Key result
RAAS inhibitors link to lower PTH, while higher aldosterone is associated with elevated levels.
Why the study?
Is higher serum aldosterone concentration associated with higher PTH, and does the use of RAAS inhibitors associate with lower PTH in a multi-ethnic cohort?
Cross-Sectional (n=5,668)
Is higher serum aldosterone concentration associated with higher PTH, and does the use of RAAS inhibitors associate with lower PTH in a multi-ethnic cohort?
Effect estimate: β = -2.327 pg/ml
Absolute Event Rate: 45% vs 47.1%
p-value: p=.006
Higher serum aldosterone is associated with higher PTH, and RAAS inhibitor use is associated with lower PTH, suggesting a potentially modifiable relationship between the RAAS and PTH.
Does not support changing RAAS inhibitor use; leaves open causal aldosterone-PTH links in diverse populations.
CONTEXT: Aldosterone and PTH are implicated in the pathogenesis of cardiovascular and skeletal diseases. An expanding body of evidence supports a bidirectional and positive physiologic relationship between aldosterone and PTH. Large population-based studies confirming this relationship, and whether it may be targeted as a potential method to mitigate the clinical consequences associated with excess aldosterone and PTH, are needed. OBJECTIVE: We hypothesized that higher aldosterone levels would associate with higher PTH, and that the use of renin-angiotensin-aldosterone system (RAAS) inhibitors would predict lower PTH in a large, multi-ethnic, community-based cohort. DESIGN, SETTING, PARTICIPANTS: We conducted cross-sectional analyses of participants in the Multi-Ethnic Study of Atherosclerosis without apparent primary hyperparathyroidism or chronic kidney disease (n = 5668). We evaluated associations of RAAS inhibitor use with PTH concentration among 1888 treated hypertensive participants. We also tested associations of serum aldosterone concentration with PTH concentration among 1547 participants with these measurements. OUTCOME: Serum PTH concentration. RESULTS: Higher aldosterone associated with higher PTH (β = 0.19 pg/ml per 1 ng/dl of aldosterone, P < .0001), and this finding was most pronounced among those with a primary hyperaldosteronism-like phenotype. There was a stepwise increment in PTH when comparing untreated normotensives, hypertensives using RAAS inhibitors, untreated hypertensives, and treated hypertensives using non-RAAS inhibitors (40.8, 45.0, 46.2, 47.1 pg/ml, respectively). The use of any RAAS inhibitor independently associated with lower PTH (β = -2.327 pg/ml per use of RAAS inhibitor, P = .006), when compared with the use of any non-RAAS inhibitor medication. CONCLUSIONS: Higher serum aldosterone concentration is associated with higher serum PTH concentration, and the use of RAAS inhibitors is associated with lower PTH concentration. These results extend prior evidence from observational and intervention studies suggesting a potentially important and modifiable relationship between the RAAS and PTH in humans.
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Brown et al. (2014) conducted a cross-sectional in Hypertension (n=5,668). Renin-angiotensin-aldosterone system (RAAS) inhibitors vs. Non-RAAS inhibitor medication was evaluated on Serum PTH concentration (β = -2.327 pg/ml, p=.006). Higher aldosterone was associated with higher PTH (P<.0001), and RAAS inhibitor use was associated with lower PTH compared to non-RAAS inhibitors (β = -2.327 pg/ml, P=.006).