Interleukin-6 and C-reactive protein in pathogenesis of diabetic nephropathy: new evidence linking inflammation, glycemic control, and microalbuminuria.

Recent studies have shown that subclinical inflammation is a part of type 2 diabetes mellitus. This study was designed to explore the relationships between low-grade inflammation and renal microangiopathy in patients with type 2 diabetes mellitus. Sixty patients with type 2 diabetes mellitus were included in the study and further divided into normoalbuminurics, microalbuminurics, and macroalbuminurics, of 20 patients each. We analyzed serum concentrations of high-sensitivity C-reactive protein (HS-CRP) and interleukin-6 (IL-6) and studied their correlation with proteinuria. The patients and a control group of 20 healthy individuals were followed-up for a period of 6 months and the markers measured again. A positive correlation was found between urinary albumin excretion and levels of HS-CRP (r = 0.781, P < .001) and IL-6 (r = 0.708, P < .001). The level of glcosylated hemoglobin (HbA1c) showed a significant positive correlation with urinary albumin excretion (r = 0.630, P < .001), CRP (r = 0.750, P < .001), and IL-6 (r = 0.680, P < .001). Levels of HbA1c, HS-CRP, and IL-6 significantly decreased in all three diabetic groups after 6 months of treatment. Also, the percentage of HbA1c decrement correlated well with the decrease percentage in HS-CRP (r = .277, P = .01). Inflammatory markers in early type 2 diabetic nephropathy are elevated and are independently associated with urinary albumin excretion. It is possible to hypothesize on the participation of locally released cytokines in the development of kidney damage.