Acute kidney injury (AKI) incidence (diagnosed by changes in serum creatinine [Cr]) following prolonged endurance events has been reported to be anywhere from 4 to 85%, and hypohydration may contribute to this. Whilst an increase in serum Cr indicates impaired kidney function, this might be influenced by muscle damage. Therefore, the use of other AKI biomarkers which can detect renal tubular injury may be more appropriate. The long-term consequences of AKI are not well understood, but there are some potential concerns of an increased subsequent risk of chronic kidney disease (CKD). Therefore, this brief review explores the effects of exercise training/competition on novel AKI biomarkers and the potential influence of fluid intake. The increase in novel AKI biomarkers following prolonged endurance events suggests renal tubular injury. This is likely due to the long duration and relatively high exercise intensity, producing increased sympathetic tone, body temperature, hypohydration, and muscle damage. Whilst muscle damage appears to be an important factor in the pathophysiology of exercise-associated AKI, it may require coexisting hypohydration. Fluid intake seems to play a role in exercise-associated AKI, as maintaining euhydration with water ingestion during simulated physical work in the heat appears to attenuate rises in AKI biomarkers. The composition of fluid intake may also be important, as high-fructose drinks have been shown to exacerbate AKI biomarkers. However, it is yet to be seen if these findings are applicable to athletes performing strenuous exercise in a temperate environment. Additionally, further work should examine the effects of repeated bouts of strenuous exercise on novel AKI biomarkers.

Following prolonged endurance events, the incidence of acute kidney injury (AKI), defined as a rapid decline in kidney function, has been reported to be anywhere from 4 to 85% [1-5]. This variable, but often high, incidence is likely due to a combination of factors, including muscle damage, sympathetic tone, body temperature, and hypohydration [1]. Of these factors, hypohydration may be of particular interest, as it is commonly seen during prolonged endurance events [6] and is relatively easy to manipulate (i.e., consume fluid to maintain euhydration). If optimizing hydration status is able to reduce the extent of AKI, then this could have implications for long-term renal function, as there are concerns that repeated AKIs (even subclinical AKIs) could increase the subsequent risk of chronic kidney disease (CKD), which describes irreversibly impaired kidney function [7]. This theory has been proposed to explain the epidemic of CKD seen in Central America among sugarcane workers, who are regularly exposed to factors that increase the risk of AKI [8]. This is of concern because CKD is associated with an increased risk of cardiovascular disease and mortality [9]. This topic, specifically kidney injury caused by working in the heat and the subsequent risk of CKD in labourers, was the focus of a recent comprehensive review by Schlader et al. [10], which will provide an excellent background for this brief, invited review. The present review will focus on the impact of exercise training/competition on AKI biomarkers in athletic populations, as well as exploring the influence of fluid intake.

In 2017, Hodgson et al. [11] conducted a systematic review of the literature observing AKI following endurance events, with a focus on serum creatinine (Cr). They reported that increases in serum Cr concentrations were seen following endurance events, but that the long-term implications were unknown [11]. Serum Cr, the principal biomarker used to clinically diagnose AKI, is a muscle breakdown product filtered by the kidneys and excreted in urine, meaning a rise, in many settings, indicates impaired kidney function. While this impaired kidney function normally indicates renal injury, in the context of prolonged endurance events, the rise in serum Cr concentrations post-exercise may simply be due to increased muscle breakdown (i.e., increased production) [1, 11] and/or a temporary reduction in renal blood flow (RBF) (i.e., reduced clearance) [12]. In this context, the use of other AKI biomarkers may be more appropriate to detect renal tubular injury [13]. Therefore, this brief review will focus on the responses of such biomarkers to exercise training/competition.

While there are many potential candidate biomarkers of AKI, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), interleukin-18, liver-type fatty acid binding protein, insulin-like growth factor binding protein 7 and tissue inhibitor metalloproteinase 2, NGAL and KIM-1 have received the most attention for exercise-associated AKI, as well as having been studied in a variety of clinical settings [13]. NGAL and KIM-1 expression are upregulated following AKI, which is thought to aid the proliferation of tubular cells [13]. An advantage of using NGAL and KIM-1 over serum Cr is that they may be able to indicate the location of kidney injury, as a rise in urinary KIM-1 (uKIM-1) indicates injury to the proximal tubule [13], whereas a rise in urinary NGAL (uNGAL) indicates injury mainly to the distal nephron [14]. Increases in NGAL and KIM-1 can be detected in blood or urine, but it is thought that the urinary forms may be more specific for determining AKI, as NGAL and KIM-1 are also expressed in organs other than the kidneys [13-15]. Therefore, this brief review will focus on uNGAL and uKIM-1.

