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Abstract: FR-PO0372

Moderate Physical Training Preserves Renal Hemodynamics and Attenuates Tenofovir-Induced Tubular Injury

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Silva, Juliana Veloso Gusmão, Universidade de Sao Paulo, São Paulo, SP, Brazil
  • Alves, Mykelly Gomes, Universidade de Sao Paulo, São Paulo, SP, Brazil
  • García, Jessica Paola, Universidade de Sao Paulo, São Paulo, SP, Brazil
  • Silva, Eloiza De Oliveira, Universidade de Sao Paulo, São Paulo, SP, Brazil
  • Gonçalves, Maikol L C, Universidade de Sao Paulo, São Paulo, SP, Brazil
  • Silva, David Bueno dos Santos da, Universidade de Sao Paulo, São Paulo, SP, Brazil
  • Monteiro, Letícia Maria, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
  • Vattimo, Maria De Fatima, Universidade de Sao Paulo, São Paulo, SP, Brazil
Background

Tenofovir Disoproxil Fumarate (TDF) nephrotoxicity is associated with tubular injury, oxidative stress, inflammation, and renal hemodynamic dysfunction. Whether exercise training protects against TDF-induced kidney injury remains unclear. We investigated the effects of moderate physical training on renal function, oxidative stress, inflammation, and renal hemodynamics in experimental TDF nephrotoxicity.

Methods

Male Wistar rats were assigned to Control, TDF, Physical Training (PT), or TDF+PT groups (n=7/group). TDF-treated animals received 600 mg/kg/day by gavage for 5 days. PT consisted of swimming exercise (60 min/day, 5 days/week, 5% body weight overload) for 28 days. Renal function was evaluated by serum creatinine, inulin clearance, and urinary NGAL. Renal hemodynamics included mean arterial pressure (MAP), renal blood flow (RBF), and renal vascular resistance (RVR). Oxidative stress markers included FOX, TBARS, thiols, and catalase activity. Renal inflammation was assessed by CD68 immunostaining.

Results

TDF induced marked renal dysfunction, characterized by reduced inulin clearance and increased serum creatinine and urinary NGAL, accompanied by hypertension, reduced RBF, increased RVR, and enhanced oxidative stress. Physical training significantly attenuated these alterations, preserving renal function and renal hemodynamics while reducing oxidative damage and macrophage infiltration. Histological analysis demonstrated mild tubulointerstitial fibrosis in TDF-treated animals, which was also attenuated by exercise training.

Conclusion

Moderate physical training protected against TDF-induced kidney injury through hemodynamic, antioxidant, and anti-inflammatory mechanisms. These findings support exercise training as a potential non-pharmacological strategy to mitigate TDF-associated nephrotoxicity.

Acknowledgment

Thank you to the University of São Paulo and CAPES.