Overnight urinary uric acid: Creatinine ratio for detection of sleep hypoxemia: Validation study in chronic obstructive pulmonary disease and obstructive sleep apnea before and after treatment with nasal continuous positive airway pressure

A. Braghiroli, C. Sacco, M. Erbetta, V. Ruga, C. F. Donner

Research output: Contribution to journalArticle

Abstract

During hypoxia ATP degradation to uric acid is increased in animal models and humans. To assess the reliability of an overnight increase in uric acid excretion as a marker of nocturnal hypoxemia, we selected 10 normal volunteers (7 males and 3 females), 29 COPD patients (26 males and 3 females), and 49 subjects with obstructive sleep apnea (OSA) (43 males and 6 females). The patients underwent standard polysomnography, which was repeated in 14 subjects with nasal continuous positive airway pressure (CPAP), and were subdivided into two groups: Group D included desaturating subjects who spent at least 1 h at Sa(O2) <90% and 15 min below 85%, and Group ND were nondesaturating subjects. The overnight change in the uric acid:creatinine ratio (ΔUA:Cr) was negative in normal subjects (-27.5 ± 9.1 [mean ± SD]) and ND groups: -19.7 ± 14.3 in COPD, -16.1 ± 13.0 in OSA. In both COPD and OSA Group D, the ratio was usually positive: ΔUA:Cr was 17.9 ± 31.4 in Group D COPD (p <0.001 versus ND) and 10.1 ± 30.7 in Group D OSA (p <0.001 versus ND and versus normal subjects) despite 4 of 15 false negative results in COPD and 8 of 20 in OSA. CPAP effective treatment induced a marked reduction ((p = 0.0024) in ΔUA:Cr, leading to a negative value. We conclude that ΔUA:Cr seems to be a promising index of significant nocturnal tissue hypoxia, with good specificity but poor sensitivity (about 30% false negative), which might be useful for the long-term follow-up of outpatients on nasal CPAP with a positive ratio at baseline.

Original languageEnglish
Pages (from-to)173-178
Number of pages6
JournalAmerican Review of Respiratory Disease
Volume148
Issue number1
Publication statusPublished - 1993

Fingerprint

Continuous Positive Airway Pressure
Validation Studies
Obstructive Sleep Apnea
Uric Acid
Chronic Obstructive Pulmonary Disease
Creatinine
Sleep
Therapeutics
Polysomnography
Hypoxia
Healthy Volunteers
Outpatients
Animal Models
Adenosine Triphosphate
Sensitivity and Specificity

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

@article{f00b322b586e44c88785368587b78fc9,
title = "Overnight urinary uric acid: Creatinine ratio for detection of sleep hypoxemia: Validation study in chronic obstructive pulmonary disease and obstructive sleep apnea before and after treatment with nasal continuous positive airway pressure",
abstract = "During hypoxia ATP degradation to uric acid is increased in animal models and humans. To assess the reliability of an overnight increase in uric acid excretion as a marker of nocturnal hypoxemia, we selected 10 normal volunteers (7 males and 3 females), 29 COPD patients (26 males and 3 females), and 49 subjects with obstructive sleep apnea (OSA) (43 males and 6 females). The patients underwent standard polysomnography, which was repeated in 14 subjects with nasal continuous positive airway pressure (CPAP), and were subdivided into two groups: Group D included desaturating subjects who spent at least 1 h at Sa(O2) <90{\%} and 15 min below 85{\%}, and Group ND were nondesaturating subjects. The overnight change in the uric acid:creatinine ratio (ΔUA:Cr) was negative in normal subjects (-27.5 ± 9.1 [mean ± SD]) and ND groups: -19.7 ± 14.3 in COPD, -16.1 ± 13.0 in OSA. In both COPD and OSA Group D, the ratio was usually positive: ΔUA:Cr was 17.9 ± 31.4 in Group D COPD (p <0.001 versus ND) and 10.1 ± 30.7 in Group D OSA (p <0.001 versus ND and versus normal subjects) despite 4 of 15 false negative results in COPD and 8 of 20 in OSA. CPAP effective treatment induced a marked reduction ((p = 0.0024) in ΔUA:Cr, leading to a negative value. We conclude that ΔUA:Cr seems to be a promising index of significant nocturnal tissue hypoxia, with good specificity but poor sensitivity (about 30{\%} false negative), which might be useful for the long-term follow-up of outpatients on nasal CPAP with a positive ratio at baseline.",
author = "A. Braghiroli and C. Sacco and M. Erbetta and V. Ruga and Donner, {C. F.}",
year = "1993",
language = "English",
volume = "148",
pages = "173--178",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society - AJRCCM",
number = "1",

