אסיף מאגר המחקר החקלאי

Enhanced urinary trypsin inhibitory activity in gentamicin-induced nephrotoxicity in rats

Year:

1988

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Volume :

176

Co-Authors:

Smetana, S., Division of Nephrology, Kaplan Hospital, Rehovot, Affiliated with Hebrew University-Hadassah Medical School, JerusalemIsrael
Khalef, S., Department of Biochemistry and Human Nutrition, Faculty of Agriculture, The Hebrew University of Jerusalem, Israel
Nitsan, Z., Agricultural Research Organization, The Volcani Center, Rehovot, Israel
Hurwitz, N., Institute of Pathology, Kaplan Hospital, Rehovot, Affiliated with Hebrew University-Hadassah Medical School, JerusalemIsrael
Miskin, A., Laboratory of Microbiology, Kaplan Hospital, Rehovot, Affiliated with Hebrew University-Hadassah Medical School, JerusalemIsrael
Bar-Khayim, Y., Division of Nephrology, Kaplan Hospital, Rehovot, Affiliated with Hebrew University-Hadassah Medical School, JerusalemIsrael
Birk, Y., Department of Biochemistry and Human Nutrition, Faculty of Agriculture, The Hebrew University of Jerusalem, Israel

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Abstract:

We delineated in rats, the relationship between trypsin inhibitory activity in the urine and the nephrotoxic effects of gentamicin, eg, proteinuria and deterioration of glomerular filtration rate (GFR), measured by creatinine clearance. Gentamicin, 70 mg/kg per day, was injected intraperitoneally for 6-10 successive days. Serum and urine gentamicin levels were determined by a microbiological test. Trypsin inhibitory activity was assayed by the casein digestion method. The results showed a steady increase in urinary trypsin inhibitory activity starting from the fourth injection day. The increased levels of urinary trypsin inhibitory activity were associated with increased levels of urinary gentamicin excretion (r = 0.36, p < 0.02, n = 50 after the fourth injection day), and were significantly higher than in control groups (p < 0.001). The urinary trypsin inhibitory activity was inversely correlated with the GFR (r = -0.45, p < 0.01, after the second injection day). The serum trypsin inhibitory activity remained unchanged throughout the study period in all groups. These data suggest that increased urinary trypsin inhibitory activity may be involved in the pathogenesis of gentamicin-induced nephrotoxicity. © 1988.

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