RAGE and Serum Copeptin Act as a Potential Biomarker for Chronic Kidney Disease with and without Type 2 Diabetes Mellitus
Divya Mishra, Roshan Alam, Mohammad Kaleem Ahmed, Pulak Raj, Saba Khan, Mustafa Khan
Adipocytes, Advanced glycation end product, Amadori products, Aminoguanidine, Autosomal dominant polycystic kidney disease, Chronic kidney disease, Copeptin, Diabetes mellitus, Nephropathy, Receptors for advanced glycation end products, Schiff base
Citation Information :
Mishra D, Alam R, Ahmed MK, Raj P, Khan S, Khan M. RAGE and Serum Copeptin Act as a Potential Biomarker for Chronic Kidney Disease with and without Type 2 Diabetes Mellitus. Indian J Med Biochem 2021; 25 (3):131-134.
The critical role of receptors for advanced glycation end products (RAGEs) and serum copeptin in the progression of chronic diseases and their complications has recently become more apparent. This review summarizes the recent contributions to the field of RAGEs and serum copeptin in chronic kidney disease (CKD). Over the past 2 decades, RAGEs have been seen to be involved in the progression of CKD, and specifically, it leads to diabetic nephropathy. Although several in vitro and in vivo studies highlighten the detrimental role of AGEs accumulation in tissue injury. Recent studies have focused on the novel mechanisms that contribute to end-organ injury as a result of AGEs accumulation, as well as novel targets of therapy in kidney disease. Serum copeptin is related to the severity of the disease in autosomal dominant polycystic kidney disease (ADPKD), and it helps in the prediction of future renal events (decline in renal function and increase in total kidney volume). The main purpose of this review is to evaluate critically the role of RAGE and serum copeptin as a prognostic biomarker for renal outcomes in ADPKD, and it will be potentially helpful as a predictive marker of treatment response. As the prevalence and the incidence of CKD rises all over the world, nowadays it is very essential to identify the therapeutic strategies which must either delay the progression and aggressiveness of CKD or to improve the mortality rate in this population. The main focus of this review is to highlight the recent studies that enhance our current understanding of the mechanisms that mediate AGEs-induced progression in CKD as well as novel treatment strategies that have the potential to avoid this disease process. This review presents current knowledge regarding the roles of RAGE and copeptin in CKD with and without diabetes mellitus. Studies from human subjects are presented to highlight the breadth of evidence linking RAGE and copeptin to CKD consequences of these metabolic disorders.
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