Administration Of Gentamicin Research Articles

Carissa carandas Linn. fruit extract ameliorates gentamicin–induced nephrotoxicity in rats via attenuation of oxidative stress

ObjectiveTo elucidate the mechanism of action of methanolic extract of Carissa carandas fruits (MCCF) in attenuation of diabetic nephropathy using gentamicin induced nephrotoxicity model. MethodsExtract was daily administered to Sprague Dawley rats at doses of 100, 200 and 400 mg/kg for 8 days along with intramuscular injection of gentamicin (80 mg/kg). After completion of the study, serum was analyzed for blood urea nitrogen, albumin and creatinine; urine (24 h) was analyzed for albumin and creatinine. Kidney was evaluated for its biochemical and morphological changes. ResultsExtract at doses of 200 and 400 mg/kg significantly normalized the nephrotoxic biomarkers in serum and urine and increased the kidney antioxidant activities which were altered due to gentamicin toxicity. The histological findings reveal that MCCF was capable of protecting the kidney against gentamicin toxicity. ConclusionsExtract ameliorated oxidative stress generated by gentamicin administration, which is one of the mechanisms for its preventive action against diabetic nephropathy.

EVALUATION OF GENTAMICIN DOSES FOR TREATING CHILDREN WITH SEVERE PNEUMONIA

Administration of gentamicin in pediatric with severe pneumonia cases is a rational use of antibiotic. Gentamicin as a narrow therapeutic range agent (0.5 to 10 mg/L) should be followed by monitoring using TDM in order to know the levels of drug in the patient’s body so it does not cause toxicity or effects of drugs that are too small. This study aimed to estimate levels of gentamicin in serum after administration pediatric with pneumonia at Dr. Sardjito Hospital and assesed the improvement of clinical outcomes.The study was conducted retrospectively and data were obtained from medical record of pediatric inpatient, 1 month-16 years, whose recieved gentamicin in Dr. Sardjito Hospital in period between January 2009-April 2014. Clinical outcomes were namely body temperature, respiratory rate, chest retraction, and leucocyte number. The data were analyzed descriptively including the patient characteristics, estimated blood levels of gentamicin, estimated gentamicin for adjusment dose. In order to determine the effect of clinical outcome parameter on the success of therapy. Data were analyzed statistically using chi square on SPSS program. The results showed that the average of blood levels of gentamicin in all 31 patients were in therapeutic range (0.5 to 10 mg/L). However there were 20 patients (64,52%) had the level of gentamicin at > 10 mg/L and 10 patient (32,26%) had < 0,5 mg/L. The research also showed that 8 patient had improvement in the clinical outcome although 23 patient not yet had improvement in these parameters. Keywords: severe pneumonia, gentamicin, dose evaluation, estimate levels, clinical outcome

Gentamicin sulphate permeation through porcine intestinal epithelial cell monolayer.

Gentamicin is an aminoglycoside antibiotic widely used in combination with dimethyl sulphoxide (DMSO) in topical drug formulations. It is not known, however, whether DMSO can enhance the permeation of gentamicin through biological membranes, leading to oto- and nephrotoxic side effects. A simple and reliable high-performance liquid chromatographic (HPLC) method was applied for the quantitative determination of gentamicin collected from the apical and basolateral compartments of the porcine intestinal epithelial cell line IPEC-J2 cell monolayer using fluorometric derivatisation of the analyte with fluorenylmethyloxycarbonyl chloride (FMOC) prior to chromatographic run in the presence and absence of 1% DMSO. The lack of change in transepithelial electrical resistance (TER) demonstrated that gentamicin and 1% DMSO did not affect IPEC-J2 cell monolayer integrity via the disruption of cell membranes. Chromatographic data also ascertained that gentamicin penetration across the cell monolayer even in the presence of 1% DMSO was negligible at 6 h after the beginning of apical gentamicin administration. This study further indicates that the addition of this organic solvent does not increase the incidence of toxic effects related to gentamicin permeation.

