The significance of serum SLC7A11 levels in the occurrence of vascular calcification in maintenance peritoneal dialysis patients

Author:

Wu Jing1,Zhang Junling1,Tang Qiong1,Zhu Huixian1,Chen Yan1,Xiong Hua1,Jiang Hongwei1ORCID

Affiliation:

1. Department of Nephrology The Affiliated Hospital of Jiangnan University Wuxi Jiangsu Province China

Abstract

AbstractAimThis research aimed to explore the serum levels of solute carrier family 7 member 11 (SLC7A11) in patients with maintenance peritoneal dialysis (MPD) and its correlation with vascular calcification (VC) and clinical results.MethodsThis present prospective observational cohort study enrolled 189 patients with MPD who were undergoing regular peritoneal dialysis for over 3 months in our hospital from February 2020 to July 2022. The abdominal aortic calcification score was used to assess the VC condition of MPD patients. The serum SLC7A11, interleukin (IL)‐6, IL‐1β and C‐reactive protein levels were measured by enzyme‐linked immunosorbent assay (ELISA). Demographic and clinical statistics were collected. All patients were followed up for 1 year and the overall survival time (OS) of all patients were recorded. All data used SPSS 18.0 for statistical analyses.ResultsPatients with moderate/severe calcification in MPD had a longer duration of dialysis, higher serum levels of phosphate (P) and calcium (Ca) and lower serum levels of SLC7A11. Spearman's analysis revealed a negative correlation between serum SLC7A11 levels and the levels of P, Ca and IL‐1β. Additionally, we observed an association between serum SLC7A11 levels and clinical prognosis as well as the extent of VC in MPD patients. Multivariate logistic regression analysis indicated that dialysis duration, SLC7A11, and P were risk factors for VC in MPD patients.ConclusionThe serum SLC7A11 levels decreased remarkably in MPD patients with moderate/severe calcification. This study may provide new targets and comprehensive approach to cardiovascular protection in patients with chronic kidney disease.image

Publisher

Wiley

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