Diabetic kidney disease (DKD) is one of the most common microvascular complications of type 2 diabetes mellitus (T2DM), affecting up to 40% of diabetic patients and accounting for the leading cause of end-stage renal disease worldwide \[1\]. The progression of DKD involves multiple mechanisms, including oxidative stress, endothelial dysfunction, and most importantly, chronic inflammation \[2\].
Systemic inflammation plays a central role in renal injury by promoting glomerular and tubulointerstitial damage. the neutrophil-to-lymphocyte ratio (NLR) and systemic inflammatory index (SII) has emerged as a readily accessible markers of subclinical inflammation. Elevated NLR and SII levels have been significantly associated with increased urinary albumin excretion and decreased estimated glomerular filtration rate (eGFR) in T2DM patients \[3\]. It was demonstrated that patients in the highest NLR tertile had a higher prevalence of DKD, independent of confounders \[4\].
High-sensitivity C-reactive protein (hsCRP), is widely used to evaluate systemic inflammation. Recent studies have shown a strong association between elevated hsCRP levels and DKD development \[5\].Some studies provided genetic evidence supporting a causal relationship between higher hsCRP and diabetic nephropathy \[6\].
Monocyte chemoattractant protein-1 (MCP-1) is a chemokine involved in monocyte recruitment to inflamed renal tissues. Elevated serum and urinary MCP-1 levels have been found to predict microalbuminuria and eGFR decline in T2DM patients \[7,8\].
Identifying these markers may help in early diagnosis, risk stratification, and monitoring progression of DKD.