Marathon Running and Cell-Cycle Arrest Biomarkers of Acute Kidney Injury

Todd Leckie, Daniel Fitzpatrick, Alan Richardson, Alex Hunter, Rob Galloway, Rachael Grimaldi, Lui Forni, Luke Hodgson

Research output: Contribution to journalArticlepeer-review


Endurance exercise is known to cause a rise in serum creatinine. It is not known to what extent this rise reflects renal stress and a potential acute kidney injury (AKI). Increases in Insulin Like Growth Factor Binding Protein 7 (IGFBP7) and Tissue Inhibitor of Metalloprotinases-2 (TIMP-2), urinary biomarkers of cell cycle arrest and renal stress, are associated with the development of AKI.

Repeated measures study

Runners were recruited at the 2019 Brighton Marathon (UK) and provided urine and blood samples at baseline, immediately post-race and 24hrs post-race. Serum creatinine, urinary creatinine and urinary IGFBP7 and TIMP-2 were analysed from the samples.

Seventy nine participants (23 females, 56 males), aged 43 ± 10yrs (mean ± SD), finish time 243 ± 40mins were included for analysis. Serum creatinine increased over the race by 40 ± 26% (p<0.001), TIMP-2 increased by 555 ± 697% (p<0.001) and IGFBP7 increased by 1094 ± 1491% (p<0.001) over the race. A subset of twenty-two participants supplied samples 24 hours post-race, reporting values similar to baseline at for all variables by this time. Significant increases (p<0.01) were seen in markers when corrected for urinary creatinine.

This study is the first to report large rises in IGFBP7 and TIMP-2 following marathon running. This suggests that rises in creatinine are not fully explained by changes in production and clearance and may reflect a state of kidney stress, or injury.

Original languageEnglish
JournalJournal of Science and Medicine in Sport
Publication statusAccepted/In press - 22 Oct 2022


  • Acute kidney injury
  • biomarker
  • endurance
  • running
  • IGFBP7
  • TIMP-2


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