Systemic and local impact of glucose and glucose degradation products in peritoneal dialysis solution

Abstract

The main osmotic agent used in the peritoneal dialysis (PD) solution is glucose because of its great osmotic power, simple metabolism, and safety. Once into the systemic circulation, however, glucose can be a cause for metabolic complications including hyperglycemia, obesity, and dyslipidemia. The glucose absorbed from peritoneal cavity leads to insulin resistance and hyperglycemia, which is associated with oxidative stress. Long-term exposure of peritoneal membrane to glucose in PD solution also has local effects such as functional and structural changes leading to peritoneal membrane failure. Moreover, the intraperitoneal glucose absorption induces conditions similar to postprandial hyperglycemia, which is a proven independent risk factor of coronary artery disease in patients with type 2 diabetes. Though speculative, glucose toxicity might explain a higher mortality of PD patients after the first few years compared with those on hemodialysis. Glucose degradation products (GDPs) induce apoptosis of peritoneal mesothelial cells (PMCs), renal tubular epithelial cells, and endothelial cells, and facilitating epithelial mesenchymal transition of PMCs. GDPs provide a stronger reactivity than glucose in the formation of advanced glycation end-products, a known cause for microvascular complications and arteriosclerosis. Unfortunately, clinical studies using a low-GDP PD solution have provided mixed results on the residual renal function, peritonitis, peritoneal membrane function, and mortality; consistent outcome data are not readily available at present.