An issue for consideration when studying urinary biomarkers is that the concentration of urine itself can vary substantially, and thus a rise in a urinary biomarker may be due to an increase in urine concentration, rather than an increase in biomarker production. To account for this, a variety of corrections have been applied in the literature, including correction for urinary Cr and urine osmolality [5, 16-21]. When measured in close proximity to exercise, it is thought that urine osmolality may be the more appropriate correction, as urinary Cr may be increased due to muscle damage [17, 19].

The previously mentioned risk factors for exercise-associated AKI may all contribute to AKI by reducing RBF [12, 22, 23]. A reduction in RBF may lead to renal is-chaemia and subsequent renal ATP depletion, which can initiate AKI [24]. During exercise, increased sympathetic tone serves to increase blood flow to the skeletal muscles, while increased core body temperature increases blood flow to the skin, both of which may reduce RBF [12, 22]. Indeed, this notion is supported by the finding that RBF decreases as exercise intensity increases [12]. Additionally, if exercise involves repeated eccentric muscle contractions, it can cause skeletal muscle damage [25], which may result in extracellular fluid entering the muscle cells [23]. These effects may decrease plasma volume and activate the renin-angiotensin-aldosterone system (RAAS), which may contribute to reduced RBF during exercise [23]. Damage to skeletal muscle may also lead to leakage of cellular contents into the circulation, including myoglobin, which is thought to scavenge nitric oxide, potentially resulting in renal vasoconstriction [23]. Furthermore, hypohydration, although a modifiable factor, is commonly present towards the end of endurance events [6]. Typically, hypohydration decreases plasma volume (resulting in subsequent RAAS activation), increases circulating vasopressin, and increases core body temperature during exercise, all of which may further reduce RBF [22, 23, 26-29]. During exercise, these factors may combine to reduce RBF (Fig. 1), which has been reported to fall by as much as 75% during vigorous exercise [12].

Fig. 1.

Schematic representing how exercise may reduce renal blood flow and thus increase the risk of AKI. AKI, acute kidney injury.

Fig. 1.

Schematic representing how exercise may reduce renal blood flow and thus increase the risk of AKI. AKI, acute kidney injury.

Close modal

In agreement with the often high incidence of AKI (as defined by serum Cr) measured following prolonged endurance events, increases in uNGAL [3, 16, 30] and uKIM-1 [3, 30] have also been reported after these events. These increases appear to be due to increased biomarker production, rather than simply urine concentration, as in one of these studies, urine specific gravity did not change from pre- to post-marathon [3]. Additionally, in another study, the increase in uNGAL from pre- to post-ultramarathon remained significant after correction for urinary Cr [16]. Taken together, these findings suggest that prolonged endurance events may cause renal tubular injury, rather than just muscle damage and/or a temporary reduction in RBF.

Given that uNGAL and uKIM-1 concentrations are sometimes only presented in their uncorrected form [3, 30], and that when they are corrected, it is often only for urinary Cr [5, 16, 17, 21], which may be inappropriate post-exercise [17, 19], this paragraph will compare uncorrected concentrations between studies. Prolonged endurance events, such as marathons and ultramarathons, appear to be the forms of exercise that produce the highest post-exercise uNGAL concentrations [3, 5, 15-21, 30-32]. This may be due to the combination of long duration and relatively high-intensity exercise. This theory could explain the comparatively lower uNGAL concentrations reported after an 800 m run (high intensity, but very short duration; [17]) and prolonged walking (long duration, but low intensity; [18]). Comparing the response of uKIM-1 to different forms of exercise is more challenging as there is less data available and there appears to be higher variability in baseline readings [3, 18, 19, 30].

Although exercise duration and intensity appear to be important factors determining the extent of kidney injury, the mechanisms are not fully understood. Increases in exercise duration and intensity are likely to align with increases in sympathetic tone, muscle damage and core body temperature. For example, Bongers et al. [19] documented greater rises in uNGAL and osmolality-corrected uNGAL following 107 min of exercise, compared to after the initial 30 min of this exercise, but the lack of a control group meant that no single risk factor could be isolated. Using a crossover design, Junglee et al. [15] demonstrated that uNGAL following exercise in the heat was significantly higher when the exercise was preceded by a bout of downhill muscle-damaging running (compared to flat less-muscle-damaging running). It has also been shown that continuous upper body cooling during exercise in the heat attenuated the increase in uNGAL [32]. The findings from these crossover studies suggest that muscle damage is an important factor in the pathophysiology of exercise-associated AKI and that an increase in core body temperature exacerbates kidney injury. A summary of the studies mentioned in this section of the review that examined the effect of exercise training/competition on uKIM-1 and/or uNGAL concentrations is presented in Table 1.

