College of Medicine and Public Health and Medicine, Flinders University, Adelaide, South Australia, Australia.
Department of Renal Medicine, Flinders Medical Centre, Adelaide, South Australia, Australia.
Nephrology (Carlton). 2019 Dec;24(12):1225-1232. doi: 10.1111/nep.13578. Epub 2019 May 5.
Following surgical removal of one kidney, the other enlarges and increases its function. The mechanism for the sensing of this change and the growth is incompletely understood but begins within days and compensatory renal hypertrophy (CRH) is the dominant contributor to the growth. In many individuals undergoing nephrectomy for cancer or kidney donation this produces a substantial and helpful increase in renal function. Two main mechanisms have been proposed, one in which increased activity by the remaining kidney leads to hypertrophy, the second in which there is release of a kidney specific factor in response to a unilateral nephrectomy that initiates CRH. Whilst multiple growth factors and pathways such as the mTORC pathway have been implicated in experimental studies, their roles and the precise mechanism of CRH are not defined. Unrestrained hypoxia inducible factor activation in renal cancer promotes growth and may play an important role in driving CRH.
在切除一个肾脏后，另一个肾脏会增大并增加其功能。这种变化和生长的感知机制尚不完全清楚，但在几天内就开始了，代偿性肾肥大（CRH）是生长的主要贡献者。在许多因癌症或肾脏捐献而接受肾切除术的患者中，这会显著增加肾功能。有两种主要的机制被提出，一种是剩余肾脏的活动增加导致肥大，另一种是单侧肾切除后释放一种肾脏特异性因子，从而引发 CRH。虽然在实验研究中已经涉及多种生长因子和途径，如 mTORC 途径，但它们在 CRH 中的作用和确切机制尚不清楚。肾细胞癌中不受限制的缺氧诱导因子激活促进生长，可能在驱动 CRH 中发挥重要作用。
