Lipid peroxidation and its correlations with urinary levels of oxalate, citric acid, and osteopontin in patients with renal calcium oxalate stones.
OBJECTIVE
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-beta-glucosaminidase (NAG), beta-galactosidase (GAL), alphaGST, piGST, 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 alphaGST, NAG, and GAL were also noted in the patients with stones; however, urinary piGST showed no statistically significant difference compared with the controls. Urinary TBARS and MDA had statistically significant correlations with alphaGST, GAL, NAG, Ca, and oxalate, but had no correlation with piGST, citrate, OPN, Mg, and P. Urinary citrate had a negative, linear, and statistically significant correlation with alphaGST, 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.
Huang
Ho-Shiang
HS
Department of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Ma
Ming-Chieh
MC
Chen
Chau-Fong
CF
Chen
Jun
J
D000118:Acetylglucosaminidase / Q000652:urine; D015415:Biomarkers / Q000652:urine; D002129:Calcium Oxalate / Q000032:analysis*; D019343:Citric Acid / Q000652:urine*; D005260:Female; D005982:Glutathione Transferase / Q000652:urine*; D006801:Humans; D007527:Isoenzymes / Q000652:urine; D007669:Kidney Calculi / Q000737:chemistry / Q000652:urine*; D007684:Kidney Tubules / Q000293:injuries / Q000378:metabolism; D015227:Lipid Peroxidation; D008274:Magnesium / Q000652:urine; D008297:Male; D008315:Malondialdehyde / Q000652:urine; D008875:Middle Aged; D053495:Osteopontin; D010070:Oxalates / Q000652:urine*; D010758:Phosphorus / Q000652:urine; D012307:Risk Factors; D012795:Sialoglycoproteins / Q000652:urine*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D001616:beta-Galactosidase / Q000652:urine
D015415:Biomarkers; D007527:Isoenzymes; D010070:Oxalates; C506895:SPP1 protein, human; D012795:Sialoglycoproteins; D017392:Thiobarbituric Acid Reactive Substances; D053495:Osteopontin; D002129:Calcium Oxalate; D010758:Phosphorus; D019343:Citric Acid; D008315:Malondialdehyde; D005982:Glutathione Transferase; D001616:beta-Galactosidase; D000118:Acetylglucosaminidase; D008274:Magnesium