Urinary N-acetyl-β-D-glucosaminidase (NAG) was measured in 108 diabetic patients with or without clinical diabetic nephropathy, and the correlation between urinary NAG activity and proteinuria, serum creatinine, and HbAI level were studied. The results obtained were as follows. 1) The urinary NAG activity levels of non-diabetic controls, diabetics without proteinuria, diabetics with intermittent proteinuria and diabetics with persistent proteinuria were 2.74±1.41 (n=48), 7.70±4.62 (n=48), 12.26±6.35 (n=35) and 19.63±13.07 U/g creatinine (n=25), respectively. Such a marked and stepwise increment of urinary NAG activity suggests that the enzyme may represent a useful indicator of early diabetic renal involvement. 2) No correlation was noted between urinary NAG activity and serum creatinine level. 3) A significant positive correlation was observed between urinary NAG activity and HbAI level (r=0.28, n=75, p<0.02). However, further investigations are required to evaluate the relation between the state of metabolic control and the urinary NAG activity, since insulin-dependent poor control patients were more common among diabetics with persistent proteinuria who formed the high urinary NAG activity group.
Recently, it has been found that the HbAI level tends to be high in renal failure without diabetes. In the present study, we investigated whether HbAI could be used as an indicator of control in patients with renal failure as well as in diabetic patients. The correlations between HbAI and BUN, or serum creatinine for a duration of 8 weeks prior to blood collection were investigated. The best correlation was found between HbAI and BUN, or serum creatinine also at 1 to 2 weeks before blood collection. It was found that a better correlation existed between HbAI and BUN (r=0.59, n=32, p<0.001) than between HbAI and serum creatinine (r=0.42, n=31, p<0.02) at 1 to 2 weeks before. It appeared, therefore, that HbAI was produced by carbamylation of urea, and HbAI could be used as an indicator of the state of renal failure of 1 to 2 weeks before in patients with renal failure without impaired glucose tolerance.