Response to Sympathetic Hyperactivity in Hypertensive Chronic Kidney Disease Patients Is Reduced During Standard Treatment
We thank Schlaich et al1 for their comment. We fully agree that the pathogenesis may vary in the various disease conditions known to have sympathetic hyperactivity. Essential hypertension is a heterogenous condition. Indeed, apart from their studies, several other investigators have shown that angiotensin-converting enzyme inhibitor and/or angiotensin II antagonists have little or no effect on sympathetic activity in essential hypertensive patients.2–4 On the other hand, the landmark article by Converse et al,5 in which they show that dialysis patients with their native kidneys still present have high muscle sympathetic nerve activity, whereas bilaterally nephrectomized dialysis patients have muscle sympathetic nerve activity comparable to control subjects, provides definite proof that the diseased kidneys are critically involved in the pathogenesis of sympathetic hyperactivity. Experimental evidence has shown that already limited kidney damage, not necessarily affecting kidney function, can result in sympathetic activation.6 We put forward that, apart from chronic kidney disease, such a condition of (limited) kidney damage may be present in many disease states, resulting in activation of both the renin and the sympathetic system.