Do beta-blockers combined with RAS inhibitors make sense after all to protect against renal injury?

In chronic kidney disease (CKD) sympathetic overactivity is stimulated by signals from the diseased kidney activating hypothalamic centers. In addition, breakdown of circulating catecholamines is decreased. Indications for beta-blockers are cardio- and renoprotection. Cardioprotection is important because cardiovascular (CV) death is two- to 20-fold more likely in CKD than end-stage kidney disease; consequently, beta-blockers, with their adverse effect on CV risk profile, should be avoided. Controlled prospective evidence for renoprotection by beta-blockers in nondiabetic CKD with hard end points is lacking, but renoprotection by antihypertensive agents was first documented by administering beta-blockers in patients with diabetic nephropathy. Renoprotection by beta-blockers was seen experimentally. Furthermore, controlled studies documented a beneficial effect on albuminuria as a surrogate marker for renoprotection in diabetic and nondiabetic patients. Renin-angiotensin system blockade is the undoubted first-line treatment in CKD. Several points argue for ancillary treatment with beta-blockers: in CKD often four or more different antihypertensive drugs are required and cardiac indications are frequent.