Sherry G Mansour1,2, Thomas G Martin3, Wassim Obeid4, Rachel W Pata5, Karen M Myrick6, Lidiya Kukova1, Yaqi Jia4, Petter Bjornstad7,8, Joe M El-Khoury1, Chirag R Parikh9. 1. Program of Applied Translational Research, Department of Medicine and. 2. Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut. 3. Department of Biomedical Sciences and. 4. Division of Nephrology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland. 5. Department of Physical Therapy, Quinnipiac University, North Haven, Connecticut; and. 6. University of Saint Joseph, School of Interdisciplinary Health and Science, West Hartford, Connecticut. 7. Division of Endocrinology, Department of Pediatrics and. 8. Division of Nephrology, Department of Medicine, University of Colorado, Aurora, Colorado. 9. Division of Nephrology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland; chirag.parikh@jhmi.edu.
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. PODCAST: This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2019_08_13_CJASNPodcast_19_09_.mp3.
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. PODCAST: This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2019_08_13_CJASNPodcast_19_09_.mp3.
Authors: Brice M R Appenzeller; Claude Schummer; Sophie Boura Rodrigues; Robert Wennig Journal: J Chromatogr B Analyt Technol Biomed Life Sci Date: 2007-02-01 Impact factor: 3.205
Authors: Mark A Perazella; Steven G Coca; Isaac E Hall; Umo Iyanam; Madiha Koraishy; Chirag R Parikh Journal: Clin J Am Soc Nephrol Date: 2010-01-14 Impact factor: 8.237
Authors: Edward D Siew; Lorraine B Ware; Tebeb Gebretsadik; Ayumi Shintani; Karel G M Moons; Nancy Wickersham; Frederick Bossert; T Alp Ikizler Journal: J Am Soc Nephrol Date: 2009-07-23 Impact factor: 10.121
Authors: Ravindra L Mehta; John A Kellum; Sudhir V Shah; Bruce A Molitoris; Claudio Ronco; David G Warnock; Adeera Levin Journal: Crit Care Date: 2007 Impact factor: 9.097
Authors: Danielle L Kirkman; Natalie Bohmke; Salvatore Carbone; Ryan S Garten; Paula Rodriguez-Miguelez; Robert L Franco; Jason M Kidd; Antonio Abbate Journal: Am J Physiol Renal Physiol Date: 2020-12-07
Authors: Ugochukwu Ugwuowo; Yu Yamamoto; Tanima Arora; Ishan Saran; Caitlin Partridge; Aditya Biswas; Melissa Martin; Dennis G Moledina; Jason H Greenberg; Michael Simonov; Sherry G Mansour; Ricardo Vela; Jeffrey M Testani; Veena Rao; Keith Rentfro; Wassim Obeid; Chirag R Parikh; F Perry Wilson Journal: Am J Kidney Dis Date: 2020-06-04 Impact factor: 8.860
Authors: Erik Hansson; Jason Glaser; Kristina Jakobsson; Ilana Weiss; Catarina Wesseling; Rebekah A I Lucas; Jason Lee Kai Wei; Ulf Ekström; Julia Wijkström; Theo Bodin; Richard J Johnson; David H Wegman Journal: Nutrients Date: 2020-06-02 Impact factor: 5.717
Authors: Numan A AlAbdan; Omar A Almohammed; Maryam S Altukhaim; Mahfooz A Farooqui; Mubarak I Abdalla; Hazza Q Al Otaibi; Norah R Alshuraym; Shahad N Alghusun; Lama H Alotaibi; Abdullah A Alsayyari Journal: BMC Nephrol Date: 2022-02-07 Impact factor: 2.388
Authors: Michael J Stacey; Neil E Hill; Iain T Parsons; Jenny Wallace; Natalie Taylor; Rachael Grimaldi; Nishma Shah; Anna Marshall; Carol House; John P O'Hara; Stephen J Brett; David R Woods Journal: PLoS One Date: 2022-02-17 Impact factor: 3.240
Authors: Whitley C Atkins; Cory L Butts; Melani R Kelly; Chris Troyanos; R Mark Laursen; Andrew Duckett; Dawn M Emerson; Megan E Rosa-Caldwell; Brendon P McDermott Journal: Front Physiol Date: 2022-01-03 Impact factor: 4.566
Authors: Loris A Juett; Katharine L Midwood; Mark P Funnell; Lewis J James; Stephen A Mears Journal: Eur J Appl Physiol Date: 2021-09-15 Impact factor: 3.078