The role of volume regulation and thermoregulation in aki during marathon running

Sherry G. Mansour, Thomas G. Martin, Wassim Obeid, Rachel W. Pata, Karen M. Myrick, Lidiya Kukova, Yaqi Jia, Petter Bjornstad, Joe M. El-Khoury, Chirag Parikh

Research output: Contribution to journalArticle

Abstract

Background and objectives Marathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage. Design, setting, participants, & measurements To investigate the etiology, we examined volume and thermoregulatory responses as possible mechanisms in runners’ AKI using a prospective cohort of runners in the 2017 Hartford Marathon. Vitals, blood, and urine samples were collected in 23 runners 1 day premarathon and immediately and 1 day postmarathon. We measured copeptin at each time point. Continuous core body temperature, sweat sodium, and volume were assessed during the race. The primary outcome of interest was AKI, defined by AKIN criteria. Results Runners ranged from 22 to 63 years old; 43% were men. Runners lost a median (range) of 2.34 (0.50–7.21) g of sodium and 2.47 (0.36–6.81) L of volume via sweat. After accounting for intake, they had a net negative sodium and volume balance at the end of the race. The majority of runners had increases in core body temperature to 38.4 (35.8–41)°C during the race from their baseline. Fifty-five percent of runners developed AKI, yet 74% had positive urine microscopy for acute tubular injury. Runners with more running experience and increased participation in prior marathons developed a rise in creatinine as compared with those with lesser experience. Sweat sodium losses were higher in runners with AKI versus non-AKI (median, 3.41 [interquartile range (IQR), 1.7–4.8] versus median, 1.4 [IQR, 0.97–2.8] g; P=0.06, respectively). Sweat volume losses were higher in runners with AKI versus non-AKI (median, 3.89 [IQR, 1.49–5.09] versus median, 1.66 [IQR, 0.72–2.84] L; P=0.03, respectively). Copeptin was significantly higher in runners with AKI versus those without (median, 79.9 [IQR, 25.2–104.4] versus median, 11.3 [IQR, 6.6–43.7]; P=0.02, respectively). Estimated temperature was not significantly different. Conclusions All runners experienced a substantial rise in copeptin and body temperature along with salt and water loss due to sweating. Sodium and volume loss via sweat as well as plasma copeptin concentrations were associated with AKI in runners.

Original languageEnglish (US)
Pages (from-to)1297-1305
Number of pages9
JournalClinical Journal of the American Society of Nephrology
Volume14
Issue number9
DOIs
StatePublished - Sep 6 2019

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Sweat
Body Temperature Regulation
Sodium
Body Temperature
Urine
Sweating
Nephrons
Wounds and Injuries
Microscopy
Creatinine
Salts
Biomarkers
Temperature
copeptins
Water

ASJC Scopus subject areas

  • Epidemiology
  • Critical Care and Intensive Care Medicine
  • Nephrology
  • Transplantation

Cite this

The role of volume regulation and thermoregulation in aki during marathon running. / Mansour, Sherry G.; Martin, Thomas G.; Obeid, Wassim; Pata, Rachel W.; Myrick, Karen M.; Kukova, Lidiya; Jia, Yaqi; Bjornstad, Petter; El-Khoury, Joe M.; Parikh, Chirag.

In: Clinical Journal of the American Society of Nephrology, Vol. 14, No. 9, 06.09.2019, p. 1297-1305.

Research output: Contribution to journalArticle

Mansour, Sherry G. ; Martin, Thomas G. ; Obeid, Wassim ; Pata, Rachel W. ; Myrick, Karen M. ; Kukova, Lidiya ; Jia, Yaqi ; Bjornstad, Petter ; El-Khoury, Joe M. ; Parikh, Chirag. / The role of volume regulation and thermoregulation in aki during marathon running. In: Clinical Journal of the American Society of Nephrology. 2019 ; Vol. 14, No. 9. pp. 1297-1305.
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abstract = "Background and objectives Marathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage. Design, setting, participants, & measurements To investigate the etiology, we examined volume and thermoregulatory responses as possible mechanisms in runners’ AKI using a prospective cohort of runners in the 2017 Hartford Marathon. Vitals, blood, and urine samples were collected in 23 runners 1 day premarathon and immediately and 1 day postmarathon. We measured copeptin at each time point. Continuous core body temperature, sweat sodium, and volume were assessed during the race. The primary outcome of interest was AKI, defined by AKIN criteria. Results Runners ranged from 22 to 63 years old; 43{\%} were men. Runners lost a median (range) of 2.34 (0.50–7.21) g of sodium and 2.47 (0.36–6.81) L of volume via sweat. After accounting for intake, they had a net negative sodium and volume balance at the end of the race. The majority of runners had increases in core body temperature to 38.4 (35.8–41)°C during the race from their baseline. Fifty-five percent of runners developed AKI, yet 74{\%} had positive urine microscopy for acute tubular injury. Runners with more running experience and increased participation in prior marathons developed a rise in creatinine as compared with those with lesser experience. Sweat sodium losses were higher in runners with AKI versus non-AKI (median, 3.41 [interquartile range (IQR), 1.7–4.8] versus median, 1.4 [IQR, 0.97–2.8] g; P=0.06, respectively). Sweat volume losses were higher in runners with AKI versus non-AKI (median, 3.89 [IQR, 1.49–5.09] versus median, 1.66 [IQR, 0.72–2.84] L; P=0.03, respectively). Copeptin was significantly higher in runners with AKI versus those without (median, 79.9 [IQR, 25.2–104.4] versus median, 11.3 [IQR, 6.6–43.7]; P=0.02, respectively). Estimated temperature was not significantly different. Conclusions All runners experienced a substantial rise in copeptin and body temperature along with salt and water loss due to sweating. Sodium and volume loss via sweat as well as plasma copeptin concentrations were associated with AKI in runners.",
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AU - Martin, Thomas G.

