Increases in serum leptin levels during peritoneal dialysis are associatedwith inflammation and a decrease in lean body mass

Leptin, secreted from fat cells, functions as a lipostat mechanism through modulation of satiety signals. Markedly elevated leptin levels have been do cumented in uremic patients, especially in those who are treated by periton eal dialysis (PD). However, the role of hyperleptinemia in uremic patients is not clear, and it is not known whether elevated leptin levels contribute to uremic anorexia and changes in body composition. In this prospective st udy, serum leptin, C-reactive protein (CRP), plasma insulin, and body compo sition (dual-energy x-ray absorptiometry) were measured in 36 patients (53 +/- 1 yr) close to start and after about 1 yr of PD. In addition, markers o f dialysis adequacy and urea kinetics were followed during treatment with P D. During PD, the total body fat mass (20.5 +/- 1.0 to 22.9 +/- 1.3 kg; P < 0.01), truncal fat mass (11.5 +/- 0.7 to 13.2 +/- 0.9 kg; P < 0.001), and serum leptin levels (20.1 +/- 3.8 to 35.6 +/- 6.8 ng/ml; P < 0.01) increase d markedly, especially in patients with diabetes mellitus. Twenty-five PD p atients that lost lean body mass during PD had significantly (P < 0.05) ele vated initial CRP levels (14 +/- 2 mg/L) compared to 11 patients (<10 mg/L) who gained lean body mass during PD. A significant increase in serum lepti n levels (20.9 +/- 4.2 to 42.7 +/- 4.0 ng/ml; P < 0.001) was observed in th ose patients who lost lean body mass, whereas no such change (18.4 +/- 8.4 to 19.2 +/- 6.4 ng/ml) was observed in the patients that gained lean body m ass during PD treatment. The present longitudinal results demonstrate that serum leptin level and body fat content increase markedly during PD, especi ally in diabetic patients. Patients that lost lean body mass during PD had higher initial CRP levels and increased their serum leptin levels significa ntly during PD compared to those patients that gained lean body mass. Addit ional studies are therefore needed to elucidate the role of hyperleptinemia and inflammation in causing anorexia, protein-malnutrition, and changes in body composition during treatment with PD.