Evaluation of Subclinical Uremic Cardiomyopathy using Speckle Tracking Echocardiography Serum Soluble Klotho and Fibroblast Growth Factor-23

Abdel Moniem, El Hassan Mohamed Ayman; Zeid, Montasser Mohamed Hussein; El Gohary, Iman Ezzat; El Hadidi, Abeer Shawky; Abdelkhalek, Hoda Shehata; Gawish, Rasha Ibrahim Abd Elrazek

doi:10.21608/svuijm.2024.298903.1902

Evaluation of Subclinical Uremic Cardiomyopathy using Speckle Tracking Echocardiography Serum Soluble Klotho and Fibroblast Growth Factor-23

Document Type : Original research articles

Authors

¹ Nephrology and Transplantation Unit, Internal Medicine Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt.

² Clinical and Chemical Pathology Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt.

³ Cardiology Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt.

10.21608/svuijm.2024.298903.1902

Abstract

Background: Uremic cardiomyopathy (UC) is being described to contribute to left ventricular (LV) dysfunction. Fibroblast growth factor-23 (FGF-23) and soluble alpha-Klotho (a-klotho) are thought to be involved in the pathogenesis of UC. Despite heart failure being the most common cardiovascular disease in chronic kidney disease (CKD), ejection fraction evaluation is still challenging.
Objectives: We aimed to evaluate the myocardial performance of both ventricles in uremic patients using speckle tracking echocardiography (STE) and its possible relation to serum soluble a-Klotho and FGF-23.
Patients and methods: This cross-sectional study included 45 hemodialysis (HD) patients and 45 patients with moderate CKD stages 3 and 4. Global longitudinal strain (GLS) and right ventricular free-wall strain (RVFWS) obtained by STE were used to evaluate both ventricular performances.
Results: Impaired GLS ≤ 16% was found in 46.7% of HD patients and 28.9% of CKD patients (p = 0.082). Impaired RVFWS ≤ 20% was found in 44.4% of HD patients and 24.4% of CKD patients (p = 0.046). In HD patients, impaired GLS is associated with a history of hypertension (p = 0.011), left ventricular mass index (LVMI) (p=0.041), and RVFWS (p = 0.030). The history of hypertension in HD patients (p = 0.013) and LVMI in CKD patients (p = 0.051), independently predicted compromised GLS.
Conclusion: Reduced subclinical LV and right ventricular systolic function existed in patients with moderate CKD and became worse in dialysis patients. The history of hypertension in HD patients and LVMI in CKD were key determinants of impaired GLS.

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