The clinical triad of hypertension (HT), chronic kidney disease (CKD), and cardiovascular disease (CVD) associated with a concomitant presence of cardiovascular (CV) risk factors portends a serious cardiorenal risk profile. HT and CKD represent a frequently interlinked disorder, defined as hypertensive nephrosclerosis. HT represents a major risk factor for ESRD in 25–30% of patients starting renal replacement therapy. On the other hand, CKD represents the most common cause of secondary hypertension, with a prevalence increasing progressively from 85 to 95% as GFR falls from 85 to 15 mL/min/1.73 m2. Hypertensive nephrosclerosis is classified into two phenotypes, benign and malignant forms, and is characterized by mild-to-severe renovascular changes. It is determined by neurohormonal, metabolic, inflammatory, vascular, and genetic factors. The presence of two APOLI risk alleles defines a subgroup of Afro-Americans characterized by more severe proteinuria at baseline and more rapid progression to ESRD. Further, several hypertensive phenotypes are reported in CKD namely white-coat HT, masked HT, nocturnal HT, absence of nocturnal dipping, resistant, and refractory HT. Novel classes of antidiabetic and antihypertensive medications including Finerenone, a MR antagonist, and SGLT2 inhibitors have improved significantly blood pressure control, reduced cardiovascular complications and progression to ESRD in CKD patients.