AU - Obeid, Wassim

AU - Pata, Rachel W.

AU - Myrick, Karen M.

AU - Kukova, Lidiya

AU - Jia, Yaqi

AU - Bjornstad, Petter

AU - El-Khoury, Joe M.

AU - Parikh, Chirag

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N2 - Background and objectives Marathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage. Design, setting, participants, & measurements To investigate the etiology, we examined volume and thermoregulatory responses as possible mechanisms in runners’ AKI using a prospective cohort of runners in the 2017 Hartford Marathon. Vitals, blood, and urine samples were collected in 23 runners 1 day premarathon and immediately and 1 day postmarathon. We measured copeptin at each time point. Continuous core body temperature, sweat sodium, and volume were assessed during the race. The primary outcome of interest was AKI, defined by AKIN criteria. Results Runners ranged from 22 to 63 years old; 43% were men. Runners lost a median (range) of 2.34 (0.50–7.21) g of sodium and 2.47 (0.36–6.81) L of volume via sweat. After accounting for intake, they had a net negative sodium and volume balance at the end of the race. The majority of runners had increases in core body temperature to 38.4 (35.8–41)°C during the race from their baseline. Fifty-five percent of runners developed AKI, yet 74% had positive urine microscopy for acute tubular injury. Runners with more running experience and increased participation in prior marathons developed a rise in creatinine as compared with those with lesser experience. Sweat sodium losses were higher in runners with AKI versus non-AKI (median, 3.41 [interquartile range (IQR), 1.7–4.8] versus median, 1.4 [IQR, 0.97–2.8] g; P=0.06, respectively). Sweat volume losses were higher in runners with AKI versus non-AKI (median, 3.89 [IQR, 1.49–5.09] versus median, 1.66 [IQR, 0.72–2.84] L; P=0.03, respectively). Copeptin was significantly higher in runners with AKI versus those without (median, 79.9 [IQR, 25.2–104.4] versus median, 11.3 [IQR, 6.6–43.7]; P=0.02, respectively). Estimated temperature was not significantly different. Conclusions All runners experienced a substantial rise in copeptin and body temperature along with salt and water loss due to sweating. Sodium and volume loss via sweat as well as plasma copeptin concentrations were associated with AKI in runners.

AB - Background and objectives Marathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage. Design, setting, participants, & measurements To investigate the etiology, we examined volume and thermoregulatory responses as possible mechanisms in runners’ AKI using a prospective cohort of runners in the 2017 Hartford Marathon. Vitals, blood, and urine samples were collected in 23 runners 1 day premarathon and immediately and 1 day postmarathon. We measured copeptin at each time point. Continuous core body temperature, sweat sodium, and volume were assessed during the race. The primary outcome of interest was AKI, defined by AKIN criteria. Results Runners ranged from 22 to 63 years old; 43% were men. Runners lost a median (range) of 2.34 (0.50–7.21) g of sodium and 2.47 (0.36–6.81) L of volume via sweat. After accounting for intake, they had a net negative sodium and volume balance at the end of the race. The majority of runners had increases in core body temperature to 38.4 (35.8–41)°C during the race from their baseline. Fifty-five percent of runners developed AKI, yet 74% had positive urine microscopy for acute tubular injury. Runners with more running experience and increased participation in prior marathons developed a rise in creatinine as compared with those with lesser experience. Sweat sodium losses were higher in runners with AKI versus non-AKI (median, 3.41 [interquartile range (IQR), 1.7–4.8] versus median, 1.4 [IQR, 0.97–2.8] g; P=0.06, respectively). Sweat volume losses were higher in runners with AKI versus non-AKI (median, 3.89 [IQR, 1.49–5.09] versus median, 1.66 [IQR, 0.72–2.84] L; P=0.03, respectively). Copeptin was significantly higher in runners with AKI versus those without (median, 79.9 [IQR, 25.2–104.4] versus median, 11.3 [IQR, 6.6–43.7]; P=0.02, respectively). Estimated temperature was not significantly different. Conclusions All runners experienced a substantial rise in copeptin and body temperature along with salt and water loss due to sweating. Sodium and volume loss via sweat as well as plasma copeptin concentrations were associated with AKI in runners.

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