Brenner B M, Garcia D L, Anderson S
Renal Division, Brigham and Women's Hospital, Boston, MA 02115.
Am J Hypertens. 1988 Oct;1(4 Pt 1):335-47. doi: 10.1093/ajh/1.4.335.
A primary role for the kidney in the initiation and maintenance of hypertension has long been recognized, but the pathogenetic interactions among renal hemodynamics, hormonal and hereditary factors, and dietary sodium intake remain enigmatic. Reduction in filtration surface area, whether acquired in the course of intrinsic renal disease or after surgical renal ablation, leads to systemic hypertension as well as to progressive renal insufficiency, sequellae made even more severe by dietary sodium excess. Moreover, hypertension and progressive renal disease eventuate in some individuals born with a solitary kidney, as well as in those with more severe degrees of dysgenesis (ie, oligomeganephronia). Hypertension is also commonly observed in certain inbred rat strains in which filtration surface area is congenitally deficient. Based on these and other lines of evidence reviewed herein, we postulate that a renal abnormality that contributes to essential hypertension in the general population is a reduced number of nephrons. The consequences of this abnormality are limitations in the ability to excrete sodium and thus, salt-sensitive hypertension. Finally, congenital variability in filtration surface area may explain why only some, but not all, patients exposed to potentially injurious renal stimuli eventually manifest chronic nephropathy. This may also account for the susceptibility of subsets of Type I and Type II diabetics to develop overt glomerulopathy.
肾脏在高血压的引发和维持中所起的主要作用早已得到认可，但肾脏血流动力学、激素和遗传因素以及饮食中钠摄入之间的致病相互作用仍然是个谜。滤过表面积的减少，无论是在原发性肾脏疾病过程中获得的，还是在肾脏手术切除后出现的，都会导致系统性高血压以及进行性肾功能不全，而饮食中钠过量会使这些后遗症更加严重。此外，高血压和进行性肾脏疾病也会在一些先天性单肾个体以及发育不全程度更严重（即肾单位过少）的个体中出现。在某些先天性滤过表面积不足的近交系大鼠中也普遍观察到高血压。基于本文所回顾的这些及其他证据，我们推测，导致普通人群原发性高血压的肾脏异常是肾单位数量减少。这种异常的后果是排钠能力受限，从而导致盐敏感性高血压。最后，滤过表面积的先天性差异或许可以解释为什么只有部分而非所有受到潜在有害肾脏刺激的患者最终会出现慢性肾病。这也可能解释了Ⅰ型和Ⅱ型糖尿病患者亚组易发生明显肾小球病变的原因。
