Why the study?
Soccer is a high-intensity intermittent contact sport with underrecognized effects on kidney function.
Soccer induces transient, reversible functional kidney changes that are largely adaptive, and novel biomarkers like NGAL and KIM-1 may be more useful than serum creatinine for monitoring athletes.
Clinicians should consider exercise history to avoid misinterpreting post-soccer labs; leaves open need for prospective data on cumulative effects.
Soccer (football) is a high-intensity intermittent contact sport with underrecognized effects on kidney function. Evidence suggests it causes transient, reversible renal changes, including increased serum creatinine (SCr), reduced estimated glomerular filtration rate (eGFR), exercise-induced proteinuria, and microscopic hematuria. Soccer-related kidney abnormalities are largely functional, adaptive, and reversible, with severe kidney injury being rare. They primarily reflect hemodynamic and metabolic stress rather than intrinsic kidney damage. Although serum creatinine is the most widely used marker of kidney function, its interpretation in athletes is limited by muscle mass and exercise-induced muscle injury. Novel biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cystatin C offer greater sensitivity for detecting tubular injury and acute changes in GFR. In soccer players, transient elevations in NGAL and KIM-1 have been observed following matches, particularly under conditions leading to dehydration. Traumatic kidney injuries are rare and usually mild. Seasonal training induces adaptive renal changes in protein and urea handling. Hydration, monitoring, and individualized risk assessment support safe participation, even in athletes with pre-existing kidney vulnerability. This review summarizes the renal effects of soccer, focusing on physiological adaptations, biomarker interpretation, and kidney injury prevention.
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Jhaveri et al. (2026) studied this question.
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