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Comprehensive Review

Kidney physiology and pathophysiology during heat stress and the modification by exercise, dehydration, heat acclimation and aging

ORCID Icon, ORCID Icon, ORCID Icon, ORCID Icon, ORCID Icon & ORCID Icon
Pages 108-159 | Received 28 Aug 2020, Accepted 17 Sep 2020, Published online: 13 Oct 2020
 

ABSTRACT

The kidneys’ integrative responses to heat stress aid thermoregulation, cardiovascular control, and water and electrolyte regulation. Recent evidence suggests the kidneys are at increased risk of pathological events during heat stress, namely acute kidney injury (AKI), and that this risk is compounded by dehydration and exercise. This heat stress related AKI is believed to contribute to the epidemic of chronic kidney disease (CKD) occurring in occupational settings. It is estimated that AKI and CKD affect upwards of 45 million individuals in the global workforce. Water and electrolyte disturbances and AKI, both of which are representative of kidney-related pathology, are the two leading causes of hospitalizations during heat waves in older adults. Structural and physiological alterations in aging kidneys likely contribute to this increased risk. With this background, this comprehensive narrative review will provide the first aggregation of research into the integrative physiological response of the kidneys to heat stress. While the focus of this review is on the human kidneys, we will utilize both human and animal data to describe these responses to passive and exercise heat stress, and how they are altered with heat acclimation. Additionally, we will discuss recent studies that indicate an increased risk of AKI due to exercise in the heat. Lastly, we will introduce the emerging public health crisis of older adults during extreme heat events and how the aging kidneys may be more susceptible to injury during heat stress.

Abbreviations

ACEi=

Angiotensin converting enzyme inhibitor

AKI=

Acute kidney injury

ARF=

Acute renal failure

AT1R=

Angiotensin II type 1 receptor

CKD=

Chronic kidney disease

GFR=

Glomerular filtration rate

IGFBP7=

Insulin-like growth factor binding protein 7

IL-18=

Interleukin-18

KIM-1=

Kidney injury molecule-1

L-FABP=

Liver type fatty acid-binding protein

NGAL=

Neutrophil gelatinase-associated lipocalin

NHE3=

Sodium-hydrogen antiporter 3

NIOSH=

U.S. National Institute for Occupational Safety and Health

NOS=

Nitric oxide synthase

NSAID=

Nonsteroidal anti-inflammatory drug

PAH=

Para-aminohippurate

RSNA=

Renal sympathetic nerve activity

TIMP-2=

Tissue inhibitor of metalloproteinase-2

V˙O2max=

Maximal oxygen uptake

V1=

Vasopressin type 1 receptors

V2=

Vasopressin type 2 receptors

Disclosure statement

No conflicts of interest, financial or otherwise, are declared by the authors.

Additional information

Funding

Preparation of this manuscript and some of the original research efforts discussed herein were supported by awards from the Carl V. Gisolfi Memorial Fund from the American College of Sports Medicine Foundation (#17-00580), the Mark Diamond Research Fund from the University at Buffalo (no. SP-19-04), and the U.S. Centers for Disease Control and Prevention (R01OH011528).

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