}

TY - JOUR

T1 - Overnight urinary uric acid

T2 - Creatinine ratio for detection of sleep hypoxemia: Validation study in chronic obstructive pulmonary disease and obstructive sleep apnea before and after treatment with nasal continuous positive airway pressure

AU - Braghiroli, A.

AU - Sacco, C.

AU - Erbetta, M.

AU - Ruga, V.

AU - Donner, C. F.

PY - 1993

Y1 - 1993

N2 - During hypoxia ATP degradation to uric acid is increased in animal models and humans. To assess the reliability of an overnight increase in uric acid excretion as a marker of nocturnal hypoxemia, we selected 10 normal volunteers (7 males and 3 females), 29 COPD patients (26 males and 3 females), and 49 subjects with obstructive sleep apnea (OSA) (43 males and 6 females). The patients underwent standard polysomnography, which was repeated in 14 subjects with nasal continuous positive airway pressure (CPAP), and were subdivided into two groups: Group D included desaturating subjects who spent at least 1 h at Sa(O2) <90% and 15 min below 85%, and Group ND were nondesaturating subjects. The overnight change in the uric acid:creatinine ratio (ΔUA:Cr) was negative in normal subjects (-27.5 ± 9.1 [mean ± SD]) and ND groups: -19.7 ± 14.3 in COPD, -16.1 ± 13.0 in OSA. In both COPD and OSA Group D, the ratio was usually positive: ΔUA:Cr was 17.9 ± 31.4 in Group D COPD (p <0.001 versus ND) and 10.1 ± 30.7 in Group D OSA (p <0.001 versus ND and versus normal subjects) despite 4 of 15 false negative results in COPD and 8 of 20 in OSA. CPAP effective treatment induced a marked reduction ((p = 0.0024) in ΔUA:Cr, leading to a negative value. We conclude that ΔUA:Cr seems to be a promising index of significant nocturnal tissue hypoxia, with good specificity but poor sensitivity (about 30% false negative), which might be useful for the long-term follow-up of outpatients on nasal CPAP with a positive ratio at baseline.

AB - During hypoxia ATP degradation to uric acid is increased in animal models and humans. To assess the reliability of an overnight increase in uric acid excretion as a marker of nocturnal hypoxemia, we selected 10 normal volunteers (7 males and 3 females), 29 COPD patients (26 males and 3 females), and 49 subjects with obstructive sleep apnea (OSA) (43 males and 6 females). The patients underwent standard polysomnography, which was repeated in 14 subjects with nasal continuous positive airway pressure (CPAP), and were subdivided into two groups: Group D included desaturating subjects who spent at least 1 h at Sa(O2) <90% and 15 min below 85%, and Group ND were nondesaturating subjects. The overnight change in the uric acid:creatinine ratio (ΔUA:Cr) was negative in normal subjects (-27.5 ± 9.1 [mean ± SD]) and ND groups: -19.7 ± 14.3 in COPD, -16.1 ± 13.0 in OSA. In both COPD and OSA Group D, the ratio was usually positive: ΔUA:Cr was 17.9 ± 31.4 in Group D COPD (p <0.001 versus ND) and 10.1 ± 30.7 in Group D OSA (p <0.001 versus ND and versus normal subjects) despite 4 of 15 false negative results in COPD and 8 of 20 in OSA. CPAP effective treatment induced a marked reduction ((p = 0.0024) in ΔUA:Cr, leading to a negative value. We conclude that ΔUA:Cr seems to be a promising index of significant nocturnal tissue hypoxia, with good specificity but poor sensitivity (about 30% false negative), which might be useful for the long-term follow-up of outpatients on nasal CPAP with a positive ratio at baseline.

UR - http://www.scopus.com/inward/record.url?scp=0027322801&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027322801&partnerID=8YFLogxK

M3 - Article

C2 - 8317794

AN - SCOPUS:0027322801

VL - 148

SP - 173

EP - 178

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 1

ER -