Effect of peritoneal glucose load on plasma leptin concentration in continuous ambulatory peritoneal dialysis patients

This study was performed to investigate the effect of peritoneal glucose load on plasma leptin concentrations in the continuous ambulatory peritoneal dialysis (CAPD) performed on 13 non-diabetic ESRD patients. Plasma leptin and insulin concentrations were measured for 2 hours during a single 2 liter exchange of 1.5% glucose-based dialysate (SPD, n = 6), for 7 days of daily peritoneal dialysis (DPD, n = 7). In DPD, standard full volume (2,000 ml x 4 times/day) exchange was performed immediately after operation. In SPD, plasma leptin and insulin concentrations remained unchanged during the study. In DPD, the plasma leptin concentration increased significantly after CAPD on the first day (PD1) (11.2 +/- 5.4 to 17.0 +/- 6.0 ng/mL, p < 0.05) and this elevation seemed to persist until 7 days after operation. After CAPD, there was no significant day-to-day variation in peritoneal glucose absorption (391-465 cal). Oral intake seemed to decrease on operation day (PD0) and PD1 and then increased slowly. Plasma insulin and glucose concentrations did not significantly change after CAPD. Changes of leptin concentration were significantly correlated with the changes of peritoneal glucose absorption at PD1. In conclusion, continuous peritoneal glucose load may affect plasma leptin concentrations in CAPD patients.

A case of living-related kidney transplantation in Bartter's syndrome

Bartter's syndrome is a renal tubular disorder characterized by hypokalemia, metabolic alkalosis, increased urinary excretion of potassium and prostaglandins, a relative vascular resistance to the pressor effects of exogenous angiotensin II, and hyperplasia of the juxtaglomerular apparatus. In most patients, the glomerular filtration rate is normal and chronic renal failure does not develop. We report here on a case of living-related kidney transplantation in Bartter's syndrome, in which a non-steroidal anti-inflammatory drug is suspected to be the cause of the end-stage renal disease.