Does Proteinuria-Inducing Physical Activity Increase Biomarkers of Acute Kidney Injury?

Junglee, Naushad A.; Lemmey, Andrew; E, Burton, M; Searell, Catrin; Jones, Daniel W.; Lawley, Justin S.; Jibani, Mahdi; Macdonald, Jamie

doi:10.1159/000343417

Cited by 23 publications

(38 citation statements)

References 30 publications

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“…In this study, we found a positive correlation between pre-GXT albuminuria and pre-and post-GXT NCR. These findings are in agreement with earlier studies [6]. Otherwise, there was no correlation between post exercise albuminuria and urinary KIM.…”

Section: Discussionsupporting

confidence: 93%

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Urinary Kidney Injury Molecule-1 but Not Urinary Neutrophil Gelatinase Associated Lipocalin Is Increased after Short Maximal Exercise

Wołyniec

Ratkowski²,

Urbański³

et al. 2017

Nephron

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Background and Aims: Urinary neutrophil gelatinase associated lipocalin (uNGAL) and urinary kidney injury molecule-1 (uKIM-1) are markers of acute kidney injury. The albuminuria is a well-known abnormality after physical exercise. The aim of this study was to investigate changes in uNGAL and uKIM-1 after intensive exercise causing albuminuria. Methods: The study population consisted of 19 participants (10 males and 9 females). The mean age of participants was 35.74 years. All were fit amateur runners; the mean body mass index was 21.99 in females and 24.71 in males. The subjects underwent a graded treadmill exercise test (GXT) according to the Bruce protocol. Maximal oxygen consumption (VO₂max) was measured. Immediately before and after the test urine was collected. Urinary creatinine, albumin, NGAL, and KIM-1 were measured. Albumin to creatinine (ACR), KIM-1 to creatinine (KCR), and NGAL to creatinine (NCR) ratios were calculated. Results: The mean VO₂max was 53.68 in females and 59.54 mL/min/kg in males. Albuminuria and ACR were significantly higher after exercise. An increase in the ACR from 8.82 to 114.35 mg/g (p < 0.01) was observed. uKIM-1 increased significantly after exercise from 849.02 to 1,243.26 pg/mL (p < 0.05). KCR increased from 1,239.1 to 1,725.9 ng/g but without statistical significance (p = 0.07). There were no statistical changes in pre- and post-run uNGAL levels. There was no correlation between post-GXT albuminuria and uKIM-1. Conclusions: uKIM-1 is a very sensitive marker of kidney dysfunction. In our study, uKIM-1 increased significantly after a very short period of exercise. It is not clear if the increase in KIM-1 is caused by post-exercise albuminuria.

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Section: Discussionsupporting

confidence: 93%

“…These abnormalities of kidney function are of special interest because the kidneys are essential to maintain human homeostasis during exercise. They struggle against dehydration and acidosis, metabolize lactic acid, and generate glucose [6].…”

Section: Introductionmentioning

confidence: 99%

Urinary Kidney Injury Molecule-1 but Not Urinary Neutrophil Gelatinase Associated Lipocalin Is Increased after Short Maximal Exercise

Wołyniec

Ratkowski²,

Urbański³

et al. 2017

Nephron

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“…The follow‐up evaluations post‐exercise were needed to examine the transient changes in the urinary parameters obtained from the urine produced during the exercise. Secondly, we did not measure the other urinary tubular biomarkers, such as urinary KIM‐1 and NGAL which were also reported to transiently increase after the high‐intensity exercise . Further studies are needed to clarify which urinary tubular biomarkers are more sensitive indicators.…”

Section: Discussionmentioning

confidence: 98%

“…Post‐exercise proteinuria (ie, albuminuria) is a well‐known renal (glomerular) abnormality after high‐intensity exercise . Furthermore, several acute kidney injury biomarkers such as urinary neutrophil gelatinase associated‐lipocalin (NGAL) and kidney injury molecule‐1 (KIM‐1) were also reported to transiently increase after the high‐intensity exercise . These findings indicate the possibility that high‐intensity exercise induces not only glomerular abnormality but also tubular hypoxia/ischemia, which is one of the aggravating factors of tubulointerstitial damage.…”

Section: Introductionmentioning

confidence: 97%

Incremental short maximal exercise increases urinary liver‐type fatty acid‐binding protein in adults without CKD

