Kidney damage represents a frequent event in the course of
hypertension, ranging from a benign to a malignant form of nephropathy depending on several factors, that is, individual susceptibility, degree of
hypertension, type of etiology and underlying
kidney disease. Multiple mechanisms are involved in determination of kidney glomerular, tubular and interstitial
injuries in
hypertension. The present review article discusses relevant contributory molecular mechanisms underpinning the promotion of hypertensive renal damage, such as the renin-angiotensin-aldosterone system (RAAS), oxidative stress, endothelial dysfunction, and genetic and epigenetic determinants. We highlighted major pathways involved in the progression of
inflammation and
fibrosis leading to glomerular
sclerosis, tubular
atrophy and interstitial
fibrosis, thus providing a state of the art review of the pathogenetic background useful for a better understanding of current and future therapeutic strategies toward
hypertensive nephropathy. An adequate control of
high blood pressure, obtained through an appropriate therapeutic intervention, still represents the key strategy to achieve a satisfactory control of renal damage in
hypertension. In this regard, we reviewed the impact of currently available
antihypertensive pharmacological treatment on kidney damage, with particular regard to RAAS inhibitors. Notably, recent findings underscored the ability of the kidneys to regenerate and to repair tissue
injuries through the differentiation of resident embryonic stem cells. Pharmacological modulation of the renal endogenous reparative process (that is, with
angiotensin-converting enzyme inhibitors and AT1
angiotensin II receptor blockers), as well as future therapeutic strategies targeted to the renopoietic system, offers interesting perspectives for the management of
hypertensive nephropathy.