Urinary uric acid excretion as an indicator of severe hypoxia and mortality in patients with obstructive sleep apnea and chronic obstructive pulmonary disease

Abstract

Objective: Uric acid (UA) is the end product of adenosine triphosphate degradation, and could increase due to hypoxia. We investigated the association of UA metabolites with nocturnal hypoxemia, apnea-hypopnea index (AHI), noninvasive mechanical ventilation (NIMV) usage and five-year mortality. Materials/subjects and methods: We obtained urinary specimen before and after the night polysomnography in order to measure UA excretion and overnight change in urinary UA/creatinine ratio (ΔUA/Cr) in 75 subjects (14 controls, 15 chronic obstructive pulmonary disease (COPD) without nocturnal hypoxemia (NH), 15 COPD with NH, 16 obstructive sleep apnea syndrome (OSAS) without NH, 15 OSAS with NH). Percentage of time spent below SaO2 of 90% (T90%) for >10% of sleep time was considered as nocturnal hypoxemia. Patients were contacted after 5 years with a questionnaire including information on the use of NIMV treatment (n: 58) and urinary specimen analysis (n: 35). Results: T90% was found to be significantly correlated with UA excretion (coefficient: 0.005, 95%CI: 0.003–0.007) and ΔUA/Cr (coefficient: 0.8, 95%CI: 0.3–1.2) after adjustments for age, gender, body mass index and apnea-hypopnea index. Median and IQR (interquartile range) of baseline UA excretion were 0.79 (0.51–0.89) and 0.41 (0.31–0.55) in 10 deceased and 58 surviving patients, respectively (p = 0.001). UA excretion median and IQR of baseline and 5 years of NIMV treatment were 0.41 (0.36–0.57) and 0.29 (0.23–0.37), respectively (p = 0.01). Conclusion: UA excretion, as a marker of tissue hypoxia, may be useful in the management of OSA and COPD patients. Keywords: Uric acid, Hypoxia, Obstructive sleep apnea, COPD