The role of antihypertensive agents in preventing hypertensive glomerular damage

Hypertension is a major cause of chronic renal failure. During the last decade, we have learned that not only systemic blood pressure but probably also intrarenal, hemodynamic, and nonhemodynamic factors are involved in the progression of hypertensive renal damage. Despite better control of hypertension and a decrease in the incidence of strokes and coronary artery disease, hypertensive nephropathy has increased as a cause of end-stage renal failure. Tight control of blood pressure effectively preserves renal function, but there seems to be a level of diastolic blood pressure below which no additional benefits are obtained. However, specific hemodynamic and nonhemodynamic effects of certain antihypertensive agents, namely the calcium channel blockers and, particularly, the angiotensin-converting enzyme inhibitors, may provide additional protection that would more effectively prevent hypertensive nephropathy or significantly slow its progression. A combination of calcium channel blockers and angiotensin-converting enzyme inhibitors may in the end be found to provide the best results. Comparative long-term trials of the agents, examining their effects on the evolution of glomerular filtration rate and renal histology, are needed to help clarify the agents' role.