Changes in renal markers and acute kidney injury after marathon running

The impact of marathon running on kidney function has not been previously described.

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).

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.

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.