Abstract:Spironolactone reduced the severity of OSA and reduced blood pressure in resistant hypertension patients with moderate-to-severe OSA. These findings may assist in the treatment of OSA in patients with resistant hypertension.
“…The follow-up was 12 weeks. AHI decreased significantly in the treatment group but not in the control group [28].…”
Section: Impact Of Mineralocorticoid Receptor Antagonists On Osa Sevementioning
confidence: 68%
“…Moreover, except one study, all studies followed non-randomized, observational design. Secondly, it is difficult to judge if the effect of treatment with aldosterone antagonists was related to combatting the deleterious effects of aldosterone or to the decrease and changes in distribution of extracellular fluid during sleep by the diuretic effects of the drugs [26][27][28][29].…”
Section: Impact Of Mineralocorticoid Receptor Antagonists On Osa Sevementioning
It has been suggested that the high prevalence of obstructive sleep apnea (OSA) in resistant hypertension (RHT) may be related to the high prevalence of primary aldosteronism (PA) in patients with RHT. It has been also hypothesized that the relationship between aldosterone and OSA might be bidirectional. In patients with RHT, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. It has been postulated that aldosterone worsens OSA by promoting accumulation of fluid, which shifted in the supine position to the neck, contributes to increased upper airway resistance. Also there is growing data that PA is more frequent in patients with OSA and that the treatment of PA positively influences OSA course. Also in some studies it has been shown that patients with OSA are characterized by higher aldosterone levels and higher prevalence of PA than patients without OSA and that causal treatment of OSA might decrease aldosterone levels. Moreover, the recent guideline of the Endocrine Society on management of PA recommends to screen hypertensive patients with OSA for PA.
“…The follow-up was 12 weeks. AHI decreased significantly in the treatment group but not in the control group [28].…”
Section: Impact Of Mineralocorticoid Receptor Antagonists On Osa Sevementioning
confidence: 68%
“…Moreover, except one study, all studies followed non-randomized, observational design. Secondly, it is difficult to judge if the effect of treatment with aldosterone antagonists was related to combatting the deleterious effects of aldosterone or to the decrease and changes in distribution of extracellular fluid during sleep by the diuretic effects of the drugs [26][27][28][29].…”
Section: Impact Of Mineralocorticoid Receptor Antagonists On Osa Sevementioning
It has been suggested that the high prevalence of obstructive sleep apnea (OSA) in resistant hypertension (RHT) may be related to the high prevalence of primary aldosteronism (PA) in patients with RHT. It has been also hypothesized that the relationship between aldosterone and OSA might be bidirectional. In patients with RHT, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. It has been postulated that aldosterone worsens OSA by promoting accumulation of fluid, which shifted in the supine position to the neck, contributes to increased upper airway resistance. Also there is growing data that PA is more frequent in patients with OSA and that the treatment of PA positively influences OSA course. Also in some studies it has been shown that patients with OSA are characterized by higher aldosterone levels and higher prevalence of PA than patients without OSA and that causal treatment of OSA might decrease aldosterone levels. Moreover, the recent guideline of the Endocrine Society on management of PA recommends to screen hypertensive patients with OSA for PA.
“…One of the explanations for the high occurrence of OSA in CKD patients is sodium and water retention mediated by abnormal renin-angiotensin-aldosterone system (RAAS) activity [42]. In patients with OSA, an abnormal diurnal RAAS activity has been reported [43], and one study has shown, that both OSA severity and BP levels were reduced when adding aldosterone antagonists to the antihypertensive treatment in hypertensive OSA patients [44]. Hence, when analysing the effect of CPAP treatment, it is relevant to evaluate eventual changes in vasoactive hor-Open Journal of Nephrology mones and renal handling of sodium and water as an explanation for BP response.…”
Background: Previous studies of continuous positive airway pressure (CPAP) treatment for obstructive sleep apnoea (OSA) have shown conflicting results on the effect on blood pressure (BP), and patients with chronic kidney disease (CKD) have not been included in these studies. As OSA is a frequent comorbidity in patients with CKD, it is of relevance to evaluate the effect of CPAP treatment on BP in this population. Aim: In this prospective follow-up study, we measured the effect of short term CPAP treatment of moderate-to-severe OSA on brachial and central BP, plasma level of syndecan-1 and vasoactive hormones, renal handling of sodium, subjective sleepiness, and quality of life in patients with impaired renal function. Methods: From December 2015 until March 2017, 25 patients were invited to participate in the study at the University Clinic in Nephrology and Hypertension, Aarhus University and Holstebro Hospital. At baseline and at follow-up after three to four months of CPAP treatment, we performed 24 h brachial and central ambulatory BP measurement, blood sampling measurements of plasma concentrations of syndecan-1, renin, angiotensin II, aldosterone, vasopressin, creatinine, haemoglobin A1c, and cholesterol, cardio respiratory monitoring, 24 h urine collection for measurement of urinary excretion of albumin, aquaporin-2, and epithelial sodium channel, Epworth Sleepiness Scale (ESS), and SF-36 (quality of life). Results: At follow-up, the 17 included patients with mean baseline estimated glomerular filtration rate 66 mL/min/1.
“…1), and 6-beta-hydroxy-7-alpha-methylthiospironolactone as the main ones [2]. Spironolactone has been widely used for decades and its side effects have been studied and documented [3–8], but despite being used also in children, the dosing recommendations are based on clinical trials performed in the adult population and/or expert opinion and clinical experience. As such, studies evaluating the pharmacokinetic profile of spironolactone in pediatric age groups contribute to the refinement of evidence-based dosing recommendations in children.Fig.…”
This paper describes an LC-MS/MS method to determine the concentration of spironolactone and its metabolites 7-alpha-methylthiospironolactone and canrenone in blood plasma samples. The resulting assay is simple (using protein precipitation for sample preparation) and sensitive (the lower limit of quantification is close to 0.5 ng/ml) while requiring only 50 μl of plasma, making it especially suitable for analyzing samples obtained from pediatric and neonatal patients where sample sizes are limited. The sensitivity is achieved by using ammonium fluoride as an eluent additive, which in our case amplifies the signal from our analytes in the plasma solution on average about 70 times. The method is fully validated according to the European Medicines Agency’s guideline and used for the measurement of pediatric patients’ samples in clinical trials for evaluating oral spironolactone’s and its metabolites’ pharmacokinetics in children up to 2 years of age.
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