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Hyperuricemia and non-dipping blood pressure
Full text linkOreste Marrone,1 Maria Rosaria Bonsignore1,21National Research Council, Institute of Biomedicine and Molecular Immunology, Palermo, Italy; 2Biomedical Department of Internal and Specialistic Medicine, University of Palermo, Palermo, ItalyThe strong association between the metabolic derangements that characterize the metabolic syndrome with arterial hypertension is very well-known, as it is the common finding of hyperuricemia in the patients with the metabolic syndrome. Besides, hyperuricemia has been found to be associated with cardiovascular, renal, and metabolic diseases; including not only gout but also type 2 diabetes mellitus, although its role as a risk factor is still debated.1 We were not aware of previous studies describing an association between uric acid levels and the non-dipping 24-hour blood pressure (BP) pattern, and for that reason we were intrigued by Tutal et al’s article, regarding hypertensive patients with the metabolic syndrome.2 The authors explain some possible causes that could determine an increase in uric acid in the metabolic syndrome, and describe some pathogenetic mechanisms of systemic hypertension in their patients. We would like to point out one more possible mechanism that could link hyperuricemia to non-dipping BP.View original paper by Tutal et a
Decrease in blood pressure during continuous positive airway pressure treatment for obstructive sleep apnoea: still searching for predictive factors
Full text linkSleep Apnea and the Kidney
Full text linkPurpose of Review: There are some uncertainties about the interactions between obstructive sleep apnea (OSA) and chronic kidney disease (CKD). We critically reviewed recent studies on this topic with a focus on experimental and clinical evidence of bidirectional influences between OSA and CKD, as well as the effects of treatment of either disease. Recent Findings: Experimental intermittent hypoxia endangers the kidneys, possibly through activation of inflammatory pathways and increased blood pressure. In humans, severe OSA can independently decrease kidney function. Treatment of OSA by CPAP tends to blunt kidney function decline over time, although its effect may vary. OSA may increase cardiovascular complications and mortality in patients with end-stage renal disease (ESRD), while it seems of little harm after renal transplantation. Excessive fluid removal may explain some of the improvements in OSA severity in ESRD and after transplantation. Summary: Severe OSA and CKD do interact negatively, mainly through hypoxia and fluid retention. The moderate mutually interactive benefits that treatment of each disease exerts on the other one warrant further studies to improve patient management
The puzzle of metabolic effects of obstructive sleep apnoea in children
Full text linkIn obese children with obstructive sleep apnoea insulin resistance is common while lipids do not
show a clear patter
Sleep Apnea, Sleepiness, and Driving Risk
Full text linkObstructive sleep apnea is associated with excessive daytime sleepiness in about 50% of cases, and with increased risk of driving accidents. Treatment with continuous positive airway pressure effectively decreases such risk, but compliance with continuous positive airway pressure treatment is often suboptimal. According to the European Union Directive on driving risk, retention of a driving license in patients with obstructive sleep apnea requires assessment of sleepiness and adherence to continuous positive airway pressure treatment, but there remains uncertainty on the optimal methods to assess sleepiness on a large scale
Renal Function In European Patients Studied For Suspected Sleep Apnea. The European Sleep Apnea Database (ESADA)
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Relationship between mild to moderate renal dysfunction and obstructive sleep apnea: Data from the European sleep apnea database
Full text linkThe relationship between severity of obstructive sleep apnea (OSA) and kidney function was investigated in the European Sleep Apnea Database (ESADA), where clinical, sleep, and biochemical data of patients studied for suspected OSA in 24 sleep centres of 17 European countries are stored. After excluding patients with missing data or extremely high/low creatinine values, data from 8112 subjects (2328 female) with creatinine values ranging between 0.5 and 2.0 mg% were analyzed. Estimated glomerular filtration rate (eGFR) was obtained with the Modified Diet in Renal Disease (MDRD) equation. Patients were subdivided into two groups: group 1 (n = 3709) studied by full polysomnography; group 2 (n = 4403) studied by nocturnal cardiorespiratory monitoring. Altogether, 8.5% subjects had an eGFR<60 ml/min/1.73m2. At univariate analysis, eGFR correlated to age, comorbidities and severity of OSA in both groups. At logistic regression analysis, risk factors for eGFR<60 were in group 1: diabetes, female gender, age, body mass index, and lowest nocturnal SaO2 (r2=0.086); in group 2: hypertension, female gender, age, and lowest nocturnal SaO2 (r2=0.087). In conclusion, as expected, comorbidities, female gender and advanced age are significant risk factors for low eGFR in subjects with OSA. While traditional severity measures of OSA (apnea/hypopnea index, oxygen desaturation index) did not contribute to low eGFR, more severe nocturnal hypoxia captured by lowest nocturnal SaO2 appeared as a significant predictor in this large patient cohort. The ESADA study is supported by ResMed and Philips Respironics
