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

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Abstract

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 β-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, β-blockers, with their adverse effect on CV risk profile, should be avoided. Controlled prospective evidence for renoprotection by β-blockers in nondiabetic CKD with hard end points is lacking, but renoprotection by antihypertensive agents was first documented by administering β-blockers in patients with diabetic nephropathy. Renoprotection by β-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 β-blockers: in CKD often four or more different antihypertensive drugs are required and cardiac indications are frequent.

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Ritz, E., Rump, L.C. Do β-blockers combined with RAS inhibitors make sense after all to protect against renal injury?. Current Science Inc 9, 409–414 (2007). https://doi.org/10.1007/s11906-007-0075-6

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