After diabetes, the most common cause of end-stage kidney disease is hypertensive nephrosclerosis. Previous studies of hypertensive kidney disease have focused on the afferent arterioles and glomeruli damage and the involvement of the renin angiotensin system.
According to Valeria Victoria Costantino, PhD, and colleagues, recent novel evidence has demonstrated that persistent high blood pressure injures tubular cells, leading to epithelial-mesenchymal transition (EMT) and tubulointerstitial fibrosis. Changes in post-glomerular peritubular capillaries are caused by injury primarily determined at the glomerular level by hypertension. Those changes, in turn, induce endothelial damage and hypoxia.
Inflammation, EMT with epithelial cells dedifferentiation, and fibrosis are triggered by microvascular dysfunction by inducing hypoxic environment. Hypertensive kidney disease also includes podocyte effacement and loss, leading to disruption of the filtration barrier.
In Cells [2021;10(11), 3146; doi.org/10.3390/cells10113146], the researchers presented a review highlighting the molecular mechanisms and histologic aspects in the pathophysiology of hypertensive kidney disease, incorporating knowledge regarding EMT and tubulointerstitial fibrosis. The review also discusses the role of the Hsp70 chaperone on the angiotensin II-induced EMT after angiotensin II type 1 receptor blockage, as a possible molecular target for therapeutic strategy against hypertensive renal damage.