Advanced glycation end products (AGEs) have been noted in the peritoneal tissue of continuous ambulatory peritoneal dialysis (CAPD) patients, and this may cause an increase in membrane permeability. In vivo and in vitro kinetic analysis was carried out on furosine and pentosidine, early and late glycation products. Plasma furosine and pentosidine were measured by HPLC in patients with renal dysfunction with or without diabetes mellitus (DM) and dialysate pentosidine and furosine in CAPD patients. Only those dialysis patients without residual renal function were used in this study. Plasma furosine was remarkably high in DM, hemodialysis (HD), and CAPD patients. Plasma pentosidine appeared to depend on renal function and was not influenced by diabetic condition. Plasma pentosidine was significantly higher in CAPD than HD patients. A weak positive correlation was noted between dialysate and plasma furosine and pentosidine, indicating the main source of furosine and pentosidine in PD effluent to be plasma. Serial dialysate sampling showed furosine and pentosidine to increase linearly. Mean dialysate/plasma (D/P) of furosine and pentosidine were 0.043 and 0.012, respectively. Protein-bound product size and in situ formation of furosine in the peritoneal cavity would be the reason for these differences in D/P. In situ formation of early glycation products in the peritoneal cavity may be concluded to take place in CAPD patients, and high plasma pentosidine may lead to its accumulation in tissue, resulting, possibly, in pathological change.