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Pathophysiology and consequences of arterial stiffness in children with chronic kidney disease.
Pediatric Nephrology ( IF 2.6 ) Pub Date : 2020-09-07 , DOI: 10.1007/s00467-020-04732-y
Karolis Azukaitis 1 , Augustina Jankauskiene 1 , Franz Schaefer 2 , Rukshana Shroff 3
Affiliation  

Changes in arterial structure and function are seen early in the course of chronic kidney disease (CKD) and have been causally associated with cardiovascular (CV) morbidity. Numerous potential injuries encompassing both traditional and uremia-specific CV risk factors can induce structural arterial changes and accelerate arterial stiffening. When the buffering capacity of the normally elastic arteries is reduced, damage to vulnerable microcirculatory beds can occur. Moreover, the resultant increase to cardiac afterload contributes to the development of left ventricular hypertrophy and cardiac dysfunction. Adult studies have linked arterial stiffness with increased risk of mortality, CV events, cognitive decline, and CKD progression. Pulse wave velocity (PWV) is currently the gold standard of arterial stiffness assessment but its measurement in children is challenging due to technical difficulties and physiologic aspects related to growth and poor standardization between algorithms for calculating PWV. Nevertheless, studies in pediatric CKD have reported increased arterial stiffness in children with advanced CKD, on dialysis, and after kidney transplantation. Development of arterial stiffness in children with CKD is closely related to mineral-bone disease and hypertension, but other factors may also play a significant role. The clinical relevance of accelerated arterial stiffness in childhood on cardiovascular outcomes in adult life remains unclear, and prospective studies are needed. In this review we discuss mechanisms leading to arterial stiffness in CKD and its clinical implications, along with issues surrounding the technical aspects of arterial stiffness assessment in children.



中文翻译:

慢性肾脏病儿童动脉僵硬的病理生理学和后果。

动脉结构和功能的变化在慢性肾病 (CKD) 病程的早期可见,并且与心血管 (CV) 发病率存在因果关系。包括传统和尿毒症特异性 CV 风险因素在内的许多潜在损伤可引起结构性动脉变化并加速动脉硬化。当正常弹性动脉的缓冲能力降低时,可能会损坏脆弱的微循环床。此外,由此产生的心脏后负荷增加有助于左心室肥厚和心功能不全的发展。成人研究已将动脉僵硬与死亡风险增加、心血管事件、认知能力下降和 CKD 进展联系起来。脉搏波速度 (PWV) 目前是动脉僵硬度评估的黄金标准,但由于技术困难和与生长相关的生理方面以及计算 PWV 的算法之间的标准化差,其在儿童中的测量具有挑战性。然而,儿童 CKD 的研究报告称,晚期 CKD 儿童、透析和肾移植后动脉僵硬度增加。CKD 患儿动脉僵硬度的发展与矿物质骨病和高血压密切相关,但其他因素也可能起重要作用。儿童期动脉硬化加速与成人心血管结局的临床相关性尚不清楚,需要前瞻性研究。

更新日期:2020-09-08
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