Hypertension with co-existing renal disease.

It is generally accepted that treatment of systemic hypertension protects the kidney from haemodynamically-mediated injury. However, renal function may deteriorate during traditional antihypertensive therapy. Currently, hypertensive nephrosclerosis accounts for approximately 26% of all end-stage renal disease (ESRD) in the United States. Furthermore, in spite of aggressive treatment of hypertension, there is no evidence of a reduction in the incidence of hypertensive nephrosclerosis as a cause of ESRD. A current hypothesis states that renal protection is dependent on control of systemic hypertension (when present), and control of glomerular hypertension (when present). Since angiotensin II is a potent vasoconstrictor of the postglomerular capillary bed, which increases glomerular capillary pressure, it is attractive to hypothesize that drug therapies which can interrupt the intrarenal generation of angiotensin II (ACE inhibitors), or drug therapies which may attenuate the intrarenal actions of angiotensin II (calcium antagonists), may be renal protective. ACE inhibitors do control both systemic and glomerular hypertension. Calcium antagonists do control systemic hypertension; they may control glomerular hypertension. Long-term clinical trials in hypertensive patients, comparing the renal effects of ACE inhibitors with other antihypertensive drug classes (including calcium antagonists), have not been reported. It remains to be determined if the potential differing effects of antihypertensive drug classes on the renal microcirculation do, or do not, translate into differing renal protective advantages to patients at risk for the development and/or progression of renal disease.