Rump L C, Oberhauser V
Universitätsklinikum Freiburg.
MMW Fortschr Med. 1999 Nov 18;141(46):39-41.
Previous research in end stage renal failure has focused on the renin-angiotensin-system. Today, we know, that in chronic renal failure sympathetic overactivity plays a pivotal role for progression of the disease and overall prognosis. The unique finding is that the damaged kidneys send afferent nerve impulses to the central nervous system to increase efferent sympathetic discharge. Systemically this sympathetic overactivity contributes to hypertension and associated cardiovascular complications. Locally in the kidney neurotransmitter release is enhanced, which induces proliferation thereby promoting loss of renal function. Consequently, it has been shown that pharmacological inhibition of sympathetic nerve activity prevents glomerulosclerosis and ameliorates proteinuria in models of chronic renal failure. Thus, the pathomechanism of sympathetic overactivity is likely to open a new therapeutic avenue for the treatment of hypertensive chronic renal failure patients.
以往关于终末期肾衰竭的研究主要集中在肾素-血管紧张素系统。如今我们知道,在慢性肾衰竭中,交感神经过度活跃在疾病进展和总体预后中起着关键作用。独特的发现是,受损的肾脏会向中枢神经系统发送传入神经冲动,以增加传出交感神经放电。全身性的交感神经过度活跃会导致高血压及相关心血管并发症。在肾脏局部,神经递质释放增加,这会诱导增殖,从而促进肾功能丧失。因此,研究表明,在慢性肾衰竭模型中,药物抑制交感神经活动可预防肾小球硬化并改善蛋白尿。因此,交感神经过度活跃的发病机制可能为治疗高血压慢性肾衰竭患者开辟一条新的治疗途径。