Achieving optimal blood pressure and
albuminuria control is a major therapeutic treatment goal in patients with
renal insufficiency.
Angiotensin-converting enzyme-inhibitors (ACEIs) and
angiotensin-receptor blockers (ARB) are the mainstay of
therapy in these patients. However, despite these
therapies many patients remain at high risk of renal or
cardiovascular disease that shows a relationship with
albuminuria. Various approaches have been tested to maximize the efficacy of ACEI and ARB. Increasing the dose of an ACEI or ARB beyond the maximal registered
antihypertensive dose causes a distinct decrease in
albuminuria without additional effects on blood pressure. The combination of an ACEI and ARB is another possibility to further reduce
albuminuria. However, the alleged beneficial effects on hard renal and cardiovascular outcome are not unambiguously demonstrated. Adding a
direct renin inhibitor to an ACEI or ARB has been shown to lower
albuminuria in patients with and without diabetes. Long-term trials are currently under way to determine the effects of direct
renin inhibition on clinical outcomes. Volume excess has been shown to blunt the blood pressure and
albuminuria response to ACEI or ARB
therapy. Intervening in volume status by means of restricting
dietary sodium intake or
diuretic therapy has convincingly been shown to lower blood pressure and
albuminuria. Whether this strategy translates into a reduction in the risk of renal or cardiovascular events has not (yet) been investigated in prospective randomized trials. Various options are at hand which have been shown to maximize the blood pressure and
albuminuria response to ACEI and ARB treatment. However, long-term studies supporting the benefits of these strategies on hard renal and cardiovascular outcomes are warranted.