Diabetes mellitus (DM) can be explained as a group of multiple abnormalities characterized by hyperglycemia either due to insulin deficiency or insulin resistance (IR) or in some cases both. The resulting hyperglycemia induces several metabolic and physiological changes including formation of advanced glycation end products (AGEs) (Vlassara & Uribarri, 2014) and IR (Yki-Järvinen & Koivisto, 1984). Diabetes is also one of the leading and most common causes of end stage renal disease (ESRD), and is associated with increased mortality and morbidity, responsible for more than 47% of new ESRD cases in the US (Caramori & Rossing, 2022).

Diabetic Nephropathy (DN) is one of the most common complications found in T2DM patients. 40% of patients with T2DM and 30% of IDDM patients develop DN (Hussain et al., 2021). DN is thought to be one of the major causes leading to chronic kidney disease (CKD) and ESRD (Alicic, Rooney, & Tuttle, 2017). In a study done incorporating 4006 T2DM patients in the United Kingdom, 28% of patients developed renal failure after the average follow up of 15 years (Retnakaran et al., 2006). In India, 34.4% prevalence of DN (Hussain, Habib, & Najmi, 2019) and a composite prevalence of 62.3% of diabetic-CKD (Dash, Agarwal, Panigrahi, Mishra, & Dash, 2018) have been reported, suggesting the higher prevalence of DN in India. As per a report of American diabetes association (ADA) (2014), more than 40% of diabetic patients are estimated to develop CKD, comprising a significant number of patients further developing ESRD requiring either dialysis or renal transplantation. IR is one of the common attributes observed in patients with moderate to severe chronic renal failure (DeFronzo and Alvestrand, 1980, Eidemak et al., 1995). There are various reports suggesting a strong association of IR and hyperinsulinemia with CKD through stage I to IV, independent of diabetes (Chen et al., 2004, Soltani et al., 2015, Yamagata et al., 2007). There are multiple biochemical and signal transduction pathways that result in IR under diabetic condition. One of the major contributors to IR is post-translational glycation of insulin, which renders it inefficient to function leading to hyperinsulinemia and hyperglycaemia (Song & Schmidt, 2012).