Urinary guanidinoacetic acid excretion as an indicator of gentamicin nephrotoxicity in rats

被引：12

作者：

Kiyatake, I

Nakamura, T

Koide, H

机构：

[1] Koto Hosp, Dept Med, Div Nephrol, Koto Ku, Tokyo 1360072, Japan

[2] Urasoe Gen Hosp, Renal Unit, Okinawa, Japan

[3] Shinmatsudo Cent Gen Hosp, Dept Med, Chiba, Japan

来源：

RENAL FAILURE | 2004年 / 26卷 / 04期

关键词：

guanidinoacetic acid; N-acetyl-beta-D-glucosaminidase; beta(2)-microglobulin; glycine amidinotransferase; nephrotoxicity;

D O I：

10.1081/JDI-120039812

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：

The kidney is the main site of guanidinoacetic acid synthesis and excretion. The aim of this study was to examine whether urinary guanidinoacetic acid is a sensitive indicator for diagnosis of early-stage gentamicin nephrotoxicity. Early-stage renal injury was induced in rats by a single intravenous injection of 5, 10, or 30 mg/kg body weight gentamicin. Twenty-four hours after injection all rats were killed. Blood, urine and tissue guanidino compound concentrations were determined by high performance liquid chromatography. Glycine amidinotransferase activity in tissues was assayed according to the method of Pilsum. Urinary guanidinoacetic acid excretion was decreased in 5 mg/kg gentamicin-treated rats in comparison to that in control rats, whereas urine N-acetyl-beta-D-glucosaminidase activity and beta(2)-microglobulin were unchanged. Guanidinoacetic acid concentration and glycine amidinotransferase activity in the kidney were significantly decreased in 5, 10, and 30 mg/kg gentamicin-treated rats; the decreases were dose-dependent. These results suggest that the urine guanidinoacetic acid concentration is a more sensitive indicator of renal injury than conventional indicators such as urine N-acetyl-beta-D-glucosaminidase and beta(2)-microglobulin.

引用

页码：339 / 344

页数：6

共 14 条

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