Hemopexin, a potential biomarker for the diagnosis of chronic predisposition to acute kidney injury

In the last years, the new concept of predisposition to acquire acute kidney injury (AKI) is emerging. This concept was observed in our group when experimental animals exposed to an absolutely subnephrotoxic acute treatment with certain drugs (e.g. gentamicin and cisplatin) developed AKI when they were treated with a second insult with another drug, while control animals exposed to the same second drug experimented no toxicity. On these grounds, we decide to study if chronic exposure to nephrotoxicants might induce this predisposition to AKI and investigate how to detect this condition by the search of predisposition biomarkers. To this end, rats (Sprague-Dawley) were treated with a subtoxic dosage of the experimental nephrotoxin uranyl nitrate (UN) in the drinking water for 22 weeks, or plain water (as control). After 21 weeks both groups were treated with subtoxic regime of getamicin during 7 days. Renal function was monitored by means of serum creatinine, serum urea, proteinuria, N-acetyl-beta-D-glucosaminidase and lactate dehydrogenase excretion measurement. After and before gentamicin treatment a subset of rats were sacrificed and their kidneys used for histology. With the purpose of identifying biomarker of predisposition, proteomic studies were performed before gentamicin administration at week 21. Chronic administration of UN in drinking water during 21 weeks did not modify renal function or renal tissue integrity. However, when rats exposed to UN during 21 weeks where challenged with low doses of gentamicin, they developed an overt renal failure as shown by an increase in creatinine, urea and by histological alterations. These alterations were not observed in the control group. Using a proteomic analysis, hemopexin was detected which was validated by Western blot. Urinary excretion of hemopexin was statically higher in the exposed group than in the control group. Our results suggest that chronic exposure to UN, at doses that apparently does not produce damage, predisposes to AKI when animals were subjected to a second insult at subtoxic doses. Hemopexin protein might be potentially used as marker of chronic predisposition to ARF. This new diagnostic tool might help to reduce AKI incidence and severity, and also the associated sanitary and socioeconomic costs.

Development of an “In Situ” renal perfusion system to study the origin of urinary biomarkers in a nephrotoxicity model induced by gentamicin

Background and AimsGentamicin is an aminoglycoside antibiotic widely used for the treatment of many infectious diseases. Its main side effect is its nephrotoxicity, which occurs in 10-25% of therapeutic courses, despite proper monitoring and hydration of patients, can lead to acute kidney injury (AKI). We have previously demonstrated that urinary damage markers like albuminuria increased as a consequence of the addition of gentamicin. In the present work we aimed at specifically studying the renal handling of albuminuria in a nephrotoxicity model, through in situ renal perfusion experiments. MethodsMale Wistar rats were administrated by a single dose of gentamicin (150mg/kg), or not. After 5 days, rats were anesthetized and an extracorporeal circuit for kidney perfusion was set up. The renal artery, vein and ureter of the right kidney were ligated. The renal artery of the left kidney and the urinary bladder were canulated. A catheter was placed in the right carotid artery and connected directly to the renal artery. Urine was continuously collected from a catheter placed in the urinary bladder at 10min intervals. After 1h of renal perfusion with blood from the carotid artery, oxygenated and warm (37 °C) Krebs-dextran (40g/L of dextran) was perfused through the renal artery at 3mL/min, and was discarded through the renal vein. Albuminuria was measured in the different urine fractions. ResultsFrom the second day after gentamicin administration, albuminuria was significantly increased, as compared to control rats, in which urinary markers were undetectable. When exogenous Krebs solution prefunding the kidney, neither gentamicin rats nor control rats excreted albuminuria. As a control of the perfusion experiments, urinary markers still appeared in the urine in gentamicin rats whose kidney was perfused with its own blood. However, albuminuria was undetectable in control rats. ConclusionsOur results support the idea that excess albumin found in the urine (albuminuria) as a consequence of treatment with gentamicin comes from the blood ultrafiltrate reaching Bowman’s capsule and not from the renal parenchyma. More interestingly, our results provide and in situ method to test the origin of urinary biomarkers in different conditions.

Non-compliance in gentamicin prescribing and administration: A patient safety issue

AbstractImportance: Extensive use of antibiotics requiring dose-monitoring and weight-based prescribing can reduce compliance, risking morbidity, and mortality from sepsis. Objective: To determine if gentamicin was being prescribed according to recommendations in the British National Formulary and trust guidelines. Methods: All patients prescribed gentamicin in a one-month period on electronic prescribing were included. Data comprised demographics, admission specialty, dosing regime prescribed, number of doses received, actual dose, and recorded reasons for non-administration. Results: 374 patients were prescribed gentamicin over one month. 223 were prescribed stat doses (207 received, 16 not given; 93% compliance). The remaining 151 patients were on multidose prescriptions, between 3 and 7 doses. 25 received zero doses, 41 a single dose, 50 patients received two doses, and 35 received three doses or greater (23% compliance with guidelines). Conclusion: Antibiotics are essential in treating and preventing...

