Introduction 1 2 3 4 As in many other complications of chronic renal failure, patients often do not report symptoms of hypertension, so an active screening approach is needed to prevent end-organ damage. This article aims to give a short overview of the different pathophysiological pathways that lead to hypertension in CKD in order to explain how these can be targeted by different therapeutic approaches. Pathophysiology of hypertension in CKD 3 5 1 Fig. 1 BP CO TPR PTH Na  6 7 8 9 10 5 11 12 13 14 15 16 17 18 16 19 20 13 20 21 22 23 24 L 25 26 27 25 28 29 30 31 32 33 34 35 36 37 38 39 40 41 Management 42 1 5 43 2 44 45 Fig. 2 CBP ABPM HBP BP BMI  46 47 48 49 46 44 Once hypertension has been confirmed, good management should not focus only on pharmacological therapy, but also on detection and treatment of end-organ damage and, where appropriate, improvement of the dialysis regime and consideration of therapeutic life-style changes. 50 45 46 51 52 12 53 54 55 56 3 57 58 43 5 46 59 60 61 10 16 42 62 63 63 64 65 68 69 46 47 70 59 71 72 42 2 2 42 Calcium channel blockers are very potent anti-hypertensive drugs and, therefore, useful as add-on therapy in children with resistant hypertension. Dihydropyridine (DHP) drugs (e.g. nifedipine, amlodipine) act mainly as vasodilators and do not have cardiac side effects. Amlodipine has pediatric labeling and is available as a suspension, and doses need not to be adjusted to renal function. 73 74 74 Beta blockers can be used as second-line therapy for renal hypertension in children. However, they are contraindicated in asthma and can cause fatigue. All beta blockers require dose reduction with progression of CKD. They should be used with caution in heart failure, and their adverse metabolic effects make them less suitable for diabetics. The largest clinical experience, especially for infants, is available for propranolol. A sustained-release form of this drug allows once daily administration in larger children. However, other agents, such as atenolol, which have the advantage of being both long acting and β1-selective, may be preferred in clinical practice. Other drugs are used less commonly, mainly due to their more severe side-effects profiles. Alpha blockers (such as prazosin) can be used in patients who also require them for control of bladder emptying or Raynaud’s phenomenon. Centrally acting alpha agonists (such as clonidine) act via reduction of sympathetic nervous outflow. Rebound hypertension after discontinuation is a major problem of this drug. The vasodilators hydralazine and minoxidil are less suitable in CKD as they are less effective and cause salt and water retention. 42 47 46 70 Conclusion Adequate management of hypertension in CKD requires an active screening approach in order to prevent the significant renal deterioration and cardiovascular morbidity and mortality associated with high blood pressure. Owing to the plethora of different pathophysiological mechanisms involved, a whole range of therapeutic options is available. Non-pharmacological options should not be disregarded for obese children or for children on hemodialysis. Inhibitors of the renin–angiotensin system should be preferred for proteinuric patients and, probably, also for non-proteinuric patients. Multiple drug therapy is often necessary to reach target blood pressure below the 90th percentile. For this, diuretics and calcium channel blockers are the most suitable options.