Acute kidney stress (AKS) is a clinically significant yet underrecognized complication among endurance athletes. This review synthesizes current evidence regarding the epidemiology, pathophysiology, risk factors, clinical features, diagnostic strategies, management, and preventive approaches for AKS during endurance exercise. Focusing on mechanism-based understanding and guideline-driven recommendations, the article offers practical implications for clinicians overseeing athlete care.
Endurance exercise, encompassing marathons, triathlons, and ultra-distance events, is associated with transient alterations in renal function. While the majority of athletes recover without sequelae, a subset experiences AKS, which may predispose to acute kidney injury (AKI) and, rarely, chronic kidney disease (CKD). Understanding the intricate mechanisms and clinical trajectory of AKS is essential for healthcare professionals managing athletes, facilitating the development of targeted prevention and management strategies.
AKS during endurance sports is reported in 10-40% of marathon and ultramarathon participants, with variations based on event duration, environmental conditions, and individual susceptibility. Although most cases are subclinical, a minority progress to overt AKI requiring medical intervention. Population-based studies suggest a growing incidence parallel to the rising popularity of endurance sports, emphasizing the need for heightened clinician awareness and structured surveillance.
The pathogenesis of AKS in endurance athletes is multifactorial. Key mechanisms include renal hypoperfusion due to splanchnic vasoconstriction, dehydration-induced plasma volume contraction, heat stress, and elevated sympathetic drive. Exercise-induced muscle breakdown (rhabdomyolysis) contributes myoglobinuria, further exacerbating tubular injury. Oxidative stress and inflammatory cytokine release potentiate renal endothelial dysfunction. Recent research highlights the role of subclinical acute tubular necrosis and the interplay between renal perfusion, filtration pressure, and systemic inflammatory milieu during prolonged exercise.
Predisposing factors for AKS during endurance exercise include intense or prolonged activity, inadequate hydration, high ambient temperatures, use of nonsteroidal anti-inflammatory drugs (NSAIDs), pre-existing renal impairment, and genetic susceptibility to rhabdomyolysis. Male sex, older age, and lower baseline fitness further increase risk. Athletes with comorbidities such as hypertension or diabetes require special consideration due to heightened vulnerability.
AKS is often asymptomatic, detected via biochemical markers such as transient rises in serum creatinine and blood urea nitrogen. In more severe cases, symptoms may include oliguria, myalgia, nausea, and dark urine suggestive of rhabdomyolysis. Physical findings are generally nonspecific. It is critical to distinguish physiological, reversible AKS from evolving AKI that may require intervention, particularly in athletes presenting with persistent renal dysfunction or systemic symptoms.
Diagnosis is based on clinical context and laboratory evidence of renal stress, typically a rise in serum creatinine by ≥0.3 mg/dL within 48 hours or a 1.5-fold increase from baseline. Urinalysis may reveal proteinuria, hematuria, or myoglobinuria. Biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) are under investigation for early detection. Imaging is reserved for cases with suspected obstructive or intrinsic renal pathology. Differentiation from other causes of AKI, such as sepsis or volume depletion, is paramount.
Management of AKS during endurance exercise centers on prompt recognition, volume resuscitation with isotonic fluids, and avoidance of nephrotoxins. Athletes should be withdrawn from activity at the first sign of significant renal impairment. Correction of electrolyte derangements, monitoring for complications (e.g., hyperkalemia), and supportive care are essential. Severe cases may necessitate hospitalization and, rarely, renal replacement therapy. Post-event follow-up is recommended to ensure resolution and to guide return-to-activity decisions.
Recent advances focus on early detection of subclinical injury using sensitive biomarkers, non-invasive monitoring of renal perfusion, and individualized hydration strategies based on sweat rate and body composition. Novel approaches include the use of wearable biosensors for real-time assessment of renal stress and algorithms integrating environmental and physiological data for risk prediction. Research into pharmacological agents such as antioxidants and anti-inflammatory compounds is ongoing, though clinical application remains investigational.
Consensus statements from sports medicine and nephrology societies advocate for individualized hydration protocols, avoidance of NSAIDs during competition, routine screening for renal dysfunction in high-risk athletes, and education regarding early symptoms of AKI. Pre-participation assessment should identify comorbidities and modifiable risk factors. Guidelines emphasize the importance of gradual training progression, acclimatization to heat, and prompt management of exertional rhabdomyolysis.
AKS represents a clinically important, largely preventable complication of endurance exercise. Clinicians should maintain a high index of suspicion, especially in high-risk athletes, and implement evidence-based prevention and management strategies. Ongoing research into biomarkers and emerging therapies promises to refine risk stratification and enhance athlete safety. A multidisciplinary approach, incorporating education, surveillance, and individualized care, is essential to mitigate acute kidney stress and optimize outcomes in the growing population of endurance athletes.
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