Intraosseous and intravenous administration of antibiotics yields comparable plasma concentrations during experimental septic shock.

BackgroundWe aimed to investigate whether comparable antibiotic concentrations could be reached with intraosseous and intravenous administration during septic shock.MethodsIn this randomized, prospective experimental study conducted at an animal research laboratory at the University Hospital of Uppsala, eight anesthetized pigs, weighing 21.2 to 29.1 kg (mean: 25.2 ± 2.3 kg), received endotoxin infusion at 4 μg/kg/h for 6 h. At the onset of clinical shock, alternatively after 3 h of endotoxemia, they received 75 mg/kg of cefotaxime and 7 mg/kg of gentamicin either in a proximal tibial intraosseous catheter or in a peripheral intravenous catheter. Mixed venous samples were taken after 5, 15, 30, 60, 120 and 180 min and analyzed for antibiotic concentrations.ResultsFor both antibiotics, plasma concentrations after intraosseous and intravenous administration followed similar curves throughout the observation period, and peak concentrations were comparable. Mean concentration area under the curve (AUC mg × h/l) for cefotaxime was 108.1 ± 19.5 after intraosseous and 116.5 ± 11.1 after intravenous administration; ratio 0.93, (95% CI 0.71–1.19). Mean AUC for gentamicin was 28.1 ± 6.8 for intraosseous and 32.2 ± 3.5 for intravenous administration; ratio 0.87 (95% CI 0.62–1.19).ConclusionsIn this porcine septic shock model, intraosseous and intravenous administration of gentamicin and cefotaxime yielded comparable concentrations. In an emergency, intraosseous administration of these antibiotics may be considered in severe infections when venous access is difficult.

GENTAMYCIN-INDUCED NEPHROTOXICITY IN CHICKENS: MODULATORY ROLE OF MORINGA OLEIFERA

The aim of the present study was to determine whether Moringa oleifera (MOR) leaf powder, have a modulatory effect against gentamicin (GEN)-induced nephrotoxicity in chickens or not. Twenty laying hens were equally divided into four groups: First group (CON) received standard basal diet only. Second group (GEN) was injected with GEN (50mg/kg body weight, intramuscularly (i.m.), twice daily, for 5 consecutive days). Third group (GEN+MOR) was supplemented with MOR leaf powder (10gm/kg diet) daily for 12 consecutive days and injected with GEN (50mg/kg body weight, i.m., twice daily, for 5 consecutive days) starting from the day 8. Fourth group (MOR) was supplemented with MOR leaf powder (10gm/kg diet) daily for 12 consecutive days. GEN administration increased serum creatinine (Cr), blood urea nitrogen (BUN), and malonaldehyde (MDA) and decreased total protein, albumin, reduced glutathione (GSH) content as well as superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities indicating nephrotoxicity. Furthermore, histopathological findings revealed marked tubular vacuolar degeneration, focal interstitial mononuclear cells infiltrations, congestion, focal cystic change and tubular necrosis in GEN-treated kidneys. However, MOR leaf powder supplementation with GEN administration caused significant decrease of serum Cr, BUN, and MDA and increase of total protein, albumin, GSH, SOD, GPx, and CAT compared with GEN alone. Moreover, GEN+MOR treated group showed slight focal interstitial mononuclear cells infiltrations in renal tissues. These findings suggested that dietary supplementation of MOR leaf powder may prevent or reduce the GEN-induced nephrotoxicity.

Gentamicin-induced Acute Kidney Injury in Equines is associated with Marked Acute Phase Response: An Experimental Study on Donkey (Equus asinus)

Gentamicin-induced Acute Kidney Injury in Equines is associated with Marked Acute Phase Response: An Experimental Study on Donkey (Equus asinus) Recently, there is growing evidence suggesting that acute kidney injury (AKI) in human and laboratory animals is associated with an inflammatory response that could play a role in tissue damage. However, such link has not previously been addressed in equines. The present study was designed to evaluate the effect of gentamicin (GEN) administration on the development of AKI and systemic inflammatory response in equines using donkey as a model. GEN (10%) was administered intravenously in six donkeys at a dose of 20 mg kg-1 BW thrice daily for 14 consecutive days. Three other donkeys were randomly assigned to receive saline solution and served as controls. The donkeys were clinically and sonographically examined throughout the experimental period. Blood and urine (U) samples were simultaneously collected at day (D) 7, and D 14 of GEN administration. Renal specimens from all donkeys were collected at D 14 and processed for routine histopathological examination. AKI was confirmed by sonography, laboratory measurements, histopathology and immunohistochemistry.

