Age Accumulation in Peritoneal Membrane and Cavity during Peritoneal Dialysis and Its Effect on Peritoneal Structure and Function

Abstract

T he conventional dialysis solutions contain a high concentration of glucose to induce sufficient ultra filtration and to maintain fluid balance in uremic patients. During continuous ambulatory peritoneal dialysis (CAPD), the peritoneal cavity is therefore continuously exposed to high glucose for a long time. Histological examination of the peritoneum from peritoneal dialysis patients revealed duplication of submesothelial basement membrane in both diabetic and non diabetic patients and acceleration of preexisting duplication of capillary basement membrane in diabetic patients (1-4). These histologic changes, similar to diabetic complications, are believed to be due to continuous exposure of the peritoneum to an unphysiologic ally high concentration of glucose. Hyperglycemia is associated with the presence or progression of complications in non insulin-dependent diabetes mellitus (NIDDM) (1,5) and insulindependent diabetes mellitus (IDDM) (2). One of the major consequences of prolonged hyperglycemia is accelerated formation of advanced glycosylation endproducts (AGEs) on long-lived structural proteins (3). AGEs are excreted mainly by the kidneys and, therefore, serum level increases as renal function decreases (4). AGE peptide levels in spent dialysate in PD patients is higher than plasma levels (6,7). Peritoneal accumulation of AGEs was reported in PD patients (8,9). Exogenous administration of AGEs induced an increase in vascular permeability in normal animals (10) and the accumulation of AGE induced structural and functional alterations of tis sue proteins (11). Peritoneal accumulation of AGEs, structural and functional alterations of tissue proteins, and increased permeability of the peritoneal vasculature may re