GAA as an indicator of gentamicin nephrotoxicity
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 beta2-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 beta2-microglobulin.