Kanzaki Go, Tsuboi Nobuo, Haruhara Kotaro, Koike Kentaro, Ogura Makoto, Shimizu Akira, Yokoo Takashi
Division of Nephrology and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Department of Analytic Human Pathology, Nippon Medical School, Tokyo, Japan.
Hypertens Res. 2015 Oct;38(10):633-41. doi: 10.1038/hr.2015.67. Epub 2015 Jun 18.
It has been reported that there is substantial variation in the nephron number between individuals. Previous studies using autopsy kidneys have demonstrated that a low nephron number, in relation to a low birth weight, may result in hypertension (HTN) and/or chronic kidney disease (CKD). However, recent studies have revealed that the association between a low nephron number and HTN is not a universal finding. This observation indicates that a low nephron number is unlikely to be the sole factor contributing to an elevated blood pressure. In addition to the nephron number, various genetic and congenital factors may contribute to increased susceptibility to HTN and/or CKD in a complex manner. Acquired factors, including aging, obesity and related metabolic abnormalities, and various causes of renal injury, may additionally promote further nephron loss. Such a vicious cycle may induce HTN and/or CKD via the common mechanisms of renal hemodynamic maladaptation.
据报道，个体之间的肾单位数量存在显著差异。以往使用尸检肾脏的研究表明，相对于低出生体重，低肾单位数量可能导致高血压（HTN）和/或慢性肾脏病（CKD）。然而，最近的研究表明，低肾单位数量与高血压之间的关联并非普遍存在。这一观察结果表明，低肾单位数量不太可能是导致血压升高的唯一因素。除了肾单位数量外，各种遗传和先天性因素可能以复杂的方式增加患高血压和/或慢性肾脏病的易感性。包括衰老、肥胖及相关代谢异常以及各种肾损伤原因在内的后天因素，可能会进一步促使肾单位丢失。这样的恶性循环可能通过肾血流动力学适应不良的共同机制诱发高血压和/或慢性肾脏病。
