Finishing a marathon well hydrated does not spare the kidneys or the gut

The advice given to recreational marathon runners about organ stress has for years been organised around fluid. Drink enough, the reasoning goes, and the kidney injury markers that show up in post-race bloodwork stay down. A study of the 2024 Boston Marathon published this month suggests that framing is at best incomplete [s1].

Researchers sampled blood and urine from 72 runners before and after the race — 34 males and 38 females, mean age 50 ± 11 years, with a mean finish time of 3:45 ± 0:32 [s1]. Race-day conditions were mild by marathon standards: an average temperature of 19 ± 3°C and relative humidity of 47 ± 15% [s1]. This was not a heat event.

What was measured

The panel was deliberately broad. It covered markers of hydration; intestinal injury, using intestinal fatty acid binding protein and soluble CD14; skeletal muscle damage, using creatine kinase; and acute kidney injury, using tissue inhibitor of metalloproteinase 2, insulin-like growth factor binding protein 7, neutrophil gelatinase-associated lipocalin, kidney injury molecule-1 and creatinine [s1].

That list matters, because it separates the study from the many marathon papers that measure creatinine alone. Creatinine is a late and indirect signal. The tubular stress and damage markers in this panel move earlier and are more specific to what is happening inside the kidney.

The result

Every marker of organ stress or injury rose from pre-race to post-race, with fold changes spanning 1.3 to 1455 and P ≤ 0.007 across all indices [s1]. That range is wide because the markers are not comparable to one another — a small shift in creatinine and a thousandfold shift in a tubular stress product are both statistically real and mean different things biologically.

The finding the authors highlight is what did not differ. There were no differences in any index based on biological sex or on hydration status, with P ≥ 0.099 throughout [s1]. Only 25% to 34% of runners were classified as hypohydrated after the race [s1] — meaning the majority finished in reasonable fluid balance, and their kidney and gut markers rose anyway.

The authors' own conclusion is that maintaining hydration during a marathon cannot fully offset the risk of organ injury [s1].

How this sits against the wider literature

A systematic review and meta-analysis published on 1 October pooled marathon studies reporting kidney injury biomarkers before, immediately after, and 24 hours post-race [s2]. It found significant increases in most biomarkers immediately after the marathon compared with baseline, with the largest increases in the TIMP-2 × IGFBP-7 product, copeptin, urinary L-FABP, urinary MCP-1, IGFBP-7, urinary YKL-40 and TIMP-2 [s2].

The overlap with the Boston panel is close, and the direction is the same. But the meta-analysis adds something the single-race study cannot: what happens next. It describes several distinct recovery patterns — some biomarkers rose and had still not fallen at 24 hours; some rose and then declined at 24 hours while remaining above baseline; and some rose and then dropped below baseline by 24 hours [s2].

That heterogeneity is the honest summary of the field. Marathon running reliably produces a biochemical signature of kidney stress. What that signature means over days, and whether it means anything over years, is not settled by either paper.

What these studies do not establish

Neither study measured clinical outcomes. A rise in a kidney injury biomarker is not a diagnosis of acute kidney injury, and acute kidney injury by biomarker criteria is not the same as kidney failure. The Boston study is explicit that its purpose was to characterise the physiological response, not to identify harm [s1].

Sample sizes are small. Seventy-two runners at one race, on one mild day, cannot describe what happens at a hot marathon, at elite paces, or in runners much younger or older than a mean of 50 [s1]. The meta-analysis pools across studies that differ in race, population and assay, and its own risk-of-bias assessment used a pre-post tool designed for uncontrolled designs [s2].

There is also a design limitation worth naming plainly: without a non-running control group sampled on the same day, some of the pre-to-post change reflects the ordinary effects of several hours of exertion, travel and fasting rather than anything marathon-specific.

Why the hydration result is the interesting part

The practical culture around marathon fluid intake has swung twice — first toward drinking aggressively, then back after exercise-associated hyponatraemia was recognised as a serious risk of overdrinking. What the Boston data add is that the kidney and intestinal barrier signals do not appear to be primarily a fluid problem at all [s1].

That is mechanistically plausible. Splanchnic blood flow is redistributed away from the gut during prolonged exercise regardless of hydration state, and the resulting intestinal barrier stress is one candidate driver of the systemic inflammatory response that marathons produce. Renal tubular stress markers may be responding to that cascade, to sustained catecholamine and vasopressin signalling, or to muscle breakdown products, rather than to plasma volume alone.

If that is right, then interventions aimed at the gut — pacing, heat acclimation, carbohydrate and osmolality choices during the race — become as relevant as the fluid plan. The authors frame their findings as something to consider when designing interventions to minimise gastrointestinal and renal complications in recreational but competitive marathon runners [s1].

What to watch

The useful next study is a longitudinal one: the same runners, sampled across multiple race seasons, with clinical endpoints rather than biomarker endpoints. Until that exists, the biomarker literature can establish that a marathon stresses the kidney and the gut, and that the stress is not abolished by drinking well. It cannot yet say whether that stress accumulates.

Sources

• [s1] Biomarkers of organ stress and injury following the Boston Marathon — Journal of Applied Physiology, published online 16 October 2025. https://doi.org/10.1152/japplphysiol.00775.2025
• [s2] Acute Kidney Injury Biomarkers in Marathon Runners: Systematic Review and Meta-Analysis — Medicina (Kaunas), 1 October 2025. https://doi.org/10.3390/medicina61101775