Table 1.

A summary of the studies referenced in the body text that examine the effect of exercise training/competition on uNGAL and/or uKIM-1 concentrations

A summary of the studies referenced in the body text that examine the effect of exercise training/competition on uNGAL and/or uKIM-1 concentrations
A summary of the studies referenced in the body text that examine the effect of exercise training/competition on uNGAL and/or uKIM-1 concentrations

An important caveat when interpreting the effect of exercise training/competition on long-term renal function is that exercise training has been suggested to preserve renal function through the improvement of cardiometabolic risk factors [10, 33]. To our knowledge, only one study has examined the effect of bouts of exercise on consecutive days on uNGAL and uKIM-1. Bongers et al. [18] found that uncorrected and osmolality-corrected post-exercise uNGAL and uKIM-1 concentrations did not accumulate after 3 days of prolonged walking. However, the effect of repeated bouts of more strenuous exercise, which have been shown to cause higher elevations in novel AKI biomarkers, remains unknown. Serum Cr has been measured after various stages of multistage ultramarathons, but similarly, no accumulation was found [4]. In addition, individuals that developed exercise-associated AKI from an ultramarathon did not experience greater post-exercise renal dysfunction at a following ultramarathon [1]. In this study, pre-exercise blood samples were not taken, and thus pre-exercise serum Cr concentrations were approximated [1]. In this instance, it would have been beneficial to have measured pre-exercise serum Cr values, as Cr is of more use when it is in steady state. This was done by Pryor et al. [34], who showed that 6 days of heat acclimation did not affect baseline serum Cr. A potential explanation for these findings may be that changes in novel AKI biomarkers, such as uNGAL, may precede changes in serum Cr [35]. Therefore, further research is required to determine the effect of repeated bouts of strenuous exercise on novel AKI biomarkers in athletic populations.

During exercise, the increase in metabolic heat production results in sweating, and as endurance athletes rarely match their sweat losses with fluid intake, hypohydration is commonly present towards the end of endurance events [6]. Not only can hypohydration reduce RBF but it also has the potential to exacerbate exercise-associated AKI via other mechanisms. As sweat losses are hypotonic compared to plasma, failure to replace them with fluid intake typically causes a decrease in plasma volume and a rise in plasma osmolality that draws water out of the intracellular fluid compartment via osmosis [26, 27]. This results in the release of arginine vasopressin, which acts on the kidney to increase water reabsorption [26, 27]. While this process is important for water conservation, it may result in increased renal oxygen consumption [28], which could exacerbate exercise-induced renal ischaemia and subsequent kidney injury. It was recently documented that marathon runners with AKI had higher post-exercise copeptin (a surrogate marker of vasopressin) concentrations than those without [21]. Plasma hypertonicity may also result in the conversion of glucose to sorbitol in the proximal tubule [36]. Sorbitol can then be converted to fructose, which can be metabolized by fructokinase, potentially resulting in renal ATP deletion and subsequent AKI [36].

While it has been suggested that the most common cause of exercise-associated AKI is muscle damage [1], this may require coexisting hypohydration in order to cause AKI [25]. In a study where large rises in markers of muscle damage were caused by maximal eccentric contractions, but hydration status was controlled for with fluid ingestion, there was no incidence of AKI [25]. A potential explanation for this is that both muscle damage and hypohydration may act in concert to increase kidney injury via synergistic reductions in plasma volume and RAAS activation [23]. Furthermore, while Junglee et al. [15] demonstrated that muscle damage increased uNGAL, it is important to note that this was in the presence of hypohydration.

To our knowledge, only two studies have used a crossover design to investigate the effect of hypohydration during exercise/simulated physical work on novel AKI biomarkers. Butts [20] manipulated hydration status (via fluid ingestion or restriction) before and during exercise in the heat that was preceded by muscle damaging exercise. They showed no rise in uNGAL from pre- to post-exercise in either trial, and while uNGAL concentrations were higher in the hypohydrated trial at these time points, correction for urine osmolality removed this effect [20]. Conversely, Chapman et al. [32] showed, through a panel of novel AKI biomarkers, that maintaining euhydration during simulated physical work in the heat appeared to reduce injury to the proximal tubules. These results may explain the lack of effect of hydration status on osmolality-corrected uNGAL in Butts [20], as a rise in uNGAL is thought to indicate injury mainly to the distal nephron [14].

