Objectives. To determine whether lipid peroxidation plays a role in patients with calcium oxalate kidney stones and to determine the correlation of lipid peroxidation with tubular damage and the major urinary risk factors. We also used the isoenzymes of glutathione S-transferase (GST) to examine which parts of the renal tubules were injured in patients with renal stones. Methods. This clinical study included two study groups. Group 1 included 32 normal volunteers, and group 2 included 32 patients with calcium oxalate kidney stones. A 24-hour urine sample was collected from each subject, and the levels of Ca, P, Mg, oxalate, citrate, N-acetyl-β-glucosaminidase (NAG), β-galactosidase (GAL), αGST, πGST, osteopontin (OPN), thiobarbituric acid-reactive substances (TBARS), and malondialdehyde (MDA) were examined. Results. Hyperoxaluria, hypocitraturia, and low urinary OPN were the major abnormalities found in the patients with stones. Elevated urinary αGST, NAG, and GAL were also noted in the patients with stones; however, urinary πGST showed no statistically significant difference compared with the controls. Urinary TBARS and MDA had statistically significant correlations with αGST, GAL, NAG, Ca, and oxalate, but had no correlation with πGST, citrate, OPN, Mg, and P. Urinary citrate had a negative, linear, and statistically significant correlation with αGST, GAL, and NAG. Conclusions. Lipid peroxidation correlated with hyperoxaluria and renal tubular damage, indicating that hyperoxaluria can induce tubular cell injury and that this injury may be due to the production of free radicals in patients with calcium oxalate stones. Renal tubular damage in patients with stones may be limited to the proximal tubules.
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