Acute Kidney Injury Biomarker Responses to Short-Term Heat Acclimation

Pryor, Riana R.; Pryor, J. Luke; Vandermark, Lesley W.; Adams, Elizabeth L.; Brodeur, Rachel M.; Schlader, Zachary J.; Armstrong, Lawrence E.; Lee, Elaine C.; Maresh, Carl M.; Casa, Douglas J.

doi:10.3390/ijerph17041325

Cited by 15 publications

(25 citation statements)

References 62 publications

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“…There is a growing body of evidence that exhausting work in heat leads to CKD [19,[58][59][60][61][62][63][64] and the same risk factors-dehydration and muscle damage, soft drink consumption-are present, for example, in marathon runners.…”

Section: Discussionmentioning

confidence: 99%

“…The main problem is how to implement the knowledge from these studies in clinical practice. There are several facts concerning AKI biomarkers, AKI and CKD in athletes: Exercise-induced renal impairment is commonly present but temporary, Severe complications of exercise, like AKI requiring hemodialysis, are rare, Repeated episodes of AKI lead to CKD, There is no data showing that CKD could be related to sports activity, There is a growing body of evidence that exhausting work in heat leads to CKD [ 19 , 58 , 59 , 60 , 61 , 62 , 63 , 64 ] and the same risk factors—dehydration and muscle damage, soft drink consumption—are present, for example, in marathon runners. …”

Section: Discussionmentioning

confidence: 99%

“…There are over 100 biomarkers of AKI [61]. The urinary biomarkers which have been assessed in numerous studies are: chitinase 3-like protein 1 (YKL-40), MCP-1, TNF-alfa, osteopontin, DKK-1, micro RNAs, hemojuvelin, clusterin, CYR-61, cytochrome-C, epidermal growth factor, malondialdehyde, calprotectin, urine AGT angiotensinogen, matrix metalloproteinase 9, urine cysteine-rich 61, Na + /H + exchanger isoform 3 protein, netrin-1, fetuin-A and trefoil factor 3 (TFF3) [5,8,9].…”

Section: Other Promising Markers Of Aki (Ykl-40 Mcp-1 and Tnf-alfa mentioning

confidence: 99%

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Changes in Novel AKI Biomarkers after Exercise. A Systematic Review

Wołyniec

Ratkowski

Renke

et al. 2020

IJMS

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More than 100 substances have been identified as biomarkers of acute kidney injury. These markers can help to diagnose acute kidney injury (AKI) in its early phase, when the creatinine level is not increased. The two markers most frequently studied in plasma and serum are cystatin C and neutrophil gelatinase-associated lipocalin (NGAL). The former is a marker of kidney function and the latter is a marker of kidney damage. Some other promising serum markers, such as osteopontin and netrin-1, have also been proposed and studied. The list of promising urinary markers is much longer and includes cystatin C, NGAL, kidney injury molecule-1 (KIM-1), liver-type fatty-acid-binding protein (L-FABP), interleukin 18, insulin-like growth factor binding protein 7 (IGFBP-7), tissue inhibitor of metalloproteinases-2 (TIMP-2) and many others. Although these markers are increased in urine for no longer than a few hours after nephrotoxic agent action, they are not widely used in clinical practice. Only combined IGFBP-7/TIMP-2 measurement was approved in some countries as a marker of AKI. Several studies have shown that the levels of urinary AKI biomarkers are increased after physical exercise. This systematic review focuses on studies concerning changes in new AKI biomarkers in healthy adults after single exercise. Twenty-seven papers were identified and analyzed in this review. The interpretation of results from different studies was difficult because of the variety of study groups, designs and methodology. The most convincing data concern cystatin C. There is evidence that cystatin C is a better indicator of glomerular filtration rate (GFR) in athletes after exercise than creatinine and also at rest in athletes with a lean mass lower or higher than average. Serum and plasma NGAL are increased after prolonged exercise, but the level also depends on inflammation and hypoxia; therefore, it seems that in physical exercise, it is too sensitive for AKI diagnosis. It may, however, help to diagnose subclinical kidney injury, e.g., in rhabdomyolysis. Urinary biomarkers are increased after many types of exercise. Increases in NGAL, KIM-1, cystatin-C, L-FABP and interleukin 18 are common, but the levels of most urinary AKI biomarkers decrease rapidly after exercise. The importance of this short-term increase in AKI biomarkers after exercise is doubtful. It is not clear if it is a sign of mild kidney injury or physiological metabolic adaptation to exercise.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Other Promising Markers Of Aki (Ykl-40 Mcp-1 and Tnf-alfa mentioning

confidence: 99%

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Changes in Novel AKI Biomarkers after Exercise. A Systematic Review

Wołyniec

Ratkowski

Renke

et al. 2020

IJMS

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“…In our study, water restriction and intake of SB as fluid of rehydration induced a mild dehydration state similar to heat stress models [ 15 , 28 ] with a significant increase in vasopressin secretion (measured as plasma copeptin) as well as a robust stimulation of renal vasopressin receptors and polyol-fructokinase pathway enzymes including increased KHK activity [ 24 , 29 ]. Interestingly, rats receiving tap water during rehydration drank much less water but still had a lower plasma copeptin concentration as well as a mild upregulation of renal vasopressin receptors and polyol-fructokinase enzymes and KHK activity.…”