Whilst maintaining euhydration may be beneficial, it is possible that not all drinks produce the same effect. Compared to water, ingestion of a high-fructose soft drink during and after simulated physical work in the heat caused a large increase in AKI incidence and a small increase in overnight uNGAL [31]. This effect may have been mediated through activation of the vasopressin and fructokinase pathways [31, 36], and thus the disparity between the large rise in AKI incidence and small increase in overnight uNGAL may be because fructose ingestion is more likely to lead to the injury of the proximal tubules [36]. If uKIM-1 had been measured in this study, we speculate that there would have been a large difference between trials. Therefore, although research is scarce, it is possible that fluid intake (volume and composition) might represent a potential modifiable factor to influence AKI biomarkers/risk (see Fig. 2 for potential effects).

Fig. 2.

Schematic representing how fluid intake may influence the risk of exercise-associated AKI. Solid arrows refer to established pathways, dashed arrows refer to potential/conditional pathways and the arrow from water to risk of AKI refers to potential inhibition. Temp, temperature; AVP, arginine vasopressin; RAAS, renin-angiotensin-aldosterone system; ATP, adenosine triphosphate; AKI, acute kidney injury.

Fig. 2.

Schematic representing how fluid intake may influence the risk of exercise-associated AKI. Solid arrows refer to established pathways, dashed arrows refer to potential/conditional pathways and the arrow from water to risk of AKI refers to potential inhibition. Temp, temperature; AVP, arginine vasopressin; RAAS, renin-angiotensin-aldosterone system; ATP, adenosine triphosphate; AKI, acute kidney injury.

Close modal

The increase in serum Cr following prolonged endurance events, such as marathons and ultramarathons, appears to be accompanied by an increase in novel biomarkers of AKI. This suggests renal tubular injury, rather than just muscle damage and/or a temporary reduction in RBF. The large rise in AKI biomarkers often seen following marathons and ultramarathons is likely due to the long duration and relatively high exercise intensity, resulting in an increase in sympathetic tone, muscle damage, core body temperature and level of hypohydration. While it is challenging to isolate the role of these factors, due to their mechanistic interactions, it has been shown that maintaining euhydration with water ingestion during simulated physical work in the heat attenuated rises in biomarkers of AKI [32]. However, ingesting a high-fructose soft drink during simulated physical work in the heat has been shown to exacerbate markers of AKI. Unfortunately, whether these findings regarding fluid intake apply to athletes undertaking strenuous exercise in a temperate environment remains unknown. The long-term effects of exercise-associated increases in AKI biomarkers and the effect of interventions that may attenuate these rises, such as maintaining euhydration with water ingestion, are also not well understood and require further research.

L.A. Juett received travel expenses and registration fees from Danone Research to attend the 2019 Hydration for Health Scientific Conference. L.J. James has previously received funding for his research from PepsiCo., Inc. and has previously performed consultancy work for Lucozade Ribena Suntory. These previous funding/consultancy activities are in no way linked to the present article and have always been paid directly to L.J. James’s employer, not to L.J. James. The authors have no other conflicts of interest to declare.

