1.The role of calcium dysregulation in the pathogenesis of primary aldosteronism
Senzhen CHEN ; Yiling YAN ; Lili LIN ; Qiaoling YANG ; Nuoqi CHEN ; Jinfeng CHEN
Chinese Journal of Endocrinology and Metabolism 2025;41(11):966-969
Primary aldosteronism(PA) is the most common endocrine cause of secondary hypertension and is characterized by hypertension, hypokalemia, suppressed renin, and inappropriately elevated aldosterone. Increasing evidence indicates disturbances in calcium homeostasis among patients with PA. The calcium-regulatory system encompasses calcium and phosphate, parathyroid hormone(PTH), and vitamin D. Patients with PA frequently exhibit hypocalcemia, hypophosphatemia, elevated PTH, and reduced vitamin D levels. Clarifying the contribution of calcium dysregulation to PA pathogenesis is clinically relevant for mitigating target-organ damage. This review summarizes: (1) the role of aberrant calcium signaling in the development of PA; (2) characteristic features of calcium homeostasis in PA; and (3) the interactions between the renin-angiotensin-aldosterone system(RAAS) and calcium-regulatory pathways. Overall, abnormalities in calcium signaling appear integral to the pathogenesis of PA, and disrupted calcium homeostasis may aggravate target-organ injury in affected patients.
2.The role of calcium dysregulation in the pathogenesis of primary aldosteronism
Senzhen CHEN ; Yiling YAN ; Lili LIN ; Qiaoling YANG ; Nuoqi CHEN ; Jinfeng CHEN
Chinese Journal of Endocrinology and Metabolism 2025;41(11):966-969
Primary aldosteronism(PA) is the most common endocrine cause of secondary hypertension and is characterized by hypertension, hypokalemia, suppressed renin, and inappropriately elevated aldosterone. Increasing evidence indicates disturbances in calcium homeostasis among patients with PA. The calcium-regulatory system encompasses calcium and phosphate, parathyroid hormone(PTH), and vitamin D. Patients with PA frequently exhibit hypocalcemia, hypophosphatemia, elevated PTH, and reduced vitamin D levels. Clarifying the contribution of calcium dysregulation to PA pathogenesis is clinically relevant for mitigating target-organ damage. This review summarizes: (1) the role of aberrant calcium signaling in the development of PA; (2) characteristic features of calcium homeostasis in PA; and (3) the interactions between the renin-angiotensin-aldosterone system(RAAS) and calcium-regulatory pathways. Overall, abnormalities in calcium signaling appear integral to the pathogenesis of PA, and disrupted calcium homeostasis may aggravate target-organ injury in affected patients.
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