Conseguenze metaboliche dell'ipossia
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La sopravvivenza in condizioni di ipossia dipende dall’attivazione di processi cellulari complessi, con risposte
di adattamento (quali il potenziamento del trasporto di O2 attraverso l’aumento dell’eritropoiesi, l’attivazione
dell’angiogenesi e l’aumento della glicolisi anaerobica) e l’inibizione di processi metabolici che richiedono
alta disponibilità di O2. Ciò consente di mantenere l’omeostasi energetica anche in condizioni di ridotta disponibilità
di O2. Nel modello fisiologico del soggiorno ad alta quota si verificano riduzione di peso e della capacità
di lavoro associata a riduzione della massa muscolare, che però sono reversibili al ripristino di condizioni
di normossia. Le alterazioni causate dall’ipossia dipendono in parte dalla modalità di esposizione, dalla sua
durata e dalla sua intensità. Le popolazioni ben adattate all’altitudine mostrano aumento dell’efficienza dei
processi metabolici in condizioni ipossiche rispetto ai soggetti che vivono al livello del mare. Gli adattamenti
all’ipossia, invece, sono alterati o insufficienti in condizioni patologiche. Nei pazienti con broncopneumopatia
cronica ostruttiva (BPCO), si verifica una perdita di tessuto muscolare che è largamente irreversibile,
possibilmente per gli effetti dell’attivazione infiammatoria caratteristica della malattia. Nella apnea ostruttiva
nel sonno (OSA), l’ipossia è intermittente e limitata alle ore notturne. L’OSA è caratterizzata da alterazioni
del metabolismo energetico in parte secondarie all’obesità, e da una prevalente attivazione infiammatoria
rispetto alla classica risposta di adattamento all’ipossia. Alcuni dati sulla risposta all’esercizio suggeriscono
alterazioni metaboliche muscolari anche nei pazienti OSA, ma la loro interpretazione è complicata dalla
usuale coesistenza di obesità, associata ad insulino-resistenza anche nel muscolo scheletrico. Una migliore
comprensione degli adattamenti all’ipossia potrà essere utile per meglio comprendere la fisiopatologia delle
malattie respiratorie, e potrà suggerire nuovi approcci terapeutici, come sta già avvenendo nel caso della
patologia tumorale.
Summary
Survival under hypoxic conditions depends on the activation of complex cellular processes, with development
of some adaptive responses (such as increased oxygen transport obtained by increasing erythropoiesis,
activation of angiogenesis and increased glycolysis) and inhibition of the metabolic processes that
require high availability of oxygen. Such adaptations allow maintenance of energy homeostasis despite
decreased oxygen availability. In the physiological model of sojourn at high altitude, decreased body weight
is associated with a lower exercise capacity and loss of skeletal muscle mass, but these changes are
reversible on return to sea level. Hypoxia-induced alterations vary according to the features of hypoxic
exposure, depending in part on its duration and intensity. Some populations well adapted to altitude show
increased metabolic efficiency under hypoxic conditions compared to subjects living at sea level. Adaptation
to hypoxia is altered or insufficient under pathological conditions. In patients with chronic obstructive
pulmonary disease (COPD), loss of muscle mass occurs but is largely irreversible, possibly because of the
effects of the inflammatory activation typical of the disease. In obstructive sleep apnea (OSA), intermittent
hypoxia occurs during the night. OSA is characterized by altered energy metabolism, in part due to the
associated obesity, and by a predominant inflammatory activation over the classic adaptive response to
hypoxia. Some data suggest that the metabolic response of skeletal muscle may be altered in OSA patients
during exercise, but the frequent occurrence of obesity associated with insulin resistance in skeletal muscle
complicates the interpretation of these results. Further understanding of the adaptations to hypoxia will
be useful to better understand the pathophysiology of respiratory diseases, and may suggest new treatment
approaches, as it is already occurring for cancer
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