Hypertensive nephropathy: is a more physiologic approach to blood pressure control an important concern for the...

During the past 2 decades, there have been important reductions in stroke-related morbidity and mortality due to better control of hypertension. However, there has been a lesser effect on the reduction of coronary mortality and far less of an impact on all other forms of noncardiovascular disorders such as renal disease. This suggests that our ability to prevent hypertensive nephrosclerosis through traditional methods of lowering blood pressure may not be as effective as was once thought, particularly in high-risk patients such as blacks, diabetics, the elderly, and patients with preexisting renal disease. One reason that may partially explain the difficulty in protecting the renal circulation from hypertensive damage is the interaction between antihypertensive medications and the aged-related decline in renal perfusion. Depending on their mechanism of action, antihypertensive agents may impair renal blood flow (through plasma volume contraction or reduction) and further aggravate the age-related decline in renal perfusion. A worsening of renal perfusion may activate counterregulatory neurohormonal mechanisms, such as the renin-angiotensin-aldosterone system, which in turn may place the patient at increased risk for the development of glomerulosclerosis through promotion of vascular or mesangial hypertrophic changes or increased intraglomerular pressure, despite an associated reduction in systemic blood pressure. Since antihypertensive agents have such varied effects on systemic and renal hemodynamics, an understanding of the antihypertensive actions in a given patient may have significant influence on renal function. Thus, an improved understanding about the effects of aging and hypertension on the renal microcirculation will hopefully facilitate a more physiologically appropriate antihypertensive medication selection with the expectation that renal function will be benefitted over the long term.