Obstructive Sleep Apnea Is Associated With Increased Urinary Albumin Excretion

Naustdal

European Respiratory Journal

et al. 2014

Chronic obstructive pulmonary disease (COPD), low lung function independent of diagnosis and markers of inflammation are all associated with increased morbidity and mortality. Microalbuminuria, reflecting endothelial dysfunction, could be a relevant inflammatory marker of potential systemic effects of COPD. We hypothesised that there was a positive association between microalbuminuria and mortality in individuals with COPD.We conducted a 12-year follow-up study of 3129 participants in the second survey of the Nord-Trøndelag Health Study (HUNT), Norway. At baseline, albuminuria was analysed in three urine samples and spirometry was performed. Among the participants, 136 had COPD and microalbuminuria, defined as a urinary albumin/creatinine ratio between 2.5 and 30.0 mg?mmol -1 . The main outcome measures were hazard ratio of all-cause mortality according to microalbuminuria.Compared to those with COPD without microalbuminuria, the adjusted hazard ratio for all-cause mortality in those with COPD and microalbuminuria was 1.54, 95% CI 1.16-2.04. This result was similar after excluding cardiovascular disease at baseline. Classifying COPD severity by Global Initiative for Chronic Obstructive Lung Disease, there was a positive association trend with increasing severity stages.Microalbuminuria is associated with all-cause mortality in individuals with COPD and could be a relevant tool in identification of patients with poor prognosis. @ERSpublications Microalbuminuria is associated with mortality in individuals with COPD in this 12-year follow-up study

Section: Resultsmentioning

confidence: 99%

COPD and microalbuminuria: a 12-year follow-up study

Naustdal

European Respiratory Journal

et al. 2014

Clinical Medicine & Research

“…Cross-sectional cohort studies have demonstrated a significant direct association between the severity of sleep apnea and the severity of renal dysfunction. [270][271][272][273][274][275][276] In addition, cohort studies of the longitudinal relationship between sleep apnea and kidney function show that apnea is independently associated with an increased risk of accelerated loss of kidney function. 277,278 Conversely, as kidney function declines, the prevalence of sleep apnea and nocturnal hypoxia increases.…”

Section: Repeated Episodes Of Acute Kidney Injurymentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

125

111

In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

“…34,35 Another explanation might be that in OSA, the heart has been preconditioned by factors such as increased sympathetic activity and intermittent hypoxia, and thus myocardial perfusion may be less affected by therapy withdrawal in the short-term. 36 There are some preliminary data from observational and non-randomized studies that OSA is associated with microangiopathy of the kidneys and skin, 37,38 and that microvascular endothelial function may be improved by CPAP therapy. 28 In the current randomized controlled trial, recurrence of OSA was not associated with impaired microvascular functionneither in the renal nor dermal microvascular system despite acute OSA-induced sympathetic nervous system activation, recurrent intermittent hypoxia and increased BP.…”

Section: Discussionmentioning

confidence: 99%

Effect of CPAP Withdrawal on myocardial perfusion in OSA: A randomized controlled trial

et al. 2016

Background and objective: Obstructive sleep apnoea (OSA) is highly prevalent and associated with an increased incidence of cardiovascular events. Endothelial dysfunction is the proposed causative mechanism. Continuous positive airway pressure (CPAP) is presumed to improve cardiovascular outcome in OSA. CPAP withdrawal was recently shown to lead to peripheral endothelial dysfunction. However, it is not known whether short-term CPAP withdrawal reduces myocardial perfusion in OSA. Methods: In this double-blind randomized controlled study, 45 patients with moderate to severe OSA previously adherent to CPAP were assigned to either subtherapeutic or continuing therapeutic CPAP for 2 weeks. The primary outcome was adenosine-induced myocardial blood flow (MBF) as a measure of endothelial function, assessed by