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Elevated Serum Markers of Acute Kidney Injury in Patients With Obstructive Sleep Apnea.
Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine 2019 Februrary 16
STUDY OBJECTIVES: Previous research revealed a positive correlation between endothelial cell injury (indicated by albuminuria) and obstructive sleep apnea (OSA). However, little else has been revealed about acute kidney injury (AKI) in patients with OSA.
METHODS: This prospective study recruited consecutive patients undergoing overnight polysomnography for evaluation of sleep apnea. Patients in whom any major disease or recent infection had been previously diagnosed were excluded. Ultimately, data from 75 patients with apnea-hypopnea indices of 5 or more were analyzed. Baseline values for the urinary albumin-creatinine ratio (UACR), serum levels for three markers of AKI (cystatin C, neutrophil gelatinase-associated lipocalin [NGAL], interleukin-18 [IL-18]), and polysomnography data were recorded and analyzed. Patients then were followed for 6 months of continuous positive airway pressure (CPAP) treatment.
RESULTS: At baseline, UACRs were greater in patients with more severe OSA ( P = .005, r = .329). All three serum markers of AKI (cystatin C, NGAL, and IL-18) studied were positively correlated with OSA severity, and two (cystatin C and IL-18) were positively correlated with the frequency of oxygen desaturation during sleep. However, none of the AKI markers had positive correlations with UACR. After 6 months of CPAP treatment, UACR and IL-18 were decreased significantly in patients with good adherence.
CONCLUSIONS: Albuminuria and levels of three serum markers of AKI (cystatin C, NGAL, IL-18) were positively correlated with OSA severity, and good adherence with CPAP treatment decreased albuminuria and interleukin-18 levels. These results may provide additional tools for assessing early renal injury in patients with OSA.
METHODS: This prospective study recruited consecutive patients undergoing overnight polysomnography for evaluation of sleep apnea. Patients in whom any major disease or recent infection had been previously diagnosed were excluded. Ultimately, data from 75 patients with apnea-hypopnea indices of 5 or more were analyzed. Baseline values for the urinary albumin-creatinine ratio (UACR), serum levels for three markers of AKI (cystatin C, neutrophil gelatinase-associated lipocalin [NGAL], interleukin-18 [IL-18]), and polysomnography data were recorded and analyzed. Patients then were followed for 6 months of continuous positive airway pressure (CPAP) treatment.
RESULTS: At baseline, UACRs were greater in patients with more severe OSA ( P = .005, r = .329). All three serum markers of AKI (cystatin C, NGAL, and IL-18) studied were positively correlated with OSA severity, and two (cystatin C and IL-18) were positively correlated with the frequency of oxygen desaturation during sleep. However, none of the AKI markers had positive correlations with UACR. After 6 months of CPAP treatment, UACR and IL-18 were decreased significantly in patients with good adherence.
CONCLUSIONS: Albuminuria and levels of three serum markers of AKI (cystatin C, NGAL, IL-18) were positively correlated with OSA severity, and good adherence with CPAP treatment decreased albuminuria and interleukin-18 levels. These results may provide additional tools for assessing early renal injury in patients with OSA.
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