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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Mineralocorticoid receptor (MR) activation exerts broad pathological effects, and large outcome trials have established the cardiorenal-protective benefits of MR antagonists. Although clinical observations in primary aldosteronism suggest an increased risk of fractures and enhanced urinary calcium excretion, indicating a potential involvement of MR in the bone–kidney axis, its causal role and underlying mechanisms remain to be clarified. We aimed to define molecular and structural skeletal consequences of aldosterone–salt loading and evaluate the protective effects of esaxerenone, a selective non-steroidal MR antagonist.
Male Sprague-Dawley rats were infused with aldosterone and provided 8% NaCl diet for 4 weeks (Aldo-HS group). A treatment group received esaxerenone mixed in a chow (0.03%) in addition to aldosterone and salt (Aldo-HS-Esax group). Control rats received vehicle. At 4 weeks, femurs were collected and trabecular bone in the distal femoral metaphysis was analyzed by histomorphometry, micro-CT, and three-dimensional bone morphometry. RNA-seq was performed on kidney and bone, followed by differential expression and weighted gene co-expression network analysis (WGCNA).
The Aldo+HS group exhibited elevated blood pressure without overt histological changes in the kidney, suggesting early-stage renal impairment. Serum calcium and phosphate, as well as parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), were unchanged across the three groups; however, Aldo-HS rats exhibited a significant increase in fractional excretion of calcium (FECa) accompanied by marked reductions in trabecular bone volume (BV/TV), indicating that bone loss occurred in the absence of overt CKD-related mineral imbalance. Consistent with histomorphometry, micro-CT and three-dimensional bone morphometry confirmed substantial loss of trabecular bone structure in Aldo-HS rats. Kidney RNA-seq revealed upregulation of oxidative stress and inflammatory markers in Aldo-HS rats, which were attenuated by esaxerenone, whereas canonical calcium transport transcripts showed no consistent alterations. WGCNA of bone transcriptome data identified a gene module enriched for extracellular matrix components (e.g., Col1a1, Col1a2, Col11a1), whose eigengene expression was also strongly negatively correlated with FECa (r = –0.97, p < 0.01). Consistently, FECa was strongly negatively correlated with BV/TV (r = –0.87, p < 0.01). Esaxerenone treatment significantly reduced FECa, preserved trabecular bone structure, and restored the expression profile of the identified gene module.
Aldosterone and salt loading induced early bone metabolic alterations through mechanisms independent of reduced glomerular filtration. These changes were associated with disrupted bone matrix gene regulation and were effectively prevented by mineralocorticoid receptor blockade. Our findings highlight a novel bone–kidney axis and support esaxerenone as a potential therapeutic agent for aldosterone-salt–induced osteopathy.
