High blood pressure (BP) is a leading contributor to premature mortality in patients with chronic kidney disease (CKD). Recently, we have experienced a change, in Hypertension Guidelines recommendations in CKD, to a more intensive lowering of BP levels. These changes are based on some trials but there is still debate about which BP goals are optimal in reducing morbidity and mortality in CKD patients.     Might intensive BP lowering have a benefical effect on all-cause mortality and cardiovascular (CV) outcomes in CKD patients? To address this issue, the Systolic Blood Pressure Intervention Trial (SPRINT) was performed. It is a landmark trial and is likely to result in a paradigm shift in the management of patients with hypertension. With non-diabetic high-risk patients, it demonstrated that intensive BP lowering to a target of <120 mm Hg is superior to routine management with a target of <140 mm Hg. Significant reductions were noted in CV and all-cause mortality, accompanied by a reduction in decompensated heart failure. An intensive strategy also reduced the risk of developing LVH among patients without baseline LVH and resulted in greater LVH regression among those with evidence of baseline LVH. Interestingly, these treatment effects did not differ between participants with and without CKD. Even in CKD patients, intensive BP lowering significantly reduced the risk of mortality.      With respect to the renal outcomes, however, careful interpretations are required since the SPRINT did not include diabetes, advanced CKD patients with eGFR less than 20 ml/min/1.73m2, and those with proteinuria over 1g per day. Although the SPRINT data showed an accelerated reduction in eGFR (only in patients without CKD at baseline) in the intensive arm, it is predominantly due to hemodynamic changes rather than to intrinsic damage in kidney tubule cells, therefore, may be considered as a pseudo-worsening of renal function. Supporting this, a longitudinal subgroup analysis of CKD participants from the SPRINT trial showed no difference in eight urine biomarkers of tubule cell damage between intensive and standard arms, despite a more pronounced lowering in eGFR in the intensive arm. Also, an updated systematic review and meta-analysis found that more intensive BP-lowering significantly reduced the risk of progression of albuminuria compared with less intensive BP-lowering.  In recent years, trials and meta-analyses have assessed intensive BP lowering, with some success. However, current data are not easily applicable to the general CKD population with hypertension. One thing is clear though: it should be only applied when there is strong evidence in favor of benefits against adverse effects or harm caused by intensive BP lowering. Therefore, the management of hypertension should be individualized based on the underlying risk of CV outcomes rather than based on absolute values alone, in a similar way to current recommendations for lipid-lowering therapy.