It has been well known that urinary excretions of total N-acetyl- β-D-glucosaminidase (NAG) as one of tubular proteinuria are usually increased in the patients with nephrotic syndrome. But nephrotic patients are merely associated with tubular dysfunctions, so it is unclear the course of increased urinary NAG excretion at the active stage of this disease. The purpose of this paper is to define the origin of the urinary NAG in nephrotic syndrome by using the rats models due to puromycin aminonucleoside (PAN) administration. Nephrotic state were induced on the fifth day after only PAN 15 mg/100 g B. W subcutaneously injected to the rats in isolated metabolic cages. Serious analysis of NAG isozyme was performed by operating the fast protein liquid chromatography (FPLC, Pharmacia) connected with DEAE cellulose column. Then NAG activity was determined by m-cresolsulfophthalein-NAG (MCP-NAG) method in urine, glomerular and tubular tissue isolated by pore sieving. Urine was dialyzed to exclude low molecular weight substances and renal tissues were homogenized and centrifuged to get the supernatants for estimating NAG isozyme. As the result three components of NAG which were B, I+II and A isozyme were detected in urine and elutes from renal tissue. NAG B isozyme with nontreated rats were 9.2±1.5%, 46.3+7.4% and 17.5+2.6% in urine, glomeruli and tubular tissue respectively. The B/I+II+A isozyme ratio in urine were changed from 0.10±0.01 to 1.06±0.21 on the active stage of PAN nephrotic rats. According to the high level of B/I+II+A in glomeruli on the early stage of nephrotic rats, it might be supposed that NAG were discharged from the glomeruli. In conclusion, it is clearly defined that the source of NAG is partly derived from glomeruli in patients with nephrotic syndrome.
