Erythrocyte oxidative stress in patients with calcium oxalate stones correlates with stone size and renal tubular damage

Ming Chieh Ma, Yih Sharng Chen, Ho-Shiang Huang

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Objective To investigate how erythrocyte oxidative stress relates to renal tubular damage and calcium oxalate stone size in patients as oxidative stress has been demonstrated to be associated with stone formation in disease progression. Methods The study included 29 controls, 29 patients with kidney stones, and 28 patients with ureteral stones. Venous blood samples were collected to measure the expression and activity of antioxidant enzymes in the isolated erythrocytes. A 24-hour urine sample was collected to measure urinary chemistry. The cellular levels of oxalate and the oxidative stress marker malondialdehyde (MDA) were determined to examine their correlations with stone size and renal tubule damage. Results Calcium oxalate stone deposition and high free radical levels in venous blood associated with high levels of urinary oxalate, glutathione S-transferases tubular damage markers, and MDA and low urinary citrate levels. Compared with the erythrocytes of controls, the erythrocytes of stone groups had significantly lower levels and activities of antioxidant proteins, namely, reduced glutathione, catalase, and copper- or zinc-superoxide dismutase. The ureteral stone group also had significantly lower erythrocyte glutathione peroxidase levels and glutathione reductase activity than the controls. Erythrocyte oxalate levels correlated positively with erythrocyte MDA levels and negatively with erythrocyte antioxidant protein activities. Erythrocyte oxidative stress, as indicated by cellular MDA levels, also correlated well with urinary glutathione S-transferases and stone size. Conclusion These results suggest that oxalate-mediated oxidative stress in erythrocytes might contribute to the tubular damage and stone accumulation in patients with hyperoxaluria.

Original languageEnglish
Pages (from-to)510.e9-510.e17
JournalUrology
Volume83
Issue number2
DOIs
Publication statusPublished - 2014 Jan 1

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Calcium Oxalate
Oxidative Stress
Erythrocytes
Kidney
Oxalates
Malondialdehyde
Antioxidants
Glutathione Transferase
Hyperoxaluria
Kidney Calculi
Glutathione Reductase
Glutathione Peroxidase
Citric Acid
Catalase
Superoxide Dismutase
Free Radicals
Glutathione
Disease Progression
Zinc
Copper

All Science Journal Classification (ASJC) codes

  • Urology

Cite this

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abstract = "Objective To investigate how erythrocyte oxidative stress relates to renal tubular damage and calcium oxalate stone size in patients as oxidative stress has been demonstrated to be associated with stone formation in disease progression. Methods The study included 29 controls, 29 patients with kidney stones, and 28 patients with ureteral stones. Venous blood samples were collected to measure the expression and activity of antioxidant enzymes in the isolated erythrocytes. A 24-hour urine sample was collected to measure urinary chemistry. The cellular levels of oxalate and the oxidative stress marker malondialdehyde (MDA) were determined to examine their correlations with stone size and renal tubule damage. Results Calcium oxalate stone deposition and high free radical levels in venous blood associated with high levels of urinary oxalate, glutathione S-transferases tubular damage markers, and MDA and low urinary citrate levels. Compared with the erythrocytes of controls, the erythrocytes of stone groups had significantly lower levels and activities of antioxidant proteins, namely, reduced glutathione, catalase, and copper- or zinc-superoxide dismutase. The ureteral stone group also had significantly lower erythrocyte glutathione peroxidase levels and glutathione reductase activity than the controls. Erythrocyte oxalate levels correlated positively with erythrocyte MDA levels and negatively with erythrocyte antioxidant protein activities. Erythrocyte oxidative stress, as indicated by cellular MDA levels, also correlated well with urinary glutathione S-transferases and stone size. Conclusion These results suggest that oxalate-mediated oxidative stress in erythrocytes might contribute to the tubular damage and stone accumulation in patients with hyperoxaluria.",
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Erythrocyte oxidative stress in patients with calcium oxalate stones correlates with stone size and renal tubular damage. / Ma, Ming Chieh; Chen, Yih Sharng; Huang, Ho-Shiang.

In: Urology, Vol. 83, No. 2, 01.01.2014, p. 510.e9-510.e17.

Research output: Contribution to journalArticle

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N2 - Objective To investigate how erythrocyte oxidative stress relates to renal tubular damage and calcium oxalate stone size in patients as oxidative stress has been demonstrated to be associated with stone formation in disease progression. Methods The study included 29 controls, 29 patients with kidney stones, and 28 patients with ureteral stones. Venous blood samples were collected to measure the expression and activity of antioxidant enzymes in the isolated erythrocytes. A 24-hour urine sample was collected to measure urinary chemistry. The cellular levels of oxalate and the oxidative stress marker malondialdehyde (MDA) were determined to examine their correlations with stone size and renal tubule damage. Results Calcium oxalate stone deposition and high free radical levels in venous blood associated with high levels of urinary oxalate, glutathione S-transferases tubular damage markers, and MDA and low urinary citrate levels. Compared with the erythrocytes of controls, the erythrocytes of stone groups had significantly lower levels and activities of antioxidant proteins, namely, reduced glutathione, catalase, and copper- or zinc-superoxide dismutase. The ureteral stone group also had significantly lower erythrocyte glutathione peroxidase levels and glutathione reductase activity than the controls. Erythrocyte oxalate levels correlated positively with erythrocyte MDA levels and negatively with erythrocyte antioxidant protein activities. Erythrocyte oxidative stress, as indicated by cellular MDA levels, also correlated well with urinary glutathione S-transferases and stone size. Conclusion These results suggest that oxalate-mediated oxidative stress in erythrocytes might contribute to the tubular damage and stone accumulation in patients with hyperoxaluria.

AB - Objective To investigate how erythrocyte oxidative stress relates to renal tubular damage and calcium oxalate stone size in patients as oxidative stress has been demonstrated to be associated with stone formation in disease progression. Methods The study included 29 controls, 29 patients with kidney stones, and 28 patients with ureteral stones. Venous blood samples were collected to measure the expression and activity of antioxidant enzymes in the isolated erythrocytes. A 24-hour urine sample was collected to measure urinary chemistry. The cellular levels of oxalate and the oxidative stress marker malondialdehyde (MDA) were determined to examine their correlations with stone size and renal tubule damage. Results Calcium oxalate stone deposition and high free radical levels in venous blood associated with high levels of urinary oxalate, glutathione S-transferases tubular damage markers, and MDA and low urinary citrate levels. Compared with the erythrocytes of controls, the erythrocytes of stone groups had significantly lower levels and activities of antioxidant proteins, namely, reduced glutathione, catalase, and copper- or zinc-superoxide dismutase. The ureteral stone group also had significantly lower erythrocyte glutathione peroxidase levels and glutathione reductase activity than the controls. Erythrocyte oxalate levels correlated positively with erythrocyte MDA levels and negatively with erythrocyte antioxidant protein activities. Erythrocyte oxidative stress, as indicated by cellular MDA levels, also correlated well with urinary glutathione S-transferases and stone size. Conclusion These results suggest that oxalate-mediated oxidative stress in erythrocytes might contribute to the tubular damage and stone accumulation in patients with hyperoxaluria.

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