Hypertension is a major independent risk factor for kidney disease and for faster renal function loss. Beyond hypertension, abnormal loss of proteins in the urine represents another major feature of progressive chronic kidney disease (CKD).

Type 2 diabetes is reaching epidemic proportions throughout the world, representing the most common cause of end-stage renal disease (ESRD). Hypertension is an important risk factor for the development of diabetic neuropathy and a crucial progression promoter. Early identification of renal impairment associated with diabetes and initiation of renoprotective therapy are imperative.

Proteinuria - initially thought to represent only a marker of renal function impairment - was subsequently found to be a major independent determinant and probably the stronger risk factor for progressive renal damage and function loss both in experimental animals and in humans.

Blood pressure (BP) reduction is invariably nephroprotective. Choice of antihypertensive strategies with highest nephroprotective effect is crucial to prevent or reverse progression to ESRD. Amongst different antihypertensive drugs, renin-angiotensin aldosterone system (RAAS) inhibitors have an incremental nephroprotective effect in proteinuric patients.

Maximal RAAS inhibition should be aimed to optimize renoprotection in hypertensive patients with CKD and proteinuria. Strong evidence suggests that achieving target BP goals via inhibition of the RAAS confers significant renal protection for diabetic patients.

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) lower BP and reduce both the progression of renal damage and adverse cardiovascular events; some important renoprotective actions seem to be independent of the antihypertensive effect.

The use of azilsartan in patients with renal impairment has received special focus. Azilsartan a selective AT1 receptor blocker, appears to be more efficacious in reducing BP than the other ARBs with a similar safety and tolerability profile. Azilsartan has also been proved to have renoprotective effects, in terms of reducing proteinuria, albuminuria and nephrinuria along with reduced tubular cast formation and glomerular injury.

Several experimental evidences indicate an interesting series of pleiotropic actions resulting in different beneficial effects in terms of renal, and endothelial function, and metabolic homeostasis.