leptin level and total fat mass.