SEIBUTSU BUTSURI KAGAKU

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NAG isozyme in urine was fractionated by cellulose acetate membrane electrophoresis to the following 3 fractions in the order from the positive pole: pre A form, A form, and B form. In healthy males, they showed 12.03±5.56%, 73.15±4.77%, and 14.81±2.90%, respectively. In females, they showed 12.87±4.70%, 65.47±4.61%, and 21.70±5.03%, respectively. With respect to percentage of each fractions, pre A form showed 10% or more both in male and female healthy subjects. On the other hand, patients with glomerular diseases such as MCNS, MN, and PGN as well as CRF showed low pre A form level of 5% or less, whereas they were comparable to that of healthy subjects in total NAG activity. The A form fraction showed 72.91±9.46% in MCNS, 64.66±7.97% in MN, and 60.65±16.41%, in PGN, 60.38±5.40% in CRF, 66.58±5.51% in DM, and 68.35±5.95% in healthy subjects. Except for CRF with a significant difference (p<0.01) from the healthy subjects, patients with other renal diseases showed no differences. The B form fraction showed 22.65±10.30% in MCNS, 31.88±9.17% in MN, 34.80±19.65% in PGN, 36.48±0.95% in CRF, 22.42±5.78% in DM, and 19.11±5.48% in healthy subjects. Any patients with renal diseases showed higher values than healthy subjects. There was no disease-specific pattern among various renal diseases. However, B form in MCNS was significantly lower than those in the other renal diseases. In 58 patients with diabetes, there was a positive relationship between urinary protein concentration and NAG with a coefficient of correlation of 0.570. With respect to each isoenzyme fractions of NAG, the coefficients of correlation were -0.544 for pre A form, 0.153 for A form, and 0.314 for B form. In renal diseases, there was a positive relationship with NAG to urinary protein excretion with a coefficient of correlation of 0.419 but no such relationship with individual isozymes.

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A placental specific antigen (CPA, 34kD, pI 5.4-5.8) has been isolated from feline placenta. The expression of the CPA were examined in various tissues of pregnant or non pregnant cat with a anti-CAP antibody. The CPA antigen did not detect in amniotic fluid in maternal peripheral serum and retroplacental serum. Immunohistochemical analysis demonstrated the antigen staining was limited to the syncytiotrophoblast cells of the placenta. The CPA concentration is increased in the tissue of placenta increasing the gestation age, and reached the peak concentration around the 37th days of pregnancy.

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