title: Enzymuria in non-insulin-dependent diabetic patients: signs of tubular cell dysfunction.
abstract: 1. To evaluate tubular damage in diabetic patients, we measured the 24 h urinary excretion of five enzymes (N-acetyl-beta-D-glucosaminidase, gamma-glutamyl transpeptidase, dipeptidyl aminopeptidase IV, alanine aminopeptidase and alkaline phosphatase) that originate in renal proximal tubular cells. 2. Studies were performed on 118 non-insulin-dependent diabetic patients, 59 non-diabetic patients with chronic renal disease and 47 normal control subjects. First, the correlation between renal function, glycaemic control and urinary enzyme excretion was investigated. Secondly, the subjects were treated by controlled diet therapy to assess the effects of better glycaemic control on urinary enzyme excretion. 3. Regardless of a diabetic or non-diabetic cause of renal dysfunction, all of the five enzymes showed abnormal urinary excretion in patients with renal insufficiency (serum creatinine concentration > 2.0 mg/dl). In diabetic patients, however, an increase in N-acetyl-beta-D-glucosaminidase excretion and a decrease in gamma-glutamyl transpeptidase excretion were noted even in those who had no signs of renal dysfunction, including microalbuminuria. Moreover, the excretion of these two enzymes had a higher degree of correlation with glycaemic control and renal function than did that of the other three enzymes. Multiple regression analysis revealed that excretion of N-acetyl-beta-D-glucosaminidase is best correlated with urinary protein (r2 = 0.35), whereas excretion of gamma-glutamyl transpeptidase is closely associated with glomerular filtration rate (r2 = 0.33). 4. In diabetic patients, diet therapy improved glycaemic control but had no effects on renal function, microalbumin excretion and beta 2-microglobulin excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Ikenaga
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: N
authors.initials: N
authors.lastname: Ishii
authors.forename: H
authors.initials: H
authors.lastname: Itoh
authors.forename: T
authors.initials: T
authors.lastname: Saruta
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine; D000469:Alkaline Phosphatase / Q000652:urine; D000626:Aminopeptidases / Q000652:urine; D018826:CD13 Antigens; D003924:Diabetes Mellitus, Type 2 / Q000178:diet therapy / Q000201:enzymology / Q000503:physiopathology* / Q000652:urine; D004152:Dipeptidyl-Peptidases and Tripeptidyl-Peptidases / Q000652:urine; D004798:Enzymes / Q000652:urine*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000652:urine; D007684:Kidney Tubules / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D005723:gamma-Glutamyltransferase / Q000652:urine
chemical_list: D004798:Enzymes; D005723:gamma-Glutamyltransferase; D000469:Alkaline Phosphatase; D000118:Acetylglucosaminidase; D000626:Aminopeptidases; D018826:CD13 Antigens; D004152:Dipeptidyl-Peptidases and Tripeptidyl-Peptidases