Kidney injury molecule-1 (Kim-1): an early biomarker for nephropathy in type II diabetic patients

Renal damage is a serious major microvascular diabetic complication implicated in the death of diabetic patients, which would necessitate the need for new biomarkers to detect early stage of diabetic nephropathy (DN). Kidney injury molecule-1 (Kim-1), a type I transmembrane protein, is undetectable in normal kidneys but markedly induced in proximal tubules after ischemic and toxic injury. So, the present study was conducted to estimate and evaluate Kim-1 as a biomarker for DN. This cross-sectional study was carried out on 60 male and female type II diabetic patients (whose serum creatinine level was less than 2 mg/dL). Diabetic patients were classified as microalbuminuric with nephropathy (urinary albumin was 30–300 mg/dL) and normoalbuminuric without nephropathy (urinary albumin was <30 mg/dL). Twenty matched apparently healthy subjects were included as control group. Patients and controls were assessed for fasting blood glucose, glycosylated hemoglobin (HbA1c), serum creatinine, blood urea nitrogen (BUN), microalbuminuria, and urinary Kim-1. Urinary Kim-1 levels were elevated significantly tenfold in type II diabetic microalbuminuric patients as compared to the control group and normoalbuminuric diabetic patient. Urinary Kim-1 levels were positively correlated with microalbuminuria, serum creatinine, BUN, duration of diabetes, and BMI. Higher urinary Kim-1 level in T2D particularly in those with nephropathy and its correlation with urinary microalbumin, serum creatinine, blood urea, and BUN may reflect the role of Kim-1 as a biomarker for diagnosis and prognosis of diabetic nephropathy among T2D patients taking into account other risk factors.