Lipid peroxidation is not the underlying cause of renal injury in hyperoxaluric rats.

Background: Hyperoxaluria is a major risk factor of calcium oxalate stone disease and renal injury is thought to be a significant initiating event. However, the relationship among oxidative stress, renal tubule injury and hyperoxaluria in the progression of nephrolithiasis is unclear, especially in animal models. In the current study, we assess the role of oxidative stress in renal tubular damage in a rat model of chronic hyperoxaluria (HYP) and chronic renal failure induced by hyperoxaluria (HRF) compared to control rats.

Ethylene glycol induces hyperoxaluria without metabolic acidosis in rats.

Ethylene glycol (EG) consumption is commonly employed as an experimental regimen to induce hyperoxaluria in animal models of calcium oxalate nephrolithiasis. This approach has, however, been criticized because EG overdose induces metabolic acidosis in humans. We tested the hypothesis that EG consumption (0.