Atlas of Cellular Dynamics during Zebrafish Adult Kidney Regeneration.

The zebrafish is a useful animal model to study the signaling pathways that orchestrate kidney regeneration, as its renal nephrons are simple, yet they maintain the biological complexity inherent to that of higher vertebrate organisms including mammals. Recent studies have suggested that administration of the aminoglycoside antibiotic gentamicin in zebrafish mimics human acute kidney injury (AKI) through the induction of nephron damage, but the timing and details of critical phenotypic events associated with the regeneration process, particularly in existing nephrons, have not been characterized. Here, we mapped the temporal progression of cellular and molecular changes that occur during renal epithelial regeneration of the proximal tubule in the adult zebrafish using a platform of histological and expression analysis techniques. This work establishes the timing of renal cell death after gentamicin injury, identifies proliferative compartments within the kidney, and documents gene expression changes associated with the regenerative response of proliferating cells. These data provide an important descriptive atlas that documents the series of events that ensue after damage in the zebrafish kidney, thus availing a valuable resource for the scientific community that can facilitate the implementation of zebrafish research to delineate the mechanisms that control renal regeneration.

Effects of antibacterial drugs on camel milk lysozyme concentration and lactoperoxidase activity

The objective of this research was to discover the potential effects of antibiotics used during lactation on innate immunity factors present in milk as lysozyme and lactoperoxidase. Intramuscular administration of oxytetracycline, amoxycillin, gentamicin and enrofloxacin to lactating camels for 3 days resulted in an appreciable amount of residues in milk for 72 hours. The antibacterial drugs caused significant inhibition of activity of lactoperoxidase and lysozyme concentration in milk of camels. It is recommended to implement withdrawal time when antibacterials are used in lactating camels to preserve the properties of the milk.

Histone deacetylase inhibitor sodium butyrate attenuates gentamicin-induced hearing loss in vivo

ObjectiveAlthough histone deacetylase (HDAC) inhibition has been shown to protect against gentamicin (GM)-induced hearing loss in vitro, its protective effect has not been proven in vivo. In the present study, the aim was to investigate the protective effect of sodium butyrate (NaB), a specific HDAC inhibitor, on GM-induced ototoxicity in vivo. MethodsForty 8-week-old albino guinea pigs were divided into two experimental groups. Group 1 (n=10) underwent bilateral ear surgery to place sponges (0.3mm3) permeated with NaB (10μl, 100mg/ml) and physiological saline (10μl; control) in the right and left round window niches, respectively. The sponges were left in place for 15days to evaluate the effects of NaB at the applied concentration. Group 2 (n=30) underwent the same bilateral ear surgery described for Group 1, except three days after surgery, the animals received intramuscular GM injections (200mg/kg/day) for 5 consecutive days. Seven days after the final GM injection, the protective effects of NaB were examined. ResultsAfter 15days of NaB treatment (10μl, 100mg/ml), an increase in histone acetylation was detected in Corti organ samples. Auditory brainstem response (ABR) threshold shifts and hair cell loss were also reduced in NaB-treated ears after GM administration. Furthermore, GM treatment increased HDAC1 expression in outer hair cells (OHCs) in vivo, and NaB blocked this action. ConclusionGM increases HDAC1 expression in OHCs, and NaB is able to block this action. Thus, it appears that the HDAC inhibitor, NaB, attenuates GM-induced hearing loss in guinea pigs.

Illustrative neonatal cases regarding drug delivery issues.

Illustrative neonatal cases regarding drug delivery issues.

