Prevention of Acute Kidney Injury Related (AKI) related by vancomycin; A Randomized Clinical Trial

Document Type : Original Article

Authors

1 Department of Community Medicine, Faculty of Medicine, Sabzevar University of Medical Sciences, Khorasan Razavi, Iran.

2 Department of Pediatrics, Faculty of Medicine, Sabzevar University of Medical Sciences, Khorasan Razavi, Iran.

3 Kidney Transplantation Complications Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

4 Department of Community Medicine, Mashhad Branch, Islamic Azad University, Mashhad, Iran.

5 General Physician, Surgical Oncology Research Center, Mashhad University of Medical Science, Mashhad, Iran.

6 Student Research Committee, Mashhad University of Medical Science, Mashhad, Iran.

7 Department of Medical Education, Faculty of Medicine, Shiraz University of Medical Sciences, Iran.

8 Noncommunicable Disease Research Center, Sabzevar University of Medical Sciences, Subedar, Iran.

Abstract

Introduction:
Acute kidney injury (AKI) is one of the potential side effects of vancomycin in children with systemic infections. We aimed to evaluate the effect of selenium on the prevention of Vancomycin-associated AKI (VA-AKI)
Materials and Methods:
This study is a parallel randomized controlled trial in Heshmatieh Hospital, Sabzevar, Iran. According to the simple random sampling method, thirty patients between 1 month and 18 years old with systemic infections were randomly assigned to two groups. The intervention and control groups were treated with vancomycin plus selenium and vancomycin alone, respectively. Urine and blood samples were obtained from patients at the beginning and seven days after the treatment to evaluate AKI among patients.
Results:
We found no significant difference between baseline BUN, creatinine, and microalbumin in the two groups (P>0.05). There was a significant difference between the two groups post-treatment urine microalbumin (P= 0.045). The frequency of AKI in the intervention group [5(33.3%)] was lower than the control group [11(73.3%)] (P = 0.02). There were few changes between the mean difference baseline and post-treatment Cr (0.1mg/dl) and BUN (2.9mg/dl). Drug efficacy was 66%, and the number needed to treat (NNT) was equal to 2.
Conclusion:
In the present study, we concluded that selenium could prevent vancomycin-induced AKI. Future investigations on the higher numbers of patients are needed.

Keywords

Main Subjects


  1. de Almeida CDC, Simoes e Silva AC, de Queiroz Oliveira JA, Batista ISF, Pereira FH, Gonçalves JE, et al. Vancomycin-associated nephrotoxicity in non-critically ill patients admitted in a Brazilian public hospital: A prospective cohort study. PLoS One. 2019; 14(9): e0222095.
  2. Hirai T, Hanada K, Kanno A, Akashi M, Itoh T. Risk factors for vancomycin nephrotoxicity and time course of renal function during vancomycin treatment. European Journal of Clinical Pharmacology. 2019;75:859-66.
  3. Tantranont N, Obi C, Luque Y, Truong LD. Vancomycin nephrotoxicity: Vancomycin tubular casts with characteristic electron microscopic findings. Clinical nephrology Case studies. 2019; 7:66.
  4. Zhang Y, Wang T, Zhang D, You H, Dong Y, Liu Y, et al. Therapeutic drug monitoring coupled with Bayesian forecasting could prevent vancomycin-associated nephrotoxicity in renal insufficiency patients: a prospective study and pharmacoeconomic analysis. Therapeutic drug monitoring. 2020;42(4):600-9.
  5. Katip W, Oberdorfer P. A monocentric retrospective study of AUC/MIC ratio of vancomycin associated with clinical outcomes and nephrotoxicity in patients with enterococcal infections. Pharmaceutics. 2021;13(9):1378.
  6. Vatankhoh S, Chopani A, Aghdam ET, Tavakoli ME, Joudyian N, Nafar H. Investigating the Prolonged Discharge Process in Pediatric Teaching Hospital of Tehran, Iran: A Cross-Sectional Study. Journal of patients safety and quality Improvement. 2021;11(1):49-53.
  7. Park SJ, Lim NR, Park HJ, Yang JW, Kim M-J, Kim K, et al. Evaluation of risk factors for vancomycin-induced nephrotoxicity. International Journal of Clinical Pharmacy. 2018; 40:1328-34.
  8. Fiorito TM, Luther MK, Dennehy PH, LaPlante KL, Matson KL. Nephrotoxicity with vancomycin in the pediatric population: a systematic review and meta-analysis. The Pediatric infectious disease journal. 2018; 37(7): 654-61.
  9. He J, Mao E, Xu W, Zhao B, Jing F, Bian X, et al. High dose vitamin C significantly reduces the nephrotoxicity of vancomycin in critically ill patients. Zhonghua wei Zhong Bing ji jiu yi xue. 2020; 32(4):468-72.
  10. He J, Xu W, Zheng X, Zhao B, Ni T, Yu P, et al. Vitamin C reduces vancomycin-related nephrotoxicity through the inhibition of oxidative stress, apoptosis, and inflammation in mice. Annals of Translational Medicine. 2021; 9(16).
  11. Peirano G, Agersø Y, Aarestrup FM, dos Prazeres Rodrigues D. Occurrence of integrons and resistance genes among sulphonamide-resistant Shigella spp. from Brazil. Journal of Antimicrobial Chemotherapy. 2005;55(3):301-5.
  12. Ali S, Qaisrani M, Farhat K, Waheed A, Afridi MF, Khan MW. To evaluate the ameliorative role of vitamin e on nephrotoxicity induced by vancomycin  in rbbits PAFMJ. 2020;70(1):169-73.
  13. Soltani R, Khorvash F, Meidani M, Badri S, Alaei S, Taheri S. Vitamin E in the prevention of vancomycin-induced nephrotoxicity. Research in pharmaceutical sciences. 2020;15(2):137.
  14. Kara A, Cetin H, Oktem F, Metin Ciris I, Altuntas I, Kaya S. Amikacin induced renal damage and the role of the antioxidants on neonatal rats. Renal failure. 2016;38(5):671-7.
  15. Patel Manali B, Deshpande S, Shah G. Evaluation of efficacy of vitamin E and N-acetyl cysteine in gentamicin-induced nephrotoxicity in rats. Renal failure. 2011;33(3):341-7.
  16. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute renal failure–definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Critical care. 2004;8(4):1-9.
  17. Nazıroǧlu M, Karaoğlu A, Aksoy AO. Selenium and high dose vitamin E administration protects cisplatin-induced oxidative damage to renal, liver and lens tissues in rats. Toxicology. 2004; 195(2-3):221-30.