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The effects of vitamin d on gentamicin-induced acute kidney injury in experimental rat model
Ender Hur1, Alev Garip, Asuman Camyar
1Department of Nephrology, Bulent Ecevit University Medical School, Esenkoy, 67100 Zonguldak, Turkey.
Abstract:
Introduction. Acute kidney injury (AKI) pathogenesis is complex. Findings of gentamicin nephrotoxicity are seen in 30% of the AKI patients. Vitamin D has proven to be effective on renin expression, inflammatory response, oxidative stress, apoptosis, and atherosclerosis. We aimed to investigate the effect of vitamin D in an experimental rat model of gentamicin-induced AKI. Methods. Thirty nonuremic Wistar albino rats were divided into 3 groups: Control group, 1 mL saline intramuscular (im) daily; Genta group, gentamicin 100 mg/kg/day (im); Genta + vitamin D, gentamicin 100 mg/kg/day (im) in addition to 1 α , 25 (OH)2D3 0.4 mcg/kg/day subcutaneously for 8 days. Blood pressures and 24-hour urine were measured. Blood urea and creatinine levels and urine tubular injury markers were measured. Renal histology was semiquantitatively assessed. Results. Urea, creatinine and urine neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were all increased in Genta group indicating AKI model. Systolic blood pressure decreased, but urine volume and glutathione increased in Genta + Vit D group compared to Control group. Histological scores indicating tubular injury increased in Genta and Genta + Vit D groups. Conclusions. Vitamin D does not seem to be effective on histological findings although it has some beneficial effects via RAS system and a promising effect on antioxidant system.
Insights
Vitamin D did not improve histological damage in gentamicin-induced acute kidney injury (AKI) in rats. However, it showed potential benefits in the renin-angiotensin system and antioxidant pathways.
Area of Science:
- Nephrology
- Pharmacology
- Biochemistry
Background:
- Acute kidney injury (AKI) is a complex condition with significant morbidity.
- Gentamicin nephrotoxicity is a common cause of AKI, observed in 30% of patients.
- Vitamin D exhibits protective effects against inflammation, oxidative stress, and apoptosis.
Purpose of the Study:
- To investigate the efficacy of vitamin D in mitigating gentamicin-induced AKI in a rat model.
- To assess the impact of vitamin D on renal function, oxidative stress markers, and kidney histology.
Main Methods:
- Thirty Wistar albino rats were divided into control, gentamicin-induced AKI, and gentamicin + vitamin D groups.
- Treatment involved daily intramuscular gentamicin (100 mg/kg) with or without subcutaneous vitamin D (0.4 mcg/kg) for 8 days.
- Parameters measured included blood pressure, urine output, serum urea, creatinine, urinary biomarkers (NGAL, KIM-1), and renal histology.
Main Results:
- Gentamicin administration successfully induced AKI, evidenced by elevated urea, creatinine, NGAL, and KIM-1.
- The vitamin D group exhibited decreased systolic blood pressure, increased urine volume, and elevated glutathione levels compared to controls.
- Despite biochemical improvements, histological assessment showed increased tubular injury in both gentamicin-treated groups.
Conclusions:
- Vitamin D demonstrated beneficial effects on the renin-angiotensin system and antioxidant capacity in gentamicin-induced AKI.
- Vitamin D did not appear to ameliorate the histological damage associated with gentamicin nephrotoxicity in this model.
- Further research is warranted to explore vitamin D's therapeutic potential in AKI management.
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