Efficacy of L‐N‐Acetyl Cysteine in the Prevention of Gentamicin Vestibulotoxicity in Rats

Objectives: Determine the effect of L-N-acetylcysteine (LNAC) on gentamicin (GM) initiated vestibulotoxicity. Methods: Wistar rats were divided into 4 groups: Group A (n = 7) had intratympanic (IT) GM (20 mg in 40 µL); group B (n = 6) had IT GM and intraperitoneal (IP) LNAC (350 mg/kg) at 24 hours and 1 hour before GM administration; group C (n = 6) had IT GM and IT LNAC (5 mg in 40 µL); and group D (n = 6) had only IT saline (40 µL). Rats were tested by ABR and cervical vestibular evoked myogenic potentials (VEMP) pretreatment, and at 1 week and 1 month posttreatment. Morphological analysis of the inner ears was performed at 1 month. Main outcome measures were the mean change in VEMP P1 latency at sound stimulation from 80 to 110 dB SPL, and hair cell count in the saccule. Results: Rats treated with IT LNAC exhibited the least change in mean VEMP latencies, although the intergroup differences were not statistically significant except for 80 dB stimulation at 1 week posttreatment. IP and IT LNAC resulted in preservation of the VEMP response in all rats, whereas 42% of rats not receiving LNAC had absent responses. Morphological analysis of the saccule revealed lower mean hair cell counts in rats not receiving LNAC. Conclusions: Systemic and IT administration of LNAC of rats treated with GM resulted in minimal variations in VEMP latencies and greater preservation of vestibular hair cells. The protective effect of LNAC in GM-initiated vestibulotoxicity is promising and warrants further research.

KIM-1 and NGAL as biomarkers of nephrotoxicity induced by gentamicin in rats

Gentamicin is a member of aminoglycosides, which has represented highly effective antimicrobial agents especially in Gram-negative infections despite their toxic effects in the kidney. Rapid diagnosis is vital to preserve renal function and to slow down renal injury. Owing to the poor sensitivity and specificity of serum creatinine (SCr) and blood urea nitrogen (BUN), new biomarkers for earlier and more accurate detection are needed. The aim of our study was to determine whether kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) may be useful biomarkers in the assessment of gentamicin-induced nephrotoxicity in rats. In this study, the two biomarkers of renal toxicity were assessed via ELISA, quantitative real-time PCR, and immunohistochemistry in rats treated with gentamicin for up to 7days. Repeated administration of gentamicin to male SD rats for 1, 3, or 7days resulted in a dose- and time-dependent increase in the expression of KIM-1 and NGAL. Changes in gene and protein expressions were found to correlate with the progressive histopathological alterations and preceded effects on traditional clinical parameters indicative of impaired kidney function. Both of the biomarkers are supported to be used as sensitive indicators of acute kidney injury caused by gentamicin.

Protective effect of naringenin against gentamicin-induced nephrotoxicity in rats

The protective effect of naringenin, a flavonoid compound isolated from citrus fruits, was investigated against nephrotoxicity induced by gentamicin (80mgkg−1/day, i.p., for eight days) in rats. Naringenin treatment (50mgkg−1/day, p.o.) was administered for eight days, starting on the same day of gentamicin administration. Gentamicin caused significant elevations of serum creatinine, and kidney tissue levels of malondialdehyde, nitric oxide, and interleukin-8, and a significant decrease in renal glutathione peroxidase activity. Naringenin treatment significantly ameliorated the changes in the measured biochemical parameters resulted from gentamicin administration. Also, naringenin markedly attenuated the histopathological renal tissue injury observed with gentamicin. Immunohistochemical examinations showed that naringenin significantly reduced the gentamicin-induced expression of kidney injury molecule-1, vascular endothelial growth factor, inducible nitric oxide synthase, and caspase-9, and increased survivin expression in the kidney tissue. It was concluded that naringenin, through its antioxidant and anti-inflammatory effects, may represent a therapeutic option to protect against gentamicin nephrotoxicity.

Comparison of Renal Biomarkers with Glomerular Filtration Rate in Susceptibility to the Detection of Gentamicin-Induced Acute Kidney Injury in Dogs

Fourteen renal biomarkers were compared with measurement of glomerular filtration rate (GFR) in detecting acute kidney injury (AKI) in beagle dogs given gentamicin (40 mg/kg/day by subcutaneous injection) for 7 consecutive days. Serum and urinary biomarkers were measured before administration of gentamicin and then on days 4 and 8 after starting administration. GFR was derived by use of a simplified equation. Increased urinary cystatin C and decreased GFR occurred from day 4 and were detected before increases in blood urea nitrogen (BUN) and serum creatinine concentrations and changes in other urinary parameters. The closest correlation was between urinary cystatin C and GFR. At termination, microscopical examination revealed extensive necrosis of proximal tubular epithelium with hyaline casts in the kidney of treated dogs. These data indicate that urinary cystatin C is the most sensitive index of kidney injury and GFR reflects the kidney functional mass.

