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Circulating KL-6, a biomarker of lung injury, in obstructive sleep apnoea

¹ Dept of Medicine, Columbia University, New York, NY, USA, and ² Dept of Medicine, Keio University School of Medicine, Tokyo, Japan.

CORRESPONDENCE: D. J. Lederer, Division of Pulmonary, Allergy and Critical Care Medicine, Columbia University College of Physicians and Surgeons, 622 W 168th St, PH-8, Room 101, New York, NY 10032, USA. Fax: 1 2123422101. E-mail: DL427{at}columbia.edu

Keywords: Alveolar wall permeability, biological markers, hypoxia, obstructive sleep apnoea

Received: October 5, 2008
Accepted December 15, 2008

In obstructive sleep apnoea (OSA), oxidative stress contributes to endothelial dysfunction in the peripheral circulation. In the lung, oxidative stress can lead to alveolar injury. The present authors hypothesised that patients with OSA would have biomarker evidence of increased alveolar wall permeability.

Sleep characteristics, brachial artery flow-mediated dilation and plasma KL-6 levels were observed in 11 otherwise healthy patients with OSA and 10 controls.

Median (interquartile range) plasma KL-6 levels were higher in patients with OSA compared with controls: 317 (232–506) U·mL^–1 versus 226 (179–257) U·mL^–1, respectively. Higher plasma KL-6 levels were associated with greater time spent asleep with an oxyhaemoglobin saturation <90%, lower nadir saturation, more frequent desaturation of >4% during sleep and lower brachial artery flow-mediated dilation. Adjustment for nadir saturation or flow-mediated dilation attenuated the association between plasma KL-6 levels and OSA.

Circulating KL-6 levels are elevated in some patients with obstructive sleep apnoea, possibly reflecting increased alveolar wall permeability.