ROLES OF HEMODYNAMIC AND TUBULAR FACTORS IN GENTAMICIN-MEDIATED NEPHROPATHY

被引：18

作者：

HISHIDA, A ^{[1
]}

NAKAJIMA, T ^{[1
]}

YAMADA, M ^{[1
]}

KATO, A ^{[1
]}

HONDA, N ^{[1
]}

机构：

[1] HAMAMATSU UNIV SCH MED, DEPT MED 1, HAMAMATSU, SHIZUOKA, JAPAN

来源：

RENAL FAILURE | 1994年 / 16卷 / 01期

关键词：

AMINOGLYCOSIDE; HYDROXYL RADICAL; RENAL BLOOD FLOW; RENIN-ANGIOTENSIN SYSTEMS; TUBULAR NECROSIS;

D O I：

10.3109/08860229409044852

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

Gentamicin (GM) often causes polyuric acute renal failure (ARF) in humans and animals. GM-mediated ARF in rats was accompanied with activated renin-angiotensin system, increased renal endothelin content, and enhanced lipid peroxidation. Suppression of the renin-angiotensin activity by desoxycorticosterone acetate and saline drinking, and treatment with superoxide dismutase attenuated the GM-induced decline in whole-kidney GFR with well-maintained RBF but did not reduce the severity of tubular necrosis. On the other hand, treatment with dimethylthiourea, a hydroxyl radical scavenger, attenuated the GM-mediated decline in GFR and lessened tubular necrosis but did not ameliorate the reduction in RBF. These data suggest contributions of both vascular and tubular factors to the GM-induced decline in GFR in rats. However, relative importance of these factors probably differs with different doses of the agent.

引用

页码：109 / 116

页数：8

共 24 条

[1]

Schor N., Ichikawa I., Rennke H.G., Troy J.L., Brenner B.M., Pathophysiology of altered glomerular function in aminoglycoside-treated rats, Kidney Int, 19, pp. 288-296, (1981)

[2]

Pavao Dos Santos O.F., Boim M.A., Barros E.J.G., Schor N., Role of platelet activating factor in gentamicin and cisplatin nephrotoxicity, Kidney Int, 40, pp. 742-747, (1991)

[3]

Baylis C., Rennke H.R., Brenner B.M., Mechanisms of the defect in glomerular ultrafiltration associated with gentamicin administration, Kidney Int, 12, pp. 344-353, (1977)

[4]

Cojocel C., Dociu N., Ceacmacudis E., Baumann K., Nephrotoxic effects of aminoglycoside treatment on renal protein reabsorption and accumulation, Nephron, 37, pp. 113-119, (1984)

[5]

Luft F.C., Evan A.V., Comparative effects of tobramycin and gentamicin on glumerular ultrastructure, J Infect Dis, 142, pp. 910-914, (1980)

[6]

Avasthi P.S., Huser J., Evan A.P., Glomerular endothelial cells in gentamicin-induced acute renal failure (ARF) in rats, Kidney Int, 16, (1979)

[7]

Blantz R.C., Konnen K.S., Tucker B.J., Angiotensin II effects upon the glomerular microcirculation and ultrafiltration coefficient of the rat, J Clin Invest, 57, pp. 419-434, (1976)

[8]

Luft F.C., Aronoff G.R., Evan A.P., Connors B.A., Weinberger M.H., Kleit S.A., The renin-angiotensin system in aminoglycoside-induced acute renal failure, J Pharmacol Exp Ther, 220, pp. 433-439, (1982)

[9]

Morin J.P., Thomas N., Toutain H., Borghi H., Fillastre J.P., Modulation of gentamicin nephrotoxicity by chronic inhibition of angiotensin-I-converting enzyme in rat, Arch Toxicol, 63, pp. 47-53, (1989)

[10]

Kosek J.C., Mazze R.I., Cousins M.J., Nephrotoxicity of gentamicin, Lab Invest, 30, pp. 48-57, (1974)

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