Urinary N-Acetyl-Beta-D Glucosaminidase Activity is Associated with Inflammation and Proteinuria in Diabetic and Non-Diabetic Patients with Different Stages of Chronic Kidney Disease

Abstract

OBJECTIVE: Clinical studies have demonstrated that tubulointerstitial rather than glomerular pathology correlates with the degree and progression of renal impairment. Urinary n-acetyl-betaD- glucosaminidase (NAG) is a biomarker of tubular damage, shown to be elevated in patients with glomerulonephritis and acute kidney injury. However, it has not been assessed longitudinally in chronic kidney disease (CKD). The aim of the present study was to determine urinary NAG activity and its possible associations with metabolic and inflammatory parameters in CKD.

MATERIAL and METHODS: A total of 72 patients (mean age: 64.5 +/- 15.7) with stage 1-5 CKD were included. Of the 72 patients 23 (32%) had diabetic nephropathy and 49 (68%) had different types of primary glomerular diseases. Fasting blood samples were collected to analyse complete blood count, urea, creatinine, albumin, lipid parameters, C-reactive protein, uric acid and parathyroid hormone. 24-hour urine was collected to determine protein excretion. Urinary NAG and creatinine levels were analysed from the first morning urine samples. The NAG index (urinary NAG/ creatinine) was used to exclude dilutional errors.

RESULTS: Mean eGFR was 38.3 +/- 21.7 ml/min. The urinary NAG index was significantly higher in stage 3 compared to stage 2 (32.1 +/- 23.5 vs. 7.5 +/- 3.3 U/gr-creatinine; p=0.002) and lower in stage 5 compared to stage 3 CKD (8.2 +/- 7.6 vs. 32.1 +/- 23.5; p=0.017). The urinary NAG index was positively correlated with 24-hour urine protein excretion (r=0.43; p=0.0001) and serum CRP (r=0.549; p=0.04) and negatively correlated with hemoglobin levels (r-0.394; p=0.004).

CONCLUSION: The present study demonstrated that urinary NAG correlates with systemic inflammation and proteinuria and may be associated with progression of CKD.