BACKGROUND: Previous studies have suggested an association between obstructive sleep apnea (OSA) and heavy proteinuria. Two recent studies cast doubt on the association between OSA and proteinuria, but neither studied the effect of disordered sleep per se on urinary protein excretion. METHODS: We prospectively studied 75 patients undergoing polysomnography for suspected OSA. We excluded patients with renal insufficiency, diabetes mellitus, and systemic lupus erythematosus and those administered angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Urine protein-creatinine (P/C) ratio was measured on the date of the polysomnography before sleep (awake P/C ratio) and on awakening (asleep P/C ratio). Severity of OSA was stratified by means of the apnea-hypopnea index (AHI). RESULTS: Twenty-six patients (35%) did not have OSA, 25 patients (33%) had mild OSA, 9 patients (12%) had moderate OSA, and 15 patients (20%) had severe OSA. Asleep P/C ratio was less than 0.2 in 96% of patients, and awake P/C ratio was less than 0.2 in 89% of patients. No patient had an asleep P/C ratio greater than 1.0. There was no correlation between log asleep P/C ratio and log AHI ( r = -0.042; P = 0.73) or log awake P/C ratio and log AHI (r = 0.004; P = 0.97). No significant differences could be shown between mean log P/C ratio for either the asleep or awake urine collection across any of the 4 OSA severity strata. CONCLUSION: We found clinically significant proteinuria to be absent in stable outpatients with OSA. Proteinuria in patients with OSA should not be attributed to sleep apnea and warrants further evaluation.
BACKGROUND: Previous studies have suggested an association between obstructive sleep apnea (OSA) and heavy proteinuria. Two recent studies cast doubt on the association between OSA and proteinuria, but neither studied the effect of disordered sleep per se on urinary protein excretion. METHODS: We prospectively studied 75 patients undergoing polysomnography for suspected OSA. We excluded patients with renal insufficiency, diabetes mellitus, and systemic lupus erythematosus and those administered angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Urine protein-creatinine (P/C) ratio was measured on the date of the polysomnography before sleep (awake P/C ratio) and on awakening (asleep P/C ratio). Severity of OSA was stratified by means of the apnea-hypopnea index (AHI). RESULTS: Twenty-six patients (35%) did not have OSA, 25 patients (33%) had mild OSA, 9 patients (12%) had moderate OSA, and 15 patients (20%) had severe OSA. Asleep P/C ratio was less than 0.2 in 96% of patients, and awake P/C ratio was less than 0.2 in 89% of patients. No patient had an asleep P/C ratio greater than 1.0. There was no correlation between log asleep P/C ratio and log AHI ( r = -0.042; P = 0.73) or log awake P/C ratio and log AHI (r = 0.004; P = 0.97). No significant differences could be shown between mean log P/C ratio for either the asleep or awake urine collection across any of the 4 OSA severity strata. CONCLUSION: We found clinically significant proteinuria to be absent in stable outpatients with OSA. Proteinuria in patients with OSA should not be attributed to sleep apnea and warrants further evaluation.
Authors: Muna T Canales; Misti L Paudel; Brent C Taylor; Areef Ishani; Reena Mehra; Michael Steffes; Katie L Stone; Susan Redline; Kristine E Ensrud Journal: Sleep Breath Date: 2010-02-26 Impact factor: 2.816
Authors: Sofia B Ahmed; Paul E Ronksley; Brenda R Hemmelgarn; Willis H Tsai; Braden J Manns; Marcello Tonelli; Scott W Klarenbach; Rick Chin; Fiona M Clement; Patrick J Hanly Journal: PLoS One Date: 2011-04-29 Impact factor: 3.240