A 22-year-old male developed severe rhabdomyolysis and acute kidney injury (AKI) after chronic nitrous oxide abuse, requiring hemodialysis. His creatine kinase (CK) level reached 45,000 U/L, far exceeding the 5,000 U/L threshold linked to AKI risk.
A case reported in Cureus on October 24, 2026, reveals risks of nitrous oxide misuse. The patient presented with muscle edema, dark urine, and elevated CK, with AKI progressing to require hemodialysis on day 11. His serum creatinine peaked at 14.10 mg/dL, far above the normal range of 0.7–1.3 mg/dL.
How N₂O Causes Muscle Damage
Nitrous oxide (N₂O) abuse, increasingly common for its euphoric effects, can cause muscle toxicity and rhabdomyolysis. The case study notes that while hypoxia and direct myotoxic effects are suspected, immobility likely played a key role in this patient’s muscle injury. The asymmetric edema distribution—thenar, gluteal, and paraspinal regions—supported this hypothesis. Prolonged immobilization during intoxication can cause muscle compression and ischemic injury, a recognized cause of rhabdomyolysis [[10,11]](javascript:void(0)).
Studies on nitrous oxide abuse describe its pharmacological effects, including heme binding, which depletes nitrous oxide and induces vasoconstrictors like endothelin-1. This mechanism may exacerbate muscle ischemia. The case aligns with findings emphasizing the role of systemic complications like AKI.
The NIH-published StatPearls defines rhabdomyolysis as skeletal muscle breakdown releasing myoglobin and creatine kinase (CK) into the bloodstream, with AKI occurring in 10–40% of severe cases. Elevated CK levels above 5,000 U/L correlate with heightened AKI risk, a threshold the patient exceeded by over nine times.
Tracking Patient Recovery and Treatment
The patient’s CK levels declined from 45,000 U/L at admission to 291 U/L before discharge, indicating improved muscle injury. However, AKI worsened, necessitating hemodialysis. Post-discharge, his creatinine stabilized at 1.80 mg/dL, suggesting partial renal recovery.
Cross-sectional imaging in the case revealed profound asymmetric edema of the left gluteal and proximal thigh muscles, with diffuse hypodensity and obliterated intermuscular fat planes. This aligns with findings noting similar patterns of muscle injury.
The patient’s serum creatinine timeline, as depicted in Figure 5 of the Cureus study, showed a rise from 1.83 mg/dL at admission to 14.10 mg/dL by day 11, prompting hemodialysis. At discharge, creatinine was 1.89 mg/dL, declining to 1.80 mg/dL at one-week follow-up. This trajectory highlights the severity of N₂O-induced AKI and the necessity of timely intervention.
Rhabdomyolysis’s Broader Health Impact
Rhabdomyolysis remains a critical condition with significant morbidity. The NIH highlights that 15% of acute renal failure cases stem from rhabdomyolysis, emphasizing early intervention. For nitrous oxide abuse, the case provides a rare but vital example of its potential to cause life-threatening complications, urging clinicians to consider it in differential diagnoses.
Readers should note that while this case links N₂O abuse to rhabdomyolysis and AKI, broader population data remain limited. The study by Shah et al. (Cureus, 2026) is a single-case report, and larger cohorts are needed to confirm these findings.