This joint consensus statement summarizes the mechanisms by which endothelial factors, including endothelin-1, the renin-angiotensin-aldosterone system, and oxidative stress, induce vascular remodeling and contribute to chronic kidney disease.
Highlights endothelial-targeted therapies in CKD; confirms pathogenic mechanisms and extends to guideline-directed research priorities.
: Kidney damage is a common consequence of arterial hypertension, but is also a cause of atherogenesis. Dysfunction and/or harm of the endothelium in glomeruli and tubular interstitium damage the function of these structures and translates into dynamic changes of filtration fraction, with progressive reduction in glomerular filtration rate, expansion of extracellular fluid volume, abnormal ion balance, and hypoxia, ultimately leading to chronic kidney disease. Considering the key role played by endothelial dysfunction in chronic kidney disease, the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension and the Japanese Society of Hypertension have critically reviewed available knowledge on the mechanisms underlying endothelial cell injury. This resulted into two articles: in the first, we herein examine the mechanisms by which endothelial factors induce vascular remodeling and the role of different players, including endothelin-1, the renin-angiotensin-aldosterone system and their interactions, and of oxidative stress; in the second, we discuss the role of endothelial dysfunction in the major disease conditions that affect the kidney.
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Rossi et al. (2017) conducted a review in Chronic Kidney Disease. Endothelial dysfunction and the imbalance between vasodilating and vasoconstricting factors, including endothelin-1 and the renin-angiotensin-aldosterone system, play a key role in the pathogenesis of chronic kidney disease.
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