Time-dependent change in the toxic effects of amikacin on renal functions

Fujimura, Akio; Sudoh, Toshiaki; Ebihara, Akio

doi:10.1016/0024-3205(94)00647-4

Cited by 5 publications

(6 citation statements)

References 10 publications

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“…A higher incidence of nephrotoxicity during the rest period has been found in many animal studies. 5,[9][10][11][12][13][14][15] In these studies aminoglycoside concentrations in the renal cortex were also higher when the aminoglycosides were administered during the rest period,579,'0,12-14 therefore an increased uptake by the kidney during the rest period is a likely cause of the increased incidence of nephrotoxicity, and this increased uptake is most likely the result of the higher AUC after administration during the rest period. Whether this increase in renal cortical uptake fully explains the higher incidence of nephrotoxicity during the night or whether the kidney is also more susceptible to injury during the night is not clear.…”

Section: Discussionmentioning

confidence: 79%

Circadian variations in serum levels and the renal toxicity of aminoglycosides in patients

Prins

Weverling

Ketel

et al. 1997

Clin Pharmacol Ther

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Animals show a faster clearance and a lower incidence of nephrotoxicity and ototoxicity when aminoglycosides are administered during the activity period. Human data on a circadian rhythm in pharmacokinetics are conflicting, and there are no data on a circadian rhythm in toxicity. When aminoglycosides are administered once daily, as is often done, a circadian rhythm in pharmacokinetics or toxicity could have clinical implications. In a prospective study we investigated the influence of drug administration time on serum drug levels and the incidence of nephrotoxicity in 221 patients with serious infections treated with gentamicin or tobramycin once daily. We did not find statistically significant differences in trough or peak levels for the three time periods (midnight to 7:30 AM, 8 AM to 3:30 PM, and 4 to 11:30 PM). Nephrotoxicity occurred significantly more frequently when the aminoglycosides were administered during the rest period (midnight to 7:30 AM; p = 0.004). In addition to the coadministration of high-dose furosemide or other nephrotoxic antibiotics and the duration of treatment, the time of administration was still an independent risk factor in a multivariate analysis.

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Section: Discussionmentioning

confidence: 79%

Circadian variations in serum levels and the renal toxicity of aminoglycosides in patients

Prins

Weverling

Ketel

et al. 1997

Clin Pharmacol Ther

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“…Temporal variation in the nephrotoxicity of aminoglycosides has been previously reported for gentamicin (27,37), tobramycin (20,21), and amikacin (8,11) with different doses and parameters of toxicity. Temporal variation in the nephrotoxicity of isepamicin has already been reported (peak toxicity at 1300 h, through toxicity at 0100 h) for high doses of isepamicin (300 mg/kg of body weight) with urinary enzyme excretion, histopathologic nephrotoxicity scores, and serum and cortical levels of isepamicin as parameters of toxicity (38).…”

mentioning

confidence: 78%

“…Nakano and Ogawa (25) were the first to demonstrate the temporal variations in the nephrotoxicity of gentamicin in mice with 50% lethal dose as a parameter of toxicity. With sublethal doses of aminoglycosides, temporal variations in the nephrotoxicity of gentamicin (27,32,37), amikacin (8,11,13), tobramycin (20,21), and isepamicin (38) were observed in experimental animals. There are actually no data on the temporal variation in the nephrotoxicity of aminoglycosides in humans.…”

mentioning

confidence: 99%

Temporal variation in nephrotoxicity of low doses of isepamicin in rats

Yoshiyama¹,

Grenier²,

Gourde³

et al. 1996

Antimicrob Agents Chemother

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The temporal variation in the nephrotoxicity of low doses of isepamicin was studied in male Sprague-Dawley rats treated with a single daily intraperitoneal injection of saline (NaCl, 0.9%) or isepamicin (80 mg/kg of body weight) at either 0800, 1400, 2000, or 0200 h for 4 and 10 days. On day 10, the cellular regeneration (incorporation of [3H] thymidine into DNA of renal cortex) and cortical accumulation of isepamicin were significantly higher in animals treated at 1400 h than at 0200 h (P < 0.01). Immunogold labeling studies showed that isepamicin was essentially localized in the lysosomes of proximal tubular cells in all treated groups, but the density of the gold particles over the lysosomes was higher in animals treated at 1400 than at 0200 h. The results of the present study show that the renal toxicity of isepamicin was maximal at 1400 h (midlight period) and minimal at 0200 h (middark period).

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“…Several other studies were done with lower doses of aminoglycosides and more sensitive parameters of toxicity such as urinary enzyme excretion (8,10,12,25,26,32,33). More recently, Fujimura et al (13) reported that the magnitude of the changes induced by amikacin on creatinine clearance and tubular function was maximal when the drug was injected at 1600 h (rest period) compared with that when the drug was injected at other times of day.…”

Section: Discussionmentioning

confidence: 99%

Effects of fasting on temporal variations in nephrotoxicity of gentamicin in rats

Beauchamp

Collin

Grenier

et al. 1996

Antimicrob Agents Chemother

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Evidence for temporal variations in the nephrotoxicity of low doses of aminoglycosides were recently shown by using specific and sensitive parameters of renal toxicity. The aim of the present study was to evaluate the effect of a short period of fasting on the temporal variations in the renal toxicity of gentamicin. Twenty-eight normally fed (i.e., food and water were available ad libitum throughout the experiment) female Sprague-Dawley rats (weight, 175 to 220 g) and 28 fasted rats (i.e., only water was available during a 12-h fast before and a 24-h fast after gentamicin injection) were used. The animals were synchronized on a 14-h light, 10-h dark cycle (lights on at 0600 h) for 1 week before gentamicin administration. In July 1993, each group of animals was treated with a single intraperitoneal injection of saline (NaCl, 0.9%) or gentamicin (150 mg/kg of body weight) at either the peak (1400 h) or the trough (0200 h) of the previously determined toxicity. On day 1, the 24-h urinary excretion of beta-galactosidase, N-acetyl-beta-D-glucosaminidase, and gamma-glutamyltransferase was significantly higher in normally fed animals treated with gentamicin at 1400 h than in their time-matched controls and in normally fed animals treated at 0200 h (P < 0.01), which had normal levels of these enzymes. By contrast, the urinary excretion of these enzymes was significantly higher in both groups of gentamicin-treated, fasted rats than in their time-matched control groups (P < 0.01), reaching levels similar to those measured in normally fed rats treated at 1400 h. The accumulation of gentamicin was significantly lower in the renal cortex of normally fed rats treated at 0200 h than in rats treated at 1400 h (P < 0.05), but this time-dependent difference was not found in fasted rats treated at 0200 and 1400 h. Immunogold labeling done on ultrathin sections and observed by electron microscopy showed a similar subcellular localization of gentamicin in normally fed and fasted rats treated at either 1400 or 0200 h. These results suggest that the feeding period is of crucial importance in the temporal variations of the nephrotoxicity of gentamicin in rats.

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Time-dependent change in the toxic effects of amikacin on renal functions

Cited by 5 publications

References 10 publications

Circadian variations in serum levels and the renal toxicity of aminoglycosides in patients

Circadian variations in serum levels and the renal toxicity of aminoglycosides in patients

Temporal variation in nephrotoxicity of low doses of isepamicin in rats

Effects of fasting on temporal variations in nephrotoxicity of gentamicin in rats

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