1.
Hoffman
MD
,
Weiss
RH
.
Does acute kidney injury from an ultramarathon increase the risk for greater subsequent injury?
Clin J Sport Med
.
2016
;
26
(
5
):
417
22
. .
2.
Kao
WF
,
Hou
SK
,
Chiu
YH
,
Chou
SL
,
Kuo
FC
,
Wang
SH
, et al
Effects of 100-km ultramarathon on acute kidney injury
.
Clin J Sport Med
.
2015
;
25
(
1
):
49
54
. .
3.
Mansour
SG
,
Verma
G
,
Pata
RW
,
Martin
TG
,
Perazella
MA
,
Parikh
CR
.
Kidney injury and repair biomarkers in marathon runners
.
Am J Kidney Dis
.
2017
;
70
(
2
):
252
61
. .
4.
Lipman
GS
,
Krabak
BJ
,
Waite
BL
,
Logan
SB
,
Menon
A
,
Chan
GK
.
A prospective cohort study of acute kidney injury in multi-stage ultramarathon runners: the biochemistry in endurance runner study (BIERS)
.
Res Sports Med
.
2014
;
22
(
2
):
185
92
. .
5.
Poussel
M
,
Touzé
C
,
Allado
E
,
Frimat
L
,
Hily
O
,
Thilly
N
, et al
Ultramarathon and renal function: does exercise-induced acute kidney injury really exist in common conditions?
Front Sports Act Living
.
2020 Jan 21
;
1
:
71
. .
6.
Cheuvront
SN
,
Haymes
EM
.
Thermoregulation and marathon running
.
Sport Med
.
2001
;
31
(
10
):
743
62
.
7.
Coca
SG
,
Singanamala
S
,
Parikh
CR
.
Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis
.
Kidney Int
.
2012
;
81
(
5
):
442
8
. .
8.
Weiner
DE
,
McClean
MD
,
Kaufman
JS
,
Brooks
DR
.
The central american epidemic of CKD
.
Clin J Am Soc Nephrol
.
2013
;
8
(
3
):
504
11
. .
9.
Go
AS
,
Chertow
GM
,
Fan
D
,
McCulloch
CE
,
Hsu
CY
.
Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization
.
N Engl J Med
.
2004
;
351
(
13
):
1296
305
. .
10.
Schlader
ZJ
,
Hostler
D
,
Parker
MD
,
Pryor
RR
,
Lohr
JW
,
Johnson
BD
, et al
The potential for renal injury elicited by physical work in the heat
.
Nutrients
.
2019
;
11
(
9
):
2087
. .
11.
Hodgson
L
,
Walter
E
,
Venn
R
,
Galloway
R
,
Pitsiladis
Y
,
Sardat
F
, et al
Acute kidney injury associated with endurance events: is it a cause for concern? A systematic review
.
BMJ Open Sport Exerc Med
.
2017
;
3
(
1
):
e000093
.
12.
Poortmans
JR
.
Exercise and renal function
.
Sports Med
.
1984 Mar–Apr
;
1
(
2
):
125
53
. .
13.
Kashani
K
,
Cheungpasitporn
W
,
Ronco
C
.
Biomarkers of acute kidney injury: the pathway from discovery to clinical adoption
.
Clin Chem Lab Med
.
2017
;
55
(
8
):
1074
89
. .
14.
Helanova
K
,
Spinar
J
,
Parenica
J
.
Diagnostic and prognostic utility of neutrophil gelatinase-associated lipocalin (NGAL) in patients with cardiovascular diseases: review
.
Kidney Blood Press Res
.
2014
;
39
(
6
):
623
9
.
15.
Junglee
NA
,
Di Felice
U
,
Dolci
A
,
Fortes
MB
,
Jibani
MM
,
Lemmey
AB
, et al
Exercising in a hot environment with muscle damage: effects on acute kidney injury biomarkers and kidney function
.
Am J Physiol Renal Physiol
.
2013
;
305
(
6
):
F813
20
. .
16.
Lippi
G
,
Sanchis-Gomar
F
,
Salvagno
GL
,
Aloe
R
,
Schena
F
,
Guidi
GC
.
Variation of serum and urinary neutrophil gelatinase associated lipocalin (NGAL) after strenuous physical exercise
.
Clin Chem Lab Med
.
2012
;
50
(
9
):
1585
9
. .
17.
Junglee
NA
,
Lemmey
AB
,
Burton
M
,
Searell
C
,
Jones
D
,
Lawley
JS
, et al
Does proteinuria-inducing physical activity increase biomarkers of acute kidney injury?
Kidney Blood Press Res
.
2012
;
36
(
1
):
278
89
. .
18.
Bongers
CCWG
,
Alsady
M
,
Nijenhuis
T
,
Hartman
YAW
,
Eijsvogels
TMH
,
Deen
PMT
, et al
Impact of acute versus repetitive moderate intensity endurance exercise on kidney injury markers
.
Physiol Rep
.
2017
;
5
(
24
):
1
11
. .
19.
Bongers
CCWG
,
Alsady
M
,
Nijenhuis
T
,
Tulp
ADM
,
Eijsvogels
TMH
,
Deen
PMT
, et al
