The calcimimetic etelcalcetide attenuates pressure overload–induced cardiac hypertrophy in rats with and without chronic kidney disease

Q: What are the key findings of this study?

Etelcalcetide significantly attenuated cardiac hypertrophy (HW/BW 3.55 vs 5.72, p<0.05) and improved LVEF (70.6% vs 57.7%, p<0.05) in CKD/LVH rats via RAAS and cardiac FGF23 modulation.

Q: What is the clinical evidence from this study?

Population: Pressure overload-induced left ventricular hypertrophy (LVH) with or without chronic kidney disease (CKD) (n=42). Intervention: Etelcalcetide vs. Vehicle. Primary outcome: Heart weight-to-body weight ratio (HW/BW) in the CKD/LVH group (p=<0.05).

Q: What question did this study set out to answer?

To determine whether etelcalcetide attenuates pressure overload–induced left ventricular hypertrophy in rats with and without chronic kidney disease.

Hidehisa Okamoto; Shunsuke Goto; Yuma Nose; Hayaki Okamoto; Hideki Fujii

doi:10.1016/j.biopha.2026.119054

January 30, 2026Biomedicine & PharmacotherapyOpen Access

The calcimimetic etelcalcetide attenuates pressure overload–induced cardiac hypertrophy in rats with and without chronic kidney disease

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Key result

Etelcalcetide cuts cardiac hypertrophy ~38% in CKD rats via RAAS and FGF23 modulation.

P<0.05
n=42

Key Points

To determine whether etelcalcetide attenuates pressure overload–induced left ventricular hypertrophy in rats with and without chronic kidney disease.
Assigned rats to seven experimental groups (N = 6 per group): sham, CKD, CKD + etelcalcetide, LVH, LVH + etelcalcetide, CKD/LVH, and CKD/LVH + etelcalcetide.
Evaluated rats at 19 weeks of age using echocardiography, histology (WGA and Sirius Red staining), and biochemical assays for mineral and cardiac markers.
Etelcalcetide significantly improved ejection fraction in LVH (73.1 ± 1.9% vs. 66.3 ± 0.9%, P < 0.05) and CKD/LVH rats (70.6 ± 1.9% vs. 57.7 ± 1.7%, P < 0.05).
Treatment significantly lowered heart weight-to-body weight ratio in the CKD/LVH group (3.55 ± 0.07 vs. 5.72 ± 0.49, P < 0.05) and suppressed cardiomyocyte enlargement and fibrosis in both LVH and CKD/LVH groups.
Etelcalcetide significantly reduced cardiac FGF23 expression, serum aldosterone, and cardiac RAAS components without altering blood pressure, BUN, or creatinine.

PICO

P

Population

42 male Sprague-Dawley rats (8 weeks old) with experimentally induced pressure-overload left ventricular hypertrophy and/or chronic kidney disease treated for 8 weeks.

I

Intervention / Comparator

Etelcalcetide vs Vehicle (0.5 mg/kg/day subcutaneously)

O

Primary Outcome

Heart weight-to-body weight ratio (HW/BW) in the CKD/LVH group, p=<0.05

Main Result

Absolute Event Rate: 3.55% vs 5.72%

p-value: p=<0.05

Limitations

Preclinical animal model (male Sprague-Dawley rats) which may not fully translate to human patients with CKD and LVH.

Implication

Animal study demonstrates etelcalcetide reduces cardiac hypertrophy, indicating potential heart protection in chronic kidney disease.

Abstract

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Discussion

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Cite This Study

Okamoto et al. (2026) studied Pressure overload-induced left ventricular hypertrophy (LVH) with or without chronic kidney disease (CKD) (n=42). Etelcalcetide vs. Vehicle was evaluated on Heart weight-to-body weight ratio (HW/BW) in the CKD/LVH group (p=<0.05). Etelcalcetide significantly attenuated cardiac hypertrophy (HW/BW 3.55 vs 5.72, p<0.05) and improved LVEF (70.6% vs 57.7%, p<0.05) in CKD/LVH rats via RAAS and cardiac FGF23 modulation.

synapsesocial.com/papers/6980feabc1c9540dea810e22 https://doi.org/10.1016/j.biopha.2026.119054

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The calcimimetic etelcalcetide attenuates pressure overload–induced cardiac hypertrophy in rats with and without chronic kidney disease

Key Points

PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

The calcimimetic etelcalcetide attenuates pressure overload–induced cardiac hypertrophy in rats with and without chronic kidney disease

Key Points

PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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