Department of Nephrology and Rheumatology, Aichi Medical University, 1-1 Karimata, Yazako, Nagakute City, Aichi, 480-1195, Japan.
Department of Anatomy, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
Sci Rep. 2024 Mar 28;14(1):7412. doi: 10.1038/s41598-024-58148-x.
Peritoneal membrane dysfunction in peritoneal dialysis (PD) is primarily attributed to angiogenesis; however, the integrity of vascular endothelial cells can affect peritoneal permeability. Hyaluronan, a component of the endothelial glycocalyx, is reportedly involved in preventing proteinuria in the normal glomerulus. One hypothesis suggests that development of encapsulating peritoneal sclerosis (EPS) is triggered by protein leakage due to vascular endothelial injury. We therefore investigated the effect of hyaluronan in the glycocalyx on peritoneal permeability and disease conditions. After hyaluronidase-mediated degradation of hyaluronan on the endothelial cells of mice, macromolecules, including albumin and β2 microglobulin, leaked into the dialysate. However, peritoneal transport of small solute molecules was not affected. Pathologically, hyaluronan expression was diminished; however, expression of vascular endothelial cadherin and heparan sulfate, a core protein of the glycocalyx, was preserved. Hyaluronan expression on endothelial cells was studied using 254 human peritoneal membrane samples. Hyaluronan expression decreased in patients undergoing long-term PD treatment and EPS patients treated with conventional solutions. Furthermore, the extent of hyaluronan loss correlated with the severity of vasculopathy. Hyaluronan on endothelial cells is involved in the peritoneal transport of macromolecules. Treatment strategies that preserve hyaluronan in the glycocalyx could prevent the leakage of macromolecules and subsequent related complications.
腹膜透析(PD)中腹膜的膜功能障碍主要归因于血管生成;然而,血管内皮细胞的完整性会影响腹膜通透性。透明质酸是内皮糖萼的组成部分,据报道,它参与预防正常肾小球中的蛋白尿。一种假说认为,包裹性腹膜硬化症(EPS)的发展是由血管内皮损伤引起的蛋白质渗漏引发的。因此,我们研究了糖萼中透明质酸对腹膜通透性和疾病状况的影响。在用透明质酸酶降解小鼠内皮细胞上的透明质酸后,包括白蛋白和β2 微球蛋白在内的大分子漏入透析液中。然而,小分子溶质的腹膜转运不受影响。在病理上,透明质酸的表达减少;然而,血管内皮钙黏蛋白和糖萼的核心蛋白肝素硫酸的表达得到了保留。使用 254 个人的腹膜膜样本研究了内皮细胞上的透明质酸表达。在接受长期 PD 治疗的患者和接受常规溶液治疗的 EPS 患者中,透明质酸的表达减少。此外,透明质酸丢失的程度与血管病变的严重程度相关。内皮细胞上的透明质酸参与大分子的腹膜转运。保持糖萼中透明质酸的治疗策略可以防止大分子的渗漏和随后的相关并发症。