Association of Galectin-3 and IL-33/ST2 Axis with Chronic Kidney Disease Severity: Do They Play A Role in Associated Comorbidities?

Abstract

Background: Elevated Galectin-3 (Gal-3) levels and Interleukin 33 (IL-33)/suppression of tumorigenicity 2 )ST2 ( involved in the pathophysiology of incident chronic kidney disease (CKD), and renal fibrosis. Besides, IL-33 induces fibrosis of pulmonary, hepatic, skin, renal, and pancreatic tissues in a way that is dependent on ST2., whereas, plays a protective role against cardiac fibrosis and atherosclerosis. Objective: the aim of this study was to investigate the association between Gal-3 and the IL-33/ST2 axis with CKD severity and the incidence of associated multi-organ affection. Methodology: Eighty one subjects were enrolled in this study; 69 patients with CKD and 12 age-and sex-matched healthy controls. Disease severity was assessed by estimated glomerular filtration rate (eGFR), and patients were classified as having mild, moderate, or severe CKD. Serum Gal-3, IL-33, and sST2 were tested by ELISA and the expression level of Gal-3 was assessed by Real-time PCR. Results: Serum Gal-3, IL-33, ST2, and the Gal-3 gene expression levels significantly increased as the severity of CKD increases. Correlation analysis showed significant associations between serum creatinine, serum Gal-3, serum IL-33, serum ST2, and the Gal-3 gene level. Conclusion: Concentrations of sST2, and the Gal-3 gene expression were directly proportional with the level of CKD severity highlighting the important role of these mechanisms in the progression of kidney disease. Accordingly, these biomarkers may be useful tools for disease monitoring and individualized therapies to slow the advancement of CKD as well as associated diabetes and heart disease.