Chemerin, Visfatin: Key Markers of Diabetes Associated-chronic Kidney Disease

Abstract Background Diabetes Mellitus is defined as a consistent hyperglycemia occur due to deficiency of insulin or insulin resistance by the insulin-dependent cell of the body. Persistence hyperglycemia leads to accumulation of advance glycosylated end product (AGEP) which founds to damage glomerular basement membrane of the nephrons leading to kidney damage causing diabetes - associated CKD. CKD is defined as glomerular filtration rate (GFR) < 60ml/min/1.73 m² for a minimum of three month irrespective of etiology. This not only affect the patient’s normal life but also decrease the life expectancy. This study aims to provide pro-inflammatory markers for earliest diagnosis and hence the treatment planning of the diabetes – associated CKD. Method An analytical cross-sectional study was conducted at tertiary care center in south India (Chennai, SRM MEDICAL COLLEGE HOSPITAL & RESEARCH CENTRE). The total sample size was calculated to be 120, which was further divided in two equal group. Group I involve 60 diabetes-associated CKD participants (25-65 years) and Group II involved aged (25-65 years), sex matched healthy controls. Serum Chemerin and Visfatin levels were quantified among both the group. Spearman’s correlation was performed to find the correlation of these markers with e-GFR and study participants. Findings Significant elevated levels of serum Chemerin was found in diabetes-associated CKD participants [4618.875 (1650.795, 9173.230)] as compare to control participants [1566.273 (666.948, 2601.144)]. Similarly, significantly elevated levels of serum Visfatin was found in diabetes-associated CKD participants [46.450 (31.458, 100.733)] as compare to control participants [14.226 (8.865, 18.619)]. Significant negative correlation was observed between serum Chemerin and e-GFR (r = -0.413, p = 0.000003), similarly Significant negative correlation was observed between serum Visfatin and e-GFR (r = -0.647, p = 0.000000). This clearly suggests the role of these adipokines in kidney damage, hence they can act as potential pro-inflammatory markers in diabetes-associated CKD. Interpretation Above findings clearly suggest the potential of these pro-inflammatory markers in earliest diagnosis and thus treatment planning in diabetes-associated CKD.