Lack of protection against gentamicin ototoxicity by auditory conditioning with noise

IntroductionAuditory conditioning consists of the pre-exposure to low levels of a potential harmful agent to protect against a subsequent harmful exposure. ObjectiveTo confirm if conditioning with an agent different from that used to cause the trauma can also be effective. MethodsThis was an experimental study with 17 guinea pigs, divided into three groups: an ototoxic control group (Cont) that received intramuscular administration of gentamicin 160mg/kg/day for ten consecutive days, but no sound exposure; a sound control group (Sound) that was exposed to 85dB broadband noise centered at 4kHz, 30min each day for ten consecutive days, but received no ototoxic medications; and an experimental group (Expt) that received sound exposure identical to the Sound group and after each noise presentation, received gentamicin similarly to Cont group. The animals were evaluated by distortion product otoacoustic emissions (DPOAEs), brainstem auditory evoked potentials (BAEPs), and scanning electron microscopy. ResultsThe animals that were conditioned with noise did not show any protective effect compared with the ones that received only the ototoxic gentamicin administration. This lack of protection was observed functionally and morphologically. ConclusionConditioning with 85dB broadband noises, 30min a day for ten consecutive days does not protect against an ototoxic gentamicin administration of 160mg/kg/day for ten consecutive days in the guinea pig.

Evaluation of the usefulness of novel biomarkers for drug-induced acute kidney injury in beagle dogs

As kidney is a major target organ affected by drug toxicity, early detection of renal injury is critical in preclinical drug development. In past decades, a series of novel biomarkers of drug-induced nephrotoxicity were discovered and verified in rats. However, limited data regarding the performance of novel biomarkers in non-rodent species are publicly available. To increase the applicability of these biomarkers, we evaluated the performance of 4 urinary biomarkers including neutrophil gelatinase-associated lipocalin (NGAL), clusterin, total protein, and N-acetyl-β-D-glucosaminidase (NAG), relative to histopathology and traditional clinical chemistry in beagle dogs with acute kidney injury (AKI) induced by gentamicin. The results showed that urinary NGAL and clusterin levels were significantly elevated in dogs on days 1 and 3 after administration of gentamicin, respectively. Gene expression analysis further provided mechanistic evidence to support that NGAL and clusterin are potential biomarkers for the early assessment of drug-induced renal damage. Furthermore, the high area (both AUCs=1.000) under receiver operator characteristics (ROC) curve also indicated that NGAL and clusterin were the most sensitive biomarkers for detection of gentamicin-induced renal proximal tubular toxicity. Our results also suggested that NAG may be used in routine toxicity testing due to its sensitivity and robustness for detection of tissue injury. The present data will provide insights into the preclinical use of these biomarkers for detection of drug-induced AKI in non-rodent species.

Nephroprotective effect of catechin on gentamicin-induced experimental nephrotoxicity.

Gentamicin is an effective aminoglycoside antibiotic employed against severe Gram-negative bacterial infections, but induction of nephrotoxicity limits its frequent clinical use. This study was undertaken to investigate the effect of catechin hydrate on gentamicin-induced nephrotoxicity in rats. Rats were administered nephrotoxic dose of gentamicin (100 mg/kg/day, i.p.) once daily for 14 days. Gentamicin-administered rats were treated with catechin hydrate (50 mg/kg/day, per os), the treatment was started 3 days before the administration of gentamicin while it was continued for 14 days from the day of gentamicin administration. Two weeks administration of gentamicin significantly increased the serum creatinine and blood urea nitrogen levels. Renal histopathological examination of gentamicin-administered rats revealed degenerative changes in glomeruli and tubules after 2 weeks. These renal structural and functional abnormalities in gentamicin-administered rats were accompanied with renal oxidative stress as assessed in terms of marked decrease in renal-reduced glutathione (GSH). However, catechin hydrate treatment showed considerably nephroprotective action against gentamicin-induced nephrotoxicity in rats by preventing aforementioned renal structural and functional abnormalities and oxidative stress. Catechin hydrate has a potential to prevent gentamicin-induced experimental nephrotoxicity. The renoprotective effect of catechin hydrate against gentamicin-induced nephrotoxicity might be mediated through its antioxidant and possible direct nephroprotective actions.