Guidi E, Menghetti D, Milani S, Montagnino G, Palazzi P, Bianchi G
Centro di Ricerca Clinica in Nefrologia e lpertensione Arteriosa, Ospedale Niguarda Ca'Granda, Milan, Italy.
J Am Soc Nephrol. 1996 Aug;7(8):1131-8. doi: 10.1681/ASN.V781131.
In several genetic hypertensive rat strains, transplantation studies have established that the kidney carries at least a portion of the genetic message for hypertension. In man it has, of course, been more difficult to obtain clearcut results. This historical prospective observational study, double-blinded for knowledge of donors' and recipients' family history for hypertension, concerns 85 transplanted patients, not treated with cyclosporine and with stable renal function, followed up for an average of 8 yr. Both the donors' and the recipients' families were carefully characterized for presence or absence of hypertension. After transplantation, in recipients without hypertension in their own families, a kidney coming from a "hypertensive" family determines less withdrawal and more introduction of antihypertensive therapy (AHT) than a kidney from a "normotensive" family (odds ratio for AHT introduction 5.0, confidence interval, 1.4 to 17.8; P = 0.017). In recipients with familial hypertension, the origin of the kidney does not influence the prevalence of hypertension after transplantation. More detailed analyses show that, in recipients without familial hypertension, the transplantation of a "hypertensive" kidney determines a tenfold larger increase in the requirement of antihypertensive therapy than the transplantation of a "normotensive" kidney, to obtain a similar blood pressure control (P = 0.003). This results is confirmed by the analysis of time-profile trends for antihypertensive therapy, adjusted for missing data, in the most clinically stable period (2nd to 10th yr after transplantation). The transmission of familial hypertension with the kidney is thus seen only in recipients coming from "normotensive" families, because a familial tendency for hypertension blunts the effect of receiving a "hypertensive" kidney.
在几种遗传性高血压大鼠品系中，移植研究已证实，肾脏携带了至少一部分高血压的遗传信息。当然，在人类中要获得明确的结果则更加困难。这项历史性前瞻性观察研究对捐赠者和接受者的高血压家族史进行了双盲处理，涉及85例移植患者，这些患者未接受环孢素治疗且肾功能稳定，平均随访8年。对捐赠者和接受者的家庭都仔细确定了是否存在高血压。移植后，在自身家庭中无高血压的接受者中，来自“高血压”家庭的肾脏比来自“正常血压”家庭的肾脏导致更少的降压治疗停药和更多的降压治疗引入（引入降压治疗的优势比为5.0，置信区间为1.4至17.8；P = 0.017）。在有家族性高血压的接受者中，肾脏的来源不影响移植后高血压的患病率。更详细的分析表明，在无家族性高血压的接受者中，为获得相似的血压控制，移植“高血压”肾脏比移植“正常血压”肾脏导致降压治疗需求增加的幅度大十倍（P = 0.003）。在最临床稳定期（移植后第2年至第10年），对降压治疗的时间趋势进行分析，并对缺失数据进行调整，证实了这一结果。因此，只有来自“正常血压”家庭的接受者中才出现肾脏传递家族性高血压的情况，因为高血压的家族倾向会削弱接受“高血压”肾脏的影响。