Impact of acute versus prolonged exercise and dehydration on kidney function and injury
.
Physiol Rep
.
2018
;
6
(
11
):
e13734
11
. .
20.
Butts
CL
.
Dehydration, muscle damage, and exercise in the heat: impacts on renal stress, thermoregulation, and muscular damage recovery
.
Fayetteville
:
University of Arkansas
;
2018
.
21.
Mansour
SG
,
Martin
TG
,
Obeid
W
,
Pata
RW
,
Myrick
KM
,
Kukova
L
, et al
The role of volume regulation and thermoregulation in AKI during marathon running
.
Clin J Am Soc Nephrol
.
2019
;
14
(
9
):
1297
305
.
22.
Radigan
LR
,
Robinson
S
.
Effects of environmental heat stress and exercise on renal blood flow and filtration rate
.
J Appl Physiol
.
1949
;
2
(
4
):
185
91
. .
23.
Petejova
N
,
Martinek
A
.
Acute kidney injury due to rhabdomyolysis and renal replacement therapy: a critical review
.
Crit Care
.
2014
;
18
(
3
):
224
8
. .
24.
Basile
DP
,
Anderson
MD
,
Sutton
TA
.
Pathophysiology of acute kidney injury
.
Compr Physiol
.
2012
;
2
(
2
):
1303
53
. .
25.
Clarkson
PM
,
Kearns
AK
,
Rouzier
P
,
Rubin
R
,
Thompson
PD
.
Serum creatine kinase levels and renal function measures in exertional muscle damage
.
Med Sci Sports Exerc
.
2006
;
38
(
4
):
623
7
. .
26.
Cheuvront
SN
,
Kenefick
RW
.
Dehydration: physiology, assessment, and performance effects
.
Compr Physiol
.
2014
;
4
(
1
):
257
85
. .
27.
James
LJ
,
Funnell
MP
,
James
RM
,
Mears
SA
.
Does hypohydration really impair endurance performance? Methodological considerations for interpreting hydration research
.
Sports Med
.
2019
;
49
(
Suppl 2
):
103
14
. .
28.
Bragadottir
G
,
Redfors
B
,
Nygren
A
,
Sellgren
J
,
Ricksten
SE
.
Low-dose vasopressin increases glomerular filtration rate, but impairs renal oxygenation in post-cardiac surgery patients
.
Acta Anaesthesiol Scand
.
2009
;
53
(
8
):
1052
9
. .
29.
Funnell
MP
,
Mears
SA
,
Bergin-Taylor
K
,
James
LJ
.
Blinded and unblinded hypohydration similarly impair cycling time trial performance in the heat in trained cyclists
.
J Appl Physiol
.
2019
;
126
(
4
):
870
9
. .
30.
McCullough
PA
,
Chinnaiyan
KM
,
Gallagher
MJ
,
Colar
JM
,
Geddes
T
,
Gold
JM
, et al
Changes in renal markers and acute kidney injury after marathon running
.
Nephrology
.
2011
;
16
(
2
):
194
9
. .
31.
Chapman
CL
,
Johnson
BD
,
Sackett
JR
,
Parker
MD
,
Schlader
ZJ
.
Soft drink consumption during and following exercise in the heat elevates biomarkers of acute kidney injury
.
Am J Physiol Regul Integr Comp Physiol
.
2019
;
316
(
3
):
R189
98
. .
32.
Chapman
CL
,
Johnson
BD
,
Vargas
NT
,
Hostler
D
,
Parker
MD
,
Schlader
ZJ
.
Hyperthermia and dehydration during physical work in the heat both contribute to the risk of acute kidney injury
.
J Appl Physiol
.
2020 Apr 1
;
128
(
4
):
715
28
. .
33.
Stump
CS
.
Physical activity in the prevention of chronic kidney disease
.
Cardiorenal Med
.
2011
;
1
(
3
):
164
73
. .
34.
Pryor
RR
,
Pryor
JL
,
Vandermark
LW
,
Adams
EL
,
Brodeur
RM
,
Schlader
ZJ
, et al
Acute kidney injury biomarker responses to short-term heat acclimation
.
Int J Environ Res Public Health
.
2020
;
17
(
4
):
1
13
. .
35.
Laws
RL
,
Brooks
DR
,
Amador
JJ
,
Weiner
DE
,
Kaufman
JS
,
Ramírez-Rubio
O
, et al
Biomarkers of kidney injury among Nicaraguan sugarcane workers
.
Am J Kidney Dis
.
2016
;
67
(
2
):
209
17
. .
36.
Jimenez
CAR
,
Ishimoto
T
,
Lanaspa
MA
,
Rivard
CJ
,
Nakagawa
T
,
Ejaz
AA
, et al
Fructokinase activity mediates dehydration-induced renal injury
.
Kidney Int
.
2014
;
86
(
2
):
294
302
.
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This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.