Peritoneal angiogenesis in response to dialysis fluid.
In patients on peritoneal dialysis (PD) ultrafiltration failure (UFF) often develops after 3 or 4 years of treatment. Increased angiogenesis, leading to an increase in small solute transport, is a key feature of UFF. Among the pathophysiological mechanisms responsible for an increased angiogenesis, peritonitis, or just 'low-grade inflammation', such as in the uremic condition per se seem to be of importance. However, also the interaction of the peritoneal membrane with peritoneal dialysis fluids (PDF), especially those containing glucose and glucose degradation products (GDP) may be crucial in triggering an increased angiogenesis. This brief review summarizes some recent experimental evidence that PDF low in glucose and GDP, or with an alternative buffer, pyruvate, may partly prevent angiogenesis in long-term PD. The fact that rat models of PD, in which catheters are used for instillation of the PDF, usually show an exaggerated neoangiogenesis, compared to rat models in which the PDF was administered by daily intraperitoneal injections, is also commented upon. To prevent angiogenesis in PD all precautions should be taken to provide a peritonitis-free PD. Although not directly proven, the use of low-GDP solutions should be preferred to GDP-containing solutions. Furthermore, ACE inhibitors have recently been shown to be of value in preventing increases in small solute transport in long-term PD. These findings await confirmation in randomized controlled trials.
Rippe
Bengt
B
D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D005947:Glucose / Q000009:adverse effects; D006801:Humans; D007674:Kidney Diseases / Q000503:physiopathology / Q000628:therapy; D009389:Neovascularization, Pathologic / Q000209:etiology* / Q000503:physiopathology; D010530:Peritoneal Dialysis / Q000009:adverse effects*; D010537:Peritoneum / Q000098:blood supply* / Q000503:physiopathology; D051381:Rats
D005947:Glucose