Arterial
hypertension remains to be a serious problem with considerable morbidity and mortality worldwide in the present age.
Hypertension is a major risk factor for
cardiovascular diseases such as
stroke,
myocardial infarction,
renal failure, and
heart failure.
Hypertensive nephropathy is the second leading cause of death in
chronic kidney disease (CKD) around the world. Long-time
hypertension loading results in renal interstitial
fibrosis, which is associated with aberrant activation of renal fibroblasts and excessive generation of extracellular matrix (ECM)
proteins. Increasing evidence supported that
proteinuria, tubular
hypertrophy, oxidative stress, activation of
renin-
aldosterone-
angiotensin system (RAAS),
collagen turnover, chronic
inflammation, and vasoactive substances synergistically contributed to the pathogenesis of hypertensive renal
fibrosis. However, the mechanisms involving the pathogenesis of hypertensive renal
fibrosis are complex and not fully understood. Also, the effective clinical
therapy to halt or even reverse renal
fibrosis in
hypertension is still limited. In this chapter, we aimed to provide an overview of the main pathophysiologic and mechanistic features of renal
fibrosis under hypertensive state. The completion of the studies in these directions would improve our understanding of renal
fibrosis in
hypertension and also help us better screen treatment strategies for preventing renal destruction associated with
hypertension.