Chronic Kidney Disease and Arterial Stiffness: A Two-Way Path

Frontiers in Medicine

Carlos Castellaro²  Felipe Inserra³  Pedro Forcada⁴  Agustina Castellaro⁵ 

[1] Advisor of Academic Vice-Rectory Department, Maimonides University, Buenos Aires, Argentina;Department of Nephrology, Centro de Educación Médica e Investigaciones Clínicas Norberto Quirno (CEMIC) Hospital, Buenos Aires, Argentina;Master Vascular Mechanics and Arterial Hypertension, Postgraduate Department, Hypertension, Austral University, Buenos Aires, Argentina;Non-Invasive Vascular Labs, CardioArenales and Diagnóstico Integral Médico (DIM) Prevención Cardiovascular, Buenos Aires, Argentina;Pediatric Medicine of Prof. Dr. Juan P Garrahan Hospital, Buenos Aires, Argentina;

关键词: pulse wave velocity (PWV);    calcification;    CKD progression;    pulsatility;    cardiovascular events;   

DOI  :  10.3389/fmed.2021.765924

来源: DOAJ

【 摘 要 】

The kidney-heart relationship has raised interest for the medical population since its vast and complex interaction significantly impacts health. Chronic kidney disease (CKD) generates vascular structure and function changes, with significant hemodynamic effects. The early arterial stiffening in CKD patients is a consequence of the interaction between oxidative stress and chronic vascular inflammation, leading to an accelerated deterioration of left ventricular function and alteration in tissue perfusion. CKD amplifies the inflammatory cascade's activation and is responsible for altering the endothelium function, increasing the vascular tone, wall thickening, and favors calcium deposits in the arterial wall. Simultaneously, the autonomic imbalance, and alteration in other hormonal systems, also favor the overactivation of inflammatory and fibrotic mediators. Thus, hormonal disarrangement also contributes to structural and functional lesions throughout the arterial wall. On the other hand, a rise in arterial stiffening and volume overload generates high left ventricular afterload. It increases the left ventricular burden with consequent myocardial remodeling, development of left ventricular hypertrophy and, in turn, heart failure. It is noteworthy that reduction in glomerular mass of renal diseases generates a compensatory glomerular filtration overdriven associated with large-arteries stiffness and high cardiovascular events. Furthermore, we consider that the consequent alterations of the arterial system's mechanical properties are crucial for altering tissue perfusion, mainly in low resistance. Thus, increasing the knowledge of these processes may help the reader to integrate them from a pathophysiological perspective, providing a comprehensive idea of this two-way path between arterial stiffness and renal dysfunction and their impact at the cardiovascular level.

【 授权许可】

Unknown