Renal protection by antihypertensive drugs: insights from microalbuminuria studies.

摘要

During the last few years there has been a renewed interest in blood-pressure (BP)-induced kidney damage, owing to a progressive increase in the incidence and prevalence of hypertension and vascular diseases as a cause of end-stage renal disease (ESRD). The need to prevent ESRD demands continued efforts so as to identify early those people with hypertension who are at risk and to provide them with effective antihypertensive therapy. This review analyses what is needed in terms of surrogate endpoints for monitoring kidney damage and what is known about the impact of antihypertensive treatments in reducing the BP burden on the kidney in non-diabetic subjects. Although glomerular filtration rate (GFR) and proteinuria are useful surrogate endpoints for patients with nephropathy and GFR below or close to the threshold value for renal insufficiency, it is clear that monitoring changes in either GFR or proteinuria does not provide a sensitive endpoint for subjects with the mildest forms of renal disease, e.g. essential hypertensive patients who are at risk of developing kidney damage. In this case microalbuminuria may be useful, although unequivocal evidence demonstrating that microalbuminuria is a risk marker for developing renal insufficiency in non-diabetic renal diseases has not existed until now, and whether a decrease in microalbuminuria is of prognostic significance in patients with essential hypertension remains to be demonstrated. The beneficial effects of the antihypertensive agents on microalbuminuria are also proportional to BP reduction. If a large enough BP reduction is achieved there seem to be, at most, only minimal differences among the antihypertensive drug classes. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers have additional beneficial effects on microalbuminuria independent of the BP reduction, owing to their direct role in glomerular haemodynamics. The heterogeneity in the changes in urinary albumin excretion during antihypertensive treatment may be related to the different factors involved in the presence of microalbuminuria or structural end-organ damage, or both.