Over the past decades, aggressive control of blood pressure (BP) and blockade of the renin-angiotensin-aldosterone system (RAAS) were considered the cornerstones of treatment against progression of chronic kidney disease (CKD), following important background and clinical evidence on the associations of hypertension and RAAS activation with renal injury. To this end, previous recommendations included a BP target of <130/80 mm Hg for all individuals with CKD (and possibly <125/75 mm Hg for those with proteinuria >1 g/day), as well as use of angiotensin-converting-enzyme inhibitors and angiotensin receptor blockers as first-line therapy for hypertension in all CKD patients. However, long-term extensions of relevant clinical trials support a low-BP goal only for patients with proteinuria, whereas recent cardiovascular trials questioned the benefits of low systolic BP for diabetic patients, leading to more individualized recommendations. Furthermore, our previous knowledge of the specific renoprotective properties of RAAS blockers in patients with proteinuric CKD is now extended with data on the use of these agents in patients with less advanced nephropathy and/or absence of proteinuria, deriving mostly from subanalyses of cardiovascular trials. This review discusses previous and recent clinical evidence on the issues of BP reduction and RAAS blockade by type and stage of renal damage, aiming to aid clinicians in their treatment decisions for patients with CKD.