Chronic kidney disease (CKD) is not only a consequence of HTN, but also it contributes to raising and maintaining elevated blood pressure. Elevated BP causes renal damage in multiple structures through complex mechanisms. Nocturnal HTN and treatment resistance, two common conditions, increase the risk, and treatment of HTN aims to slow the progressive deterioration of renal function towards the development of end-stage renal disease (ESRD) and to reduce CV events and mortality. The target for BP reduction has been controversial for decades, as too much BP reduction may worsen the rate of progression of CKD. The relevance of the initial decrease in GFR and/or hyperkalaemia with pharmacological treatment and the extent of tubular damage should be considered. Given the available information, a target of <130/80 mmHg seems reasonable, but in the presence of albuminuria, individualised treatment should be considered. If a more stringent target of <120 mmHg is implemented, potential adverse effects should be closely monitored. Antihypertensive treatment should combine lifestyle changes with drugs targeting volume overload, sympathetic overactivity, the renin–angiotensin–aldosterone system, mineralocorticoid receptors and sodium-glucose cotransporter 2. Selection should take into account the presence or absence of albuminuria/proteinuria. Emerging agents offer new therapeutic approaches, although further studies are needed before they can be recommended for the treatment of HTN in patients with CKD.