Effluent Osteopontin levels reflect the peritoneal solute transport rate

Abstract

Long-term peritoneal dialysis (PD) is accompanied by low-grade intraperitoneal inflammation and may eventually lead to peritoneal membrane injury with a high solute transport rate and ultrafiltration failure. Osteopontin (OPN) is highly expressed through the stimulation of pro-inflammatory cytokines in many cell types. This study aimed to investigate the potential of OPN as a new indicator of peritoneal deterioration. One hundred nine continuous ambulatory PD patients were analyzed. The levels of OPN and IL-6 in peritoneal effluents or serum were analyzed by ELISA kits. The mean effluent OPN concentration was 2.39 ± 1.87 ng/mL. The OPN levels in drained dialysate were correlated with D/P Cr (p < 0.0001, R = 0.54) and D/D0 glucose (p < 0.0001, R = 0.39). Logistic regression analysis showed that the OPN levels in peritoneal effluents were an independent predictive factor for the increased peritoneal solute transport rate (PSTR) obtained by the peritoneal equilibration test (p < 0.001). The area under the receiver operating characteristic curve of OPN was 0.84 (95% CI: 0.75–0.92) in predicting the increased PSTR with a sensitivity of 86% and a specificity of 67%. The joint utilization of effluent OPN with age, effluent IL-6, and serum albumin further increased the specificity (81%). Thus, OPN may be a useful indicator of peritoneal deterioration in patients with PD.

Vascular calcification inhibitors and cardiovascular events in peritoneal dialysis patients

“…Many cytokines, like IL-1, IL-2, IL-6, and TNF-α are involved in its synthesis. OPN is involved in many physiological and pathological processes like cell adhesion, angiogenesis, apoptosis, inflammatory response, ectopic calcification, fibrosis, and tumor metastasis [43]. It facilitates the attachment of osteoclasts to the bone matrix and regulates the attachment of apatite crystals to the crystal surface.…”

“…OPN also has a role in the regulation of osteoclast differentiation, bone resorption, and bone mineralization [44]. In repair and restructuring for vascular system damage, it regulates the proliferation, migration, and aggregation of epithelial cells, smooth muscle cells, and macrophages in atherosclerosis lesions [43]. In atherosclerosis, OPN rises in parallel with the severity of calcification and atherosclerosis, so it could be a key regulator of mineral deposition in arterial tissue in disease and damage [43].…”

“…Besides, patients with high permeability were older, had been undergoing dialysis for a longer time, and had lower albumin and phosphorus levels. The authors concluded that dialysate OPN could be a good indicator for PET prediction and PD prognosis [43]. Another study focused on peritoneal membrane calcification, one of the dystrophic calcifications seen among ESRD patients.…”

“…In repair and restructuring for vascular system damage, it regulates the proliferation, migration, and aggregation of epithelial cells, smooth muscle cells, and macrophages in atherosclerosis lesions [43]. In atherosclerosis, OPN rises in parallel with the severity of calcification and atherosclerosis, so it could be a key regulator of mineral deposition in arterial tissue in disease and damage [43]. For OPN to mediate the inhibition of calcification, it must be phosphorylated in smooth muscle cells.…”