Rettig R, Schmitt B, Pelzl B, Speck T
J Hypertens. 1993 Sep;11(9):883-91. doi: 10.1097/00004872-199309000-00001.
In clinical renal transplantation studies, recipients of a renal graft from a donor with a genetic predisposition to hypertension had higher blood pressures and required more antihypertensive treatment than recipients of a renal graft from a normotensive donor. In addition, blood pressure normalization in patients suffering from essential hypertension by bilateral nephrectomy and subsequent transplantation of a kidney from a normotensive donor has been reported. The interpretation of these data may be limited by the large number of different factors that can contribute to post-transplantation hypertension in human renal transplant recipients.
In experimental renal transplantation studies the contribution of individual factors to post-transplantation hypertension can be independently assessed. Besides immunological graft rejection and hypertension-induced damage to the renal graft, a genetic predisposition to hypertension in the kidney donor has been demonstrated to be associated with post-transplantation hypertension in the recipient. Thus, normotensive recipients of a renal graft from a genetically hypertensive donor consistently developed post-transplantation hypertension in four different animal models of genetic hypertension. Furthermore, in genetically hypertensive rats bilateral nephrectomy together with transplantation of a kidney from a normotensive donor has been shown to be associated with a decrease in blood pressure.
Hypertension following renal transplantation may be due to a variety of factors, including immunological graft rejection, hypertension-induced damage to the renal transplant and a genetic predisposition to hypertension of the kidney donor. The finding that blood pressure is transplanted with the renal graft in genetic hypertension suggests a genetically determined alteration to the kidney as a major factor in the aetiology of primary hypertension. The nature of this factor is just beginning to be understood. Renal transplantation studies in rat models of genetic hypertension, combined with the tools of molecular biology, may help to provide further insights into the role of the kidney in primary hypertension.
在临床肾移植研究中,接受来自有高血压遗传易感性供体的肾移植受者,比接受来自血压正常供体的肾移植受者血压更高,且需要更多的抗高血压治疗。此外,有报道称,原发性高血压患者通过双侧肾切除并随后移植来自血压正常供体的肾脏后,血压恢复正常。这些数据的解读可能受到大量不同因素的限制,这些因素可导致人类肾移植受者移植后高血压。
在实验性肾移植研究中,可以独立评估个体因素对移植后高血压的影响。除了免疫性移植排斥和高血压对肾移植造成的损害外,已证明肾供体的高血压遗传易感性与受者移植后高血压有关。因此,在四种不同的遗传性高血压动物模型中,来自遗传性高血压供体的肾移植血压正常的受者持续出现移植后高血压。此外,在遗传性高血压大鼠中,双侧肾切除并移植来自血压正常供体的肾脏已被证明与血压降低有关。
肾移植后高血压可能由多种因素引起,包括免疫性移植排斥、高血压对肾移植的损害以及肾供体的高血压遗传易感性。在遗传性高血压中,血压随肾移植而转移这一发现表明,肾脏的基因决定改变是原发性高血压病因中的一个主要因素。这个因素的本质才刚刚开始被理解。在遗传性高血压大鼠模型中的肾移植研究,结合分子生物学工具,可能有助于进一步深入了解肾脏在原发性高血压中的作用。