Mechanisms and consequences of sympathetic hyperactivity in renal disease

Kidney impairment of different origins can lead within a short time to structural and functional maladaptations of the kidney, which may culminate in end-stage renal failure. The most common causes of chronic renal failure are due to hypertensive and diabetic renal impairment [Moore et al. 1999, Ritz et al. 1999]. Moreover, an inadequate blood pressure control in primary renal diseases further accelerates the decline of renal function. In spite of improved therapeutic measures the number of patients with chronic renal failure continues to increase dramatically [Mailloux and Haley 1998]. Cardiovascular morbidity and mortality in patients with chronic renal failure are extraordinarily high and are more frequent than that observed in the general population [Vita et al. 1999]. Measures, which can reduce the high incidence of cardiovascular complications, have priority in the treatment of chronic renal failure patients. ACE-inhibitors have been shown to be the best choice in this case. Until now a possible role for sympathetic hyperactivity has not been seriously considered although there is very good clinical and experimental evidence for such a role. This overview will give a summary of the currently known experimental and clinical findings about the role of the sympathetic nervous system in hypertension and renal disease and to expound possible therapeutic strategies.