Changes in renal markers and acute kidney injury after marathon running

Background: The impact of marathon running on kidney function has not been previously described. Methods: From 425 marathon runners, 13 women and 12 men were randomly selected and cardiovascular magnetic resonance imaging (MRI) and blood/urine biomarkers were performed 4 weeks before (baseline), immediately after (peak), and 24 h after the race (recovery). Results: Participants were 38.7 +/- 9.0 years old and completed the marathon in 256.2 +/- 43.5 min. A total of 10/25 (40.0%) met the Acute Kidney Injury Network definition of acute kidney injury (AKI) based on a rise in serum creatinine. There were parallel and similar mean rises in serum creatinine and cystatin C from baseline, to peak, and return to normal in recovery. Urine neutrophil gelatinase-associated lipocalin rose from 8.2 +/- 4.0 to 47.0 +/- 28.6 and returned to 10.6 +/- 7.2 ng/mL, P < 0.0001. Likewise, the mean urinary kidney injury molecule-1 levels were 2.6 +/- 1.6, 3.5 +/- 1.6 and 2.7 +/- 1.6 ng/mL (P = 0.001). The mean and minimum pre- and post-IVC (inferior vena cava) diameters by MRI were 24.9, 18.8 and 25.3, 17.5 mm, respectively, suggesting that runners were not volume depleted at the first post-race measurement. Conclusion: Approximately 40% of marathon runners experience a transient rise in serum creatinine that meets criteria of AKI with a parallel elevation of cystatin C, and supportive elevations of neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 in the urine. All biomarker elevations resolved by 24 h. These data suggest that AKI with a transient and minor change in renal filtration function occurs with the stress of marathon running. The impact of repetitive episodes of AKI with long-distance running is unknown.