The reno-protective role of AT(1)-receptor blockers.
In the 1970s and 1980s it became evident that progression of renal disease and blood pressure are correlated. Subsequently, it was shown that antihypertensive treatment, especially with agents that block the renin-angiotensin system (RAS), could slow the progression of diabetic renal disease. Several studies, particularly with RAS blockers, have confirmed beneficial effects on urinary albumin excretion in patients with diabetes and microalbuminuria or proteinuria. There are good reasons to explore dual blockade of the RAS with an AT(1)-receptor blocker and an ACE inhibitor. Receptor blockers may block the effects of angiotensin II more effectively than ACE inhibitors; moreover, ACE inhibitors increase bradykinins which may have positive effects on blood pressure and renal function. Such combination treatment has been found to be well tolerated and more effective in reducing blood pressure than either monotherapy. Positive effects on microalbuminuria or proteinuria have also been noted. Studies have shown that treatment with AT(1)-receptor blockers postpones end-stage renal disease and reduces the rate of decline in glomerular filtration rate (GFR) in patients with type 2 diabetes and nephropathy. Moreover, albuminuria was reduced to a greater extent with AT(1)-receptor blockers than with conventional antihypertensive therapy producing the same blood pressure reductions. In summary, AT(1)-receptor blockers are effective in all stages of diabetic renal disease, and have an excellent tolerability profile. Usually the side-effect profile is comparable with placebo. In certain situations, there may be a slight, readily reversible, increase in serum potassium. There may also be a slight reduction in GFR, reflecting a decrease in glomerular filtration pressure.
Aarhus University Hospital, Denmark. carl.erik.mogensen@afdm.au.dk
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D000419:Albuminuria / Q000209:etiology*; D057911:Angiotensin Receptor Antagonists; D019610:Cytoprotection; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy / Q000652:urine; D003928:Diabetic Nephropathies / Q000175:diagnosis; D006801:Humans; D007668:Kidney / Q000187:drug effects*; D011507:Proteinuria / Q000209:etiology; D044140:Receptor, Angiotensin, Type 1
D057911:Angiotensin Receptor Antagonists; D044140:Receptor, Angiotensin, Type 1