Yung-Ming Chen, M.D.
Department of Internal Medicine, National Taiwan University Hospital

Primary hypertension is one of the leading causes for the development of
end-stage renal disease, second only to diabetes mellitus. Additionally, hypertension per se is the most controllable risk factor in the progression of chronic renal disease (CKD), regardless of etiology. In primary hypertension, about one third of patients have trivial injury in their kidneys. However, up to 30% of hypertensive patients never receive
appropriate evaluation of their renal functions. There are studies ndicating that progression of CKD can be retarded by tight control of blood pressure (BP). The consensus is to control BP in patients with CKD to below 130/80 mmHg. Some studies suggest a even lower BP target (eg., 125/75 mmHg) in patients with proteinuria (> 1.0 g/day).
The mechanisms of the progression of CKD are complex and not fully understood. Angiotensin II plays an important role in this complex rocess, through both hemodynamic and non-hemodynamic mechanisms. Angiotensin converting enzyme inhibitor (ACEi) and type 1 angiotensin II receptor blocker (ARB) have demonstrated favorable effects on the progression of both diabetic and non-diabetic kidney diseases. Although other antihypertensive drugs have no anti-proteinuric effect, their combinations with ACEi or ARB have shown synergistic beneficial effects on renal function.
There is no convincing evidence arguing against the use of ACEi or ARB in hypertensive patients with CKD. However, following the use of ACEi or ARB, a rise of serum creatinine level as much as 30 percent of baseline is acceptable and should not be deemed as a reason to withhold treatment. Measures to prevent hyperkalemia should be implemented in CKD patients treated with either ACEi or ARB.

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