Changes in renal cortical sialic acids and colloidal iron staining associated with exercise

Zambraski, Edward J.; Bober, Mitchell C.; Goldstein, Jeffrey E.; Lakas, C. S.; Shepard, Mark D.

doi:10.1249/00005768-198104000-00004

Cited by 19 publications

(7 citation statements)

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“…Alterations in prostaglandin synthesis and loss of fixed negative charges on glomerular capillary walls by glycosaminoglycans degradation lead to changes in glomerular permeability and the role ROS in this process was previously demonstrated [42]. It was also proposed that a decrease in renal sialic acid content is associated with enhanced proteinuria in exercised dogs [7]. …”

Section: Discussionmentioning

confidence: 99%

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Biphasic Pattern of Exercise-Induced Proteinuria in Sedentary and Trained Men

Şentürk¹,

Kuru²,

Koçer³

et al. 2006

Nephron Physiol

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Background/Aims: Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. Oxidant stress has been proposed as one of different factors involved in postexercise proteinuria in rats. In this study we investigated whether reactive oxygen radicals generated during exercise play a role in exercise-induced proteinuria in sedentary and trained men. Methods: The validity of oxidant stress following stepwise maximal exercise on proteinuria was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 months. While protein carbonyl content in serum and thiobarbituric acid reactive substances (TBARS) in erythrocytes and urine were used as oxidant stress markers, total protein, albumin, β₂-microglobulin in urine were assayed for proteinuria in five consecutive specimens after exercise. Urines were collected before exercise, then 30 min, 2, 8 and 24 h postexercise. Results: Increased urinary protein levels and mixed type proteinuria were determined after 30 min of exercise in sedentary and trained subjects. Proteinuria was normalized at 2 and 8 h specimens. However, glomerular type proteinuria was identified at 24 h specimen in both groups. Oxidant stress markers were significantly elevated in sedentary and trained subjects. Antioxidant treatment prevented the increase in oxidant stress markers, urinary protein levels and the occurrence of glomerular type proteinuria after exhaustive exercise at 24 h in both groups. Conclusions: These findings suggest that the exercise-induced oxidant stress may contribute to exercise-induced proteinuria in sedentary and trained men.

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Section: Discussionmentioning

confidence: 99%

“…However the loss of fixed negative charge from the capillary wall in the glomerular tuft might be responsible for exercise-induced proteinuria [3, 7]. Another cause suggested for post-exercise proteinuria is the maximal tubular reabsorption capacity reached during heavy exercise [3,4,5, 7]. …”

Section: Introductionmentioning

confidence: 99%

Biphasic Pattern of Exercise-Induced Proteinuria in Sedentary and Trained Men

Şentürk¹,

Kuru²,

Koçer³

et al. 2006

Nephron Physiol

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“…Also, the loss of fixed negative charge from the capillary wall of the glomerular tuft may be responsible for exercise-induced proteinuria (23, 41). Still another mechanism suggested for postexercise proteinuria is the maximal tubular reabsorption capacity being exceeded during heavy exercise (23)(24)(25)41). However, the transient effects of exercise on renal function are incapable of explaining the proteinuria that occurs 24 -48 h after exercise.…”

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confidence: 99%

“…The decrease in blood flow is more apparent, and the filtration fraction increases during exercise, which facilitates the passage of proteins into the ultrafiltrate (23,24). Also, the loss of fixed negative charge from the capillary wall of the glomerular tuft may be responsible for exercise-induced proteinuria (23,41). Still another mechanism suggested for postexercise proteinuria is the maximal tubular reabsorption capacity being exceeded during heavy exercise (23)(24)(25)41).…”

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confidence: 99%

Potential sources of oxidative stress that induce postexercise proteinuria in rats

Kocer¹,

Şentürk²,

Kuru³

et al. 2008

Journal of Applied Physiology

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Exercise-induced proteinuria is a common consequence of physical activity and is caused predominantly by alterations in renal hemodynamics. Although it has been shown that exercise-induced oxidative stress can also contribute to the occurrence of postexercise proteinuria, the sources of reactive oxygen species that promote it are unknown. We investigated the enzymes nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase (XO) as possible sources of oxidative stress in postexercise proteinuria. First, we evaluated the effect of blocking the NADPH oxidase enzyme on postexercise proteinuria. We found a significant increase in urinary protein level, kidney thiobarbituric acid-reactive substances (TBARS), and protein carbonyl content after exhaustive exercise, and NADPH oxidase activity was induced by exercise. Rats that were treated with an NADPH oxidase inhibitor for 4 days before exhaustive exercise showed no increase in kidney TBARS or protein carbonyl derivative level and no proteinuria or NADPH oxidase activation. In the next set of experiments, we investigated the effect of XO blockage on postexercise proteinuria. Oxypurinol, an XO inhibitor was administered to rats for 3 days before exercise. Although XO inhibition significantly decreased kidney TBARS levels and protein carbonyl content in exercised rats, the inhibition did not prevent exercise-induced proteinuria. However, plasma and kidney XO activity was not induced by exercise, but rather it was suppressed under oxypurinol treatment. These results suggest that increased NADPH oxidase activity induced by exhaustive exercise is an important source of elevated oxidative, stress during exercise, which contributes to the occurrence of postexercise proteinuria.

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“…It is widely recognized that not only the diameter o f the pores but also the negative charges of the renal capillary mem brane are the main determinants of protein fil tration through the glomerular membrane. Al teration of the electrostatic properties of the membrane may be the cause o f PEP [14].…”

Section: Discussionmentioning

confidence: 99%

Nifedipine Reduces Postexercise Proteinuria in Young Volunteers

Cosenzi

Carraro²,

Sacerdote³

et al. 1995

Kidney Blood Press Res

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Previous studies have demonstrated that it is possible to prevent postexercise proteinuria with angiotensin-converting enzyme inhibitors. To determine whether calcium antagonists have the same effect, 40 young healthy volunteers underwent maximal aerobic exercise with and without nifedipine 10 mg per os 1 h before the first or second trial. Urinary excretion of albumin (UAE), transferrin (UTE) and α₁-microglobulin (UME) were examined before and after each trial. UAE, UTE and UME were significantly increased after exercise. Nifedipine significantly decreased UAE (p = 0.001) and UTE (p = 0.02) after exercise, and slightly decreased the maximal work load and the basal excretion of albumin. UME was unchanged. Therefore, the results of this study demonstrate that nifedipine administration before exercise significantly reduces postexercise proteinuria.

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Changes in renal cortical sialic acids and colloidal iron staining associated with exercise

Cited by 19 publications

References 0 publications

Biphasic Pattern of Exercise-Induced Proteinuria in Sedentary and Trained Men

Biphasic Pattern of Exercise-Induced Proteinuria in Sedentary and Trained Men

Potential sources of oxidative stress that induce postexercise proteinuria in rats

Nifedipine Reduces Postexercise Proteinuria in Young Volunteers

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