Background Investigation into strenuous activity and kidney function has gained interest given increasing marathon participation. Study Design Prospective observational study Setting & Participants Runners participating in the 2015 Hartford Marathon Predictor Completing a marathon Outcomes Acute kidney injury (AKI) as defined by AKI Network (AKIN) criteria. Stage 1 AKI was defined as 1.5- to 2-fold or 0.3 mg/dL increase in serum creatinine within 48 hours of day 0 and stage 2 was defined as a > 2- to 3-fold increase in creatinine. Microscopy score was defined by the number of granular casts and renal tubular epithelial cells. Measurements Samples were collected 24 hours pre-marathon (Day 0), immediately post- marathon (Day 1) and 24 hours post-marathon (Day 2). Measurements of serum creatinine, creatine kinase, and urine albumin were completed as well as urine microscopy analysis. Six injury urine biomarkers (IL-6, IL-8, IL-18, kidney injury molecule 1, neutrophil gelatinase-associated lipocalin, and tumor necrosis factor α) and two repair urine biomarkers (YKL-40 and monocyte chemoattractant protein 1) were measured. Results 22 marathon runners were included. Mean age was 44 years and 41% were male. 82% of runners developed a rise in creatinine equivalent to AKIN-defined AKI stages 1 and 2. 73% had microscopy diagnoses of tubular injury. Serum creatinine, urine albumin, and injury and repair biomarkers peaked on Day 1 and were significantly elevated compared to Day 0 and Day 2. Serum creatine kinase levels continued to significantly rise from Day 0 to Day 2. Limitations Small sample size and limited clinical data available at all time points. Conclusions Marathon runners developed AKI and urine sediments diagnostic of tubular injury. Rise in injury and repair biomarkers suggests structural damage to renal tubules occurring after marathon. The results of our study should be validated in larger cohorts with longer follow-up of kidney function.

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Background and objectivesMarathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage.Design, setting, participants, & measurementsTo 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.ResultsRunners 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.ConclusionsAll 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.PodcastThis article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2019_08_13_CJASNPodcast_19_09_.mp3

This study investigated whether haematological markers differ between young and masters marathon participants, running at similar performance levels. Nine young (31.89 ± 4.96 years) and eight masters (63.13 ± 4.61 years) runners participated. At five time points (pre-race through 54 h post-race), a complete blood cell count, basic metabolic panel and creatine kinase (CK) isoenzyme panel were assessed. Race performance was standardised using the World Masters Association Age Grading Performance Tables. Total CK levels were elevated for all participants at all time points post-race (P < 0.001). The CK-isoenzyme MB% was elevated across groups at 6, 30 and 54 h post-race (P < 0.01, P < 0.01 and P < 0.05), with masters runners having a higher CK-MB% at 30 and 54 h (P < 0.05, P < 0.05). Total white blood cell and neutrophil counts were elevated through 6 h post-race (P < 0.001), with higher levels found in younger runners (P < 0.001). When considering all blood work, masters runners had a higher number of abnormal values at 6, 30 and 54 h post-race (P < 0.05, P < 0.01 and P < 0.05). In conclusion, masters runners demonstrated sustained CK-MB elevation, which may suggest greater cardiac stress. However, future studies using additional cardiac markers should be completed to confirm these findings. In addition, masters runners showed an increased number of laboratory values outside normal range, indicating the body's reduced capacity to respond to marathon running.

Key Clinical MessageElectrocardiographic changes can be present in marathon runners. These findings may be misinterpreted as malignant by healthcare providers. For example, incomplete right bundle branch block, early ventricular repolarization, and left ventricular hypertrophy by voltage criteria alone are quite common in athletes, yet considered benign.