IntroductionObstructive sleep apnea (OSA) is common in edematous states, notably in hemodialysis patients. In this population, overnight fluid shift can play an important role on the pathogenesis of OSA. The effect of compression stockings (CS) and continuous positive airway pressure (CPAP) on fluid shift is barely known. We compared the effects of CS and CPAP on fluid dynamics in a sample of patients with OSA in hemodialysis, through a randomized crossover study.MethodsEach participant performed polysomnography (PSG) at baseline, during CPAP titration, and after 1 week of wearing CS. Neck circumference (NC) and segmental bioelectrical impedance were done before and after PSG.ResultsFourteen patients were studied (53 ± 9 years; 57% men; body mass index 29.7 ± 6.8 kg/m2). Apnea–hypopnea index (AHI) decreased from 20.8 (14.2; 39.6) at baseline to 7.9 (2.8; 25.4) during CPAP titration and to 16.7 (3.5; 28.9) events/h after wearing CS (CPAP vs. baseline, p = 0.004; CS vs. baseline, p = 0.017; and CPAP vs. CS, p = 0.017). Nocturnal intracellular trunk water was higher after wearing CS in comparison to baseline and CPAP (p = 0.03). CS reduced the fluid accumulated in lower limbs during the day, although not significantly. Overnight fluid shift at baseline, CPAP, and CS was −183 ± 72, −343 ± 220, and −290 ± 213 ml, respectively (p = 0.006). Overnight NC increased at baseline (0.7 ± 0.4 cm), decreased after CPAP (−1.0 ± 0.4 cm), and while wearing CS (−0.4 ± 0.8 cm) (CPAP vs. baseline, p < 0.0001; CS vs. baseline, p = 0.001; CPAP vs. CS, p = 0.01).ConclusionCS reduced AHI by avoiding fluid retention in the legs, favoring accumulation of water in the intracellular component of the trunk, thus avoiding fluid shift to reach the neck. CPAP improved OSA by exerting local pressure on upper airway, with no impact on fluid redistribution. CPAP performed significantly better than CS for both reduction of AHI and overnight reduction of NC. Complementary studies are needed to elucidate the mechanisms by which CPAP and CS reduce NC.

BackgroundRestless leg syndrome (RLS) is a sleep disorder with high prevalence among patients on hemodialysis. It has been postulated that high phosphate and high parathyroid hormone may be implicated in its pathogenesis. Standard international criteria and face-to-face interview are not always applied.Methodsthis was an interventional prospective study in which 19 patients (6 men, aged 48±11 years) with severe hyperparathyroidism were evaluated. RLS diagnosis and rating scale were accessed based on the International RLS Study Group pre- and post-parathyroidectomy. Patients also underwent standard polysomnography.ResultsAt baseline, RLS was present in 10 patients (52.6%), and pain was the most reported symptom associated with the diagnosis. Patients with RLS had higher serum phosphate (p = 0.008) that remained independently associated with RLS in a logistic regression model, adjusted for hemoglobin, age and gender (HR = 7.28;CI = 1.14–46.3, p = 0.035). After parathyroidectomy, there was a reduction of serum parathyroid hormone, phosphate, calcium and alkaline phosphatase, and an increase of 25(OH)-vitamin D, and Fetuin-A. Parathyroidectomy alleviated RLS (from 52% to 21%; p = 0.04), which was accompanied by a decrease in severity scale, in association with relief of pain and pruritus. Polysomnography in these patients showed an improvement of sleep parameters as measured by sleep efficiency, sleep latency and percentage of REM sleep.ConclusionRLS is associated with high levels of phosphate in patients with severe secondary hyperparathyroidism on hemodialysis. Pain is most reported complain in these patients. Parathyroidectomy provided an opportunity to relief RLS. Whether the reduction of serum phosphorus or parathyroid hormone contributed to this improvement merits further investigation.

The outlines of the current manuscript are: 1. Re-establish the link between hypertension and SDB including prevalence, mechanism, and reversal of process (i.e. improvement in hypertension with improvement in SDB), why it is important-cardiovascular mortality with numbers. 2. Re-establish the link between hypertension and CKD including same points as above. Then ask if both CKD and SDB are combined, what happens to hypertension and cardiovascular mortality. 3. Lastly, talk about links between CKD and SDB on how each process feeds on the other and is a growing, common problem.

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