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Renal excreted angiotensin converting enzyme (ACE) inhibitor captopril, and renal.hepatic bile excreted ACE inhibitor temocapril, were compared by monitoring serum ACE and renal ACE expression (protein and mRNA) in streptozotocin-induced diabetic rats. Serum ACE levels did not change in untreated diabetic rats or in those treated with temocapril, compared with normal control rats. However, serum ACE levels significantly increased in diabetic rats treated with captopril after 3 months (153.8 +/- 23.0 vs. 43.5 +/- 5.5 IU/l/37 degrees C, p < 0.01) and 6 months (113.6 +/- 9.3 vs. 36.9 +/- 2.9 IU/l/37 degrees C, p < 0.01) compared with normal control rats. Compared with normal control rats (3.6 +/- 0.4), proximal tubular ACE protein expression significantly (p < 0.01) decreased in untreated diabetic rats (1.6 +/- 1.1), but significantly (p < 0.01) increased in diabetic rats treated with captopril (3.7 +/- 0.3) and temocapril (3.5 +/- 0.4). Renal ACE mRNA levels decreased in untreated diabetic rats (125.5 +/- 20.3 vs. 313.3 +/- 53.4, p < 0.01) compared with normal control rats for 6 months. Renal ACE mRNA levels tended to increase in diabetic rats treated with captopril (184.4 +/- 51.2 vs. 125.5 +/- 20.3) and temocapril (165.4 +/- 43.2 vs. 125.5 +/- 20.3) compared with untreated diabetic rats for 6 months. In conclusion, diabetic rats had lower proximal tubular ACE protein expression and lower renal ACE mRNA levels compared with normal control rats. Furthermore, both ACE inhibitors increased renal ACE protein and mRNA expression, but differed in their effect on serum ACE levels.

Among several glycated compounds (GC) which are based on Maillard reaction, glycated hemoglobin (HbA1c) and fructosamine (FRA) have been utilized widely as a markers of diabetes. Recently, glycated albumin (GA) has been pointed out as a new indicator. For the determination of GA, spectrophotometry combined with an affinity column method has been mainly used, however the procedure is complicated. Recently a two-column HPLC method (ion-exchange column and affinity column) has been developed by Shima. We have evaluated a GA analyzer GAA-2000 based on Shima's method. After a series of fundamental and performance evaluation studies, the GAA-2000 was found to be appropriate for our study. Reference values obtained from this equipment were 10.56-16.87%. Correlation coefficients based on GA using diabetic and diabetic nephropathy patient specimens (n = 87) were: FRA (r = 0.944) greater than HbA1c (r = 0.842) greater than Glucose (r = 0.510) Superoxide dismutase (SOD) and lipid peroxidase (LPO) with are produced in relation to active oxygen did not show a good correlation. Although we tried classify the patients according to juvenile (20-39), middle (40-64) and senile (greater than 65) the method of Asada et al., we could not find any distinct tendencies.

N-Acetyl-beta-glucosaminidase (NAG) exists in renal tubules and seminal tract. We measured the NAG level in patients with urinary tract and seminal tract diseases and evaluated its clinical significance. The urinary NAG level was high in renal tubular function disorders such as glomerulonephritis, diabetic nephropathy and hydronephrosis. In these patients, NAG-isoenzyme studies indicated that the A-type isoenzyme decreased while the B-type isoenzyme increased. On the other hand, in the seminal tract disease patients, the urinary NAG level was high in benign prostatic hypertrophy with a catheter indwelling and in prostatitis. Urinary and seminal NAG-isoenzymes were measured in normal subjects. The isoenzyme patterns for urinary NAG and seminal NAG differed. The urinary NAG isoenzymes were measured in acute prostatitis patients, we found that the A-type isoenzyme decreased and the B type increased. In conclusion, when the A/B ratio of the NAG-isoenzyme is close to 24.9/75.0 in the urine, the presence of urological diseases in which seminal plasma could be mixed in, especially prostatic diseases, should be suspected.