Hyperaldosteronism is associated with a reversible secondary hyperparathyroidism due to increased renal calcium excretion. Moreover, the angiotensin II receptor is expressed by human parathyroid tissue, and angiotensin may therefore directly stimulates PTH secretion. An increased bone loss is found in patients with hyperaldosteronism. The angiotensin II receptor seems main responsible for the RAAS-initiated bone loss due to a receptor activator of NF-κB ligand-mediated activation of the osteoclasts. Available data suggest a reduced fracture rate and increased bone mineral density in patients treated with angiotensin II receptor blockers, whereas treatment with angiotensin-converting enzyme inhibitors causes the opposite effects. Mineralocorticoid receptor antagonists seem to be beneficial to bone in patients with hyperaldosteronism, but it is unknown whether this also applies to other individuals. Further long-term studies are needed to clarify the effect of RAAS inhibitors on bone health. RAAS inhibitors, are widely prescribed worldwide and beneficial as well as harmful effects may have large impact on bone health in the general population.

Authors: Lise Sofie Bislev, Tanja Sikjær, Lars Rolighed, Lars Rejnmark
Keywords: bone mineral density, bone turnover markers, fracture risk, PTH, aldosterone, renin–angiotensin–aldosterone system, ACE inhibitors, angiotensin II receptor blockers, mineralocorticoid receptor antagonists
DOI Number: 10.1007/s12018-015-9182-0      Publication Year: 2015

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