Several studies have demonstrated a bidirectional relationship between obstructive sleep apnea and primary aldosteronism (PA); however, many of these studies are limited to patients with known obstructive sleep apnea, hypertension, or PA. We evaluated the role of screening for PA in all patients referred for a diagnostic sleep study without selecting for prior diagnoses with these conditions. Plasma aldosterone and renin concentration were measured after an overnight polysomnography. Blood pressure was measured at the sleep center for all patients, while a proportion underwent 24-hour blood pressure monitoring. Of the 85 participating patients, 2 (2.4%) were identified to have likely PA based on an elevated aldosterone:renin ratio and/or clinical characteristics. Another 10 (11.8%) were identified to have possible PA based on their low or normal plasma renin concentration despite taking antihypertensive medications that are known to elevate renin. In participants with both obstructive sleep apnea and hypertension (n=40), the prevalence of likely or possible PA was 30%. However, there was no correlation between aldosterone, rennin, or aldosterone:renin ratio and the apnea-hypopnea index using multiple regression analysis adjusted for interfering medications and hypertension status. The observed high prevalence of possible PA among those with both hypertension and obstructive sleep apnea suggests that they should be routinely screened for PA.

Background Hypertensive patients with primary aldosteronism (PA) have a higher risk of cardiovascular complications than those with blood pressure-matched essential hypertension. The excess cardiovascular consequences of PA can be attributed to the pro-inflammatory effect of excessive aldosterone and mineralocorticoid receptor activation in a range of peripheral tissues and cell types. The neutrophil-to-lymphocyte ratio (NLR) is a widely available markers of inflammation which has been shown to predict cardiovascular outcome in the general population. This study aims to evaluate the use of NLR as a potential biomarker of PA and PA severity. Methods Patients with PA (n=355) were identified from two large PA databases in Australia and China, while controls (n=222) were patients with hypertension who were referred for assessment but did not meet the diagnostic criteria for PA. The NLR was retrospectively collected from routine full blood examination, prior to commencement of targeted treatment for PA. Results The NLR did not differ between PA patients and hypertensive controls (median 2.3 and 2.4, p=0.563). However, amongst patients with PA, the NLR was positively correlated with baseline and post-saline aldosterone levels (r=0.22 and p<0.001 for both) and negatively correlated with serum potassium (r=-0.15, p=0.006). Furthermore, in a logistic regression analysis of data from patients with PA, the NLR predicted the presence of co-morbid CKD (defined as eGFR < 60mL/min/1.73m 2) with an odds ratio of 1.5 (p=0.003). Conclusion Whilst the NLR did not distinguish PA from controls, it was a marker of PA severity, being associated with aldosterone concentration as well as the presence of CKD. A prospective study is needed to further clarify the role of NLR in predicting end-organ damage associated with PA.