Kosaki

Kamijo‐Ikemori

Sugaya

et al. 2020

Scandinavian Med Sci Sports

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Exercise‐induced redistribution of tissue blood flow decreases the renal blood flow in an exercise intensity‐dependent manner. However, the acute effects of incremental short maximal exercise on renal tubular conditions remain unknown. The purpose of this study was to investigate the acute effects of incremental short maximal exercise on the urinary liver‐type fatty acid‐binding protein, which is a highly sensitive tubular biomarker that correlates excellently with peritubular capillary blood flow. A total of 116 adults (aged 24‐83 years) without chronic kidney disease performed the incremental short maximal exercise using a cycling ergometer, wherein the exercise sequence consisted of commencing with a 2‐min workout period at 20 W (as a warm‐up period) and then followed by a 10‐20 W increase every 1 minute until termination criteria were reached. Urinary samples were gathered before and immediately after the exercise to evaluate the concentrations of urinary creatinine, albumin, and liver‐type fatty acid‐binding protein. Urinary excretion levels of albumin and liver‐type fatty acid‐binding protein were significantly increased post‐exercise (P < .001 and P = .008, respectively). Furthermore, the % change in urinary liver‐type fatty acid‐binding protein levels after exercise was found to correlate independently with age, estimated glomerular filtration rate at baseline, and the % change in urinary albumin (Model R2 = 0.451, P < .001). Our findings suggest that incremental short maximal exercise may lead to acute slightly adverse effects on tubular conditions, especially in young adults or adults with lower renal function, even without chronic kidney disease.

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“…albumin/creatinine ratio), its application in exercise models is likely to be flawed. Marked reductions in glomerular filtration rate and tubular dysfunction occur during high-intensity exercise, and subsequently urinary creatinine excretion becomes a nonconstant (16,41). Thus we did not use this method and normalized to urinary flow rate instead (49).…”

Section: Participantsmentioning

confidence: 99%

Exercising in a hot environment with muscle damage: effects on acute kidney injury biomarkers and kidney function

Junglee

Felice

Dolci

et al. 2013

American Journal of Physiology-Renal Physiology

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Unaccustomed strenuous physical exertion in hot environments can result in heat stroke and acute kidney injury (AKI). Both exercise-induced muscle damage and AKI are associated with the release of interleukin-6, but whether muscle damage causes AKI in the heat is unknown. We hypothesized that muscle-damaging exercise, before exercise in the heat, would increase kidney stress. Ten healthy euhydrated men underwent a randomized, crossover trial involving both a 60-min downhill muscle-damaging run (exercise-induced muscle damage; EIMD), and an exercise intensity-matched non-muscle-damaging flat run (CON), in random order separated by 2 wk. Both treatments were followed by heat stress elicited by a 40-min run at 33°C. Urine and blood were sampled at baseline, after treatment, and after subjects ran in the heat. By design, EIMD induced higher plasma creatine kinase and interleukin-6 than CON. EIMD elevated kidney injury biomarkers (e.g., urinary neutrophil gelatinase-associated lipocalin (NGAL) after a run in the heat: EIMD-CON, mean difference [95% CI]: 12 [5, 19] ng/ml) and reduced kidney function (e.g., plasma creatinine after a run in the heat: EIMD-CON, mean difference [95% CI]: 0.2 [0.1, 0.3] mg/dl), where CI is the confidence interval. Plasma interleukin-6 was positively correlated with plasma NGAL (r = 0.9, P = 0.001). Moreover, following EIMD, 5 of 10 participants met AKIN criteria for AKI. Thus for the first time we demonstrate that muscle-damaging exercise before running in the heat results in a greater inflammatory state and kidney stress compared with non-muscle-damaging exercise. Muscle damage should therefore be considered a risk factor for AKI when performing exercise in hot environments.

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Does Proteinuria-Inducing Physical Activity Increase Biomarkers of Acute Kidney Injury?

Cited by 23 publications

References 30 publications

Urinary Kidney Injury Molecule-1 but Not Urinary Neutrophil Gelatinase Associated Lipocalin Is Increased after Short Maximal Exercise

Urinary Kidney Injury Molecule-1 but Not Urinary Neutrophil Gelatinase Associated Lipocalin Is Increased after Short Maximal Exercise

Incremental short maximal exercise increases urinary liver‐type fatty acid‐binding protein in adults without CKD

Exercising in a hot environment with muscle damage: effects on acute kidney injury biomarkers and kidney function

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