Ultrafiltration is essential in peritoneal dialysis (PD) for maintenance of euvolemia, making ultrafiltration insufficiency—preferably called ultrafiltration failure—an important complication. The mechanisms of ultrafiltration and ultrafiltration failure are more complex than generally assumed, especially after long-term treatment. Initially, ultrafiltration failure is mainly explained by a large number of perfused peritoneal microvessels, leading to a rapid decline of the crystalloid osmotic gradient, thereby decreasing aquaporin-mediated free water transport. The contribution of peritoneal interstitial tissue to ultrafiltration failure is limited during the first few years of PD, but becomes more important in long-term PD due to the development of interstitial fibrosis, which mainly consists of myofibroblasts. A dual hypothesis has been developed to explain why the continuous exposure of peritoneal tissues to the extremely high dialysate glucose concentrations causes progressive ultrafiltration decline. First, glucose absorption causes an increase of the intracellular NADH/NAD⁺ ratio, also called pseudohypoxia. Intracellular hypoxia stimulates myofibroblasts to produce profibrotic and angiogenetic factors, and the glucose transporter GLUT-1. Second, the increased GLUT-1 expression by myofibroblasts increases glucose uptake in these cells, leading to a reduction of the osmotic gradient for ultrafiltration. Reduction of peritoneal glucose exposure to prevent this vicious circle is essential for high-quality, long-term PD.

超滤在维持血容量正常的腹膜透析 (PD) 中必不可少，这使得超滤不足（最好称为超滤失败）成为一种重要的并发症。超滤和超滤失败的机制比通常假设的要复杂，尤其是在长期治疗之后。最初，超滤失败的主要原因是大量灌注腹膜微血管，导致晶体渗透压梯度迅速下降，从而减少水通道蛋白介导的自由水转运。腹膜间质组织对超滤失败的贡献在 PD 的最初几年是有限的，但由于主要由肌成纤维细胞组成的间质纤维化的发展，在长期 PD 中变得更加重要。已经开发了一个双重假设来解释为什么腹膜组织持续暴露于极高的透析液葡萄糖浓度会导致进行性超滤下降。首先，葡萄糖吸收导致细胞内NADH/NAD增加⁺比率，也称为假性缺氧。细胞内缺氧刺激肌成纤维细胞产生促纤维化和血管生成因子，以及葡萄糖转运蛋白 GLUT-1。其次，肌成纤维细胞增加的 GLUT-1 表达增加了这些细胞中的葡萄糖摄取，导致超滤渗透压梯度降低。减少腹膜葡萄糖暴露以防止这种恶性循环对于高质量、长期的 PD 至关重要。