Section: Discussionmentioning

confidence: 99%

Fluid Intake Restriction Concomitant to Sweetened Beverages Hydration Induce Kidney Damage

García-Arroyo

Tapia

Muñoz-Jiménez

et al. 2020

Oxidative Medicine and Cellular Longevity

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Currently, there is the paradox of low water intake but increased intake of sugar-sweetened beverages (SB) in several populations; those habits are associated with an increased prevalence of metabolic derangements and greater chronic disease mortality. Persistent heat dehydration and increased SB intake stimulate the continued release of vasopressin and overactivation of the polyol-fructokinase pathway, synergizing each other, an effect partially mediated by oxidative stress. The objective of the present study was to evaluate whether water restriction concurrent with SB hydration can cause renal damage by stimulating similar pathways as heat dehydration. Three groups of male Wistar rats ( n = 6 ) were fluid restricted; from 10 am to 12 pm animals could rehydrate with tap water (W), or sweetened beverages, one prepared with 11% of a fructose-glucose combination (SB), or with the noncaloric edulcorant stevia (ST). A normal control group of healthy rats was also studied. The animals were followed for 4 weeks. Markers of dehydration and renal damage were evaluated at the end of the study. Fluid restriction and water hydration mildly increased urine osmolality and induced a 15% fall in CrCl while increased the markers of tubular damage by NAG and KIM-1. Such changes were in association with a mild overexpression of V1a and V2 renal receptors, polyol fructokinase pathway overactivation, and increased renal oxidative stress with reduced expression of antioxidant enzymes. Hydration with SB significantly amplified those alterations, while in stevia hydrated rats, the changes were similar to the ones observed in water hydrated rats. These data suggest that current habits of hydration could be a risk factor in developing kidney damage.

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“…Heat acclimation may represent one strategy to improve kidney function during heat exposure and minimize the risk of heat‐related kidney injury/disease. Recent observations suggest that exercise‐based heat acclimation mitigates the acute decline in glomerular filtration rate that occurs after exercise heat stress, supporting the possibility that heat acclimation confers protective renal adaptations (Omassoli et al., 2019), although this is not a consistent observation (Pryor et al., 2020). Nevertheless, it remains unknown whether the preservation of glomerular filtration rate translates into an improved or maintained urine‐concentrating ability.…”

Section: Introductionmentioning

confidence: 99%

Impact of passive heat acclimation on markers of kidney function during heat stress

Ravanelli

Barry

Schlader

et al. 2020

Experimental Physiology

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Little is known about the effect of heat acclimation on kidney function during heat stress. The purpose of this study was to determine the impact of passive heat stress and subsequent passive heat acclimation on markers of kidney function. Twelve healthy adults (seven men and five women; 26 ± 5 years of age; 72.7 ± 8.6 kg; 172.4 ± 7.5 cm) underwent passive heat stress before and after a 7 day controlled hyperthermia heat acclimation protocol. The impact of passive heat exposure on urine and serum markers of kidney function was evaluated before and after heat acclimation. Glomerular filtration rate, determined from creatinine clearance, was unchanged with passive heat stress before (pre, 133 ± 41 ml min −1 ; post, 127 ± 51 ml min −1 ; P = 0.99) and after (pre, 129 ± 46 ml min −1 ; post, 130 ± 36 ml min −1 ; P = 0.99) heat acclimation. The urine-to-serum osmolality ratio was reduced after passive heating (P < 0.01), but heat acclimation did not alter this response. In comparison to baseline, free water clearance was greater after passive heating before (pre, −0.86 ± 0.67 ml min −1 ; post, 0.40 ± 1.01 ml min −1 ; P < 0.01) but not after (pre, −0.16 ± 0.57 ml min −1 ; post, 0.76 ± 1.2 ml min −1 ; P = 0.11) heat acclimation. Furthermore, passive heating increased the fractional excretion rate of potassium (P < 0.03) but not sodium (P = 0.13) or chloride (P = 0.20). Lastly, heat acclimation reduced the fractional incidence of albuminuria after passive heating (before, 58 ± 51%; after, 8 ± 29%; P = 0.03). Collectively, these results demonstrate that passive heat stress does not alter the glomerular filtration rate. However, heat acclimation might improve urineconcentrating ability and filtration within the glomerulus.

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Acute Kidney Injury Biomarker Responses to Short-Term Heat Acclimation

Cited by 15 publications

References 62 publications

Changes in Novel AKI Biomarkers after Exercise. A Systematic Review

Changes in Novel AKI Biomarkers after Exercise. A Systematic Review

Fluid Intake Restriction Concomitant to Sweetened Beverages Hydration Induce Kidney Damage

Impact of passive heat acclimation on markers of kidney function during heat stress

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