Exertional rhabdomyolysis (ER) is a recognized complication in military and athletic populations, often resulting from prolonged, high-intensity physical activity, particularly in hot or humid environments. A recent international European Neuromuscular Centre International Workshop convened with new consensus agreement for the diagnosis of ER. The diagnosis requires 1) muscle weakness swelling or myalgia, 2) serum creatine kinase (CK) exceed 10,000IU/L and 3) CK levels peaking at 1 to 4 days after the event and normalizing to baseline within 1 to 2 weeks. [1] While most cases resolve with supportive care, approximately 10% of patients develop acute kidney injury (AKI), and a subset may require renal replacement therapy (RRT). [2,3] Recent studies have highlighted the increasing incidence of ER-related AKI in endurance athletes, underscoring the need for heightened awareness and early intervention strategies. [4,5] This case details the clinical trajectory of a young, healthy male who developed dialysis-requiring AKI following a strenuous ultra-endurance event. A 20-year-old Navy servicemember presented to the emergency department with complaints of severe lower extremity myalgia and weakness, cola-colored urine, and nausea one day after completing a 50km Spartan Ultra race (Obstacle course endurance race). The servicemember was physically active completing multiple 25km endurance events without sequelae. His medical history was remarkable for a surgically corrected clubfoot during childhood. His baseline renal function two months prior to the race was 0.8mg/dL. He denied any supplement use, recreational drugs, or herbal formulations. His family history was unremarkable for any genetic muscle disorders. He did report taking a single 800mg dose of ibuprofen during the event. His initial laboratory results demonstrated severe rhabdomyolysis with a creatine kinase (CK) level of 80,001U/L, creatinine 2.6mg/dL, myoglobinuria, and moderately elevated transaminases. The patient's McMahon Score on admission was 5, indicating a low risk (<3%) of developing severe AKI or requiring RRT. [6] The patient received 5L of intravenous Normal Saline bolus on admission followed by continuous Lactated Ringer’s solution at 200mL/hr. During the first 48 hours, he remained oliguric (~20mL/hr). Despite declining CK levels (48,774U/L – day 2, 21,852U/L – day 3, 11,039U/L – day 4), his renal function continued to worsen with creatinine peaking at 6.60mg/dL on hospital day 5. Per recommendation from nephrology, he received intravenous furosemide which increased urine output to ≈170mL/hr, however, his renal function continued to deteriorate. A renal ultrasound was completed that showed no evidence of obstruction or renal injury. Due to his worsening AKI and inadequate urine output, a Trialysis short-term dialysis catheter was inserted, and the patient completed 2 consecutive days of hemodialysis with a net ultrafiltration of 1000mL. Post dialysis, his urine output improved and exceeded 4L/day and at discharge, his creatinine had steadily improved to 2.86mg/dL.