Russell Peter Spencer, Hong Jiwon, Windsor John Albert, Itkin Maxim, Phillips Anthony Ronald John
Applied Surgery and Metabolism Laboratory, School of Biological Sciences, University of Auckland, Auckland, New Zealand.
Surgical and Translational Research Centre, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
Front Physiol. 2019 Mar 14;10:251. doi: 10.3389/fphys.2019.00251. eCollection 2019.
Renal lymphatics are abundant in the cortex of the normal kidney but have been largely neglected in discussions around renal diseases. They originate in the substance of the renal lobule as blind-ended initial capillaries, and can either follow the main arteries and veins toward the hilum, or penetrate the capsule to join capsular lymphatics. There are no valves present in interlobular lymphatics, which allows lymph formed in the cortex to exit the kidney in either direction. There are very few lymphatics present in the medulla. Lymph is formed from interstitial fluid in the cortex, and is largely composed of capillary filtrate, but also contains fluid reabsorbed from the tubules. The two main factors that contribute to renal lymph formation are interstitial fluid volume and intra-renal venous pressure. Renal lymphatic dysfunction, defined as a failure of renal lymphatics to adequately drain interstitial fluid, can occur by several mechanisms. Renal lymphatic inflow may be overwhelmed in the setting of raised venous pressure (e.g., cardiac failure) or increased capillary permeability (e.g., systemic inflammatory response syndrome). Similarly, renal lymphatic outflow, at the level of the terminal thoracic duct, may be impaired by raised central venous pressures. Renal lymphatic dysfunction, from any cause, results in renal interstitial edema. Beyond a certain point of edema, intra-renal collecting lymphatics may collapse, further impairing lymphatic drainage. Additionally, in an edematous, tense kidney, lymphatic vessels exiting the kidney via the capsule may become blocked at the exit point. The reciprocal negative influences between renal lymphatic dysfunction and renal interstitial edema are expected to decrease renal function due to pressure changes within the encapsulated kidney, and this mechanism may be important in several common renal conditions.
肾淋巴管在正常肾脏皮质中丰富，但在有关肾脏疾病的讨论中很大程度上被忽视了。它们起源于肾小叶实质内的盲端起始毛细血管，可跟随主要动静脉朝向肾门，或穿透肾包膜与包膜淋巴管相连。小叶间淋巴管中没有瓣膜，这使得皮质中形成的淋巴液能够双向流出肾脏。髓质中存在的淋巴管很少。淋巴液由皮质中的组织液形成，主要由毛细血管滤过液组成，但也含有从肾小管重吸收的液体。促成肾淋巴液形成的两个主要因素是组织液量和肾内静脉压。肾淋巴管功能障碍定义为肾淋巴管无法充分引流组织液，可通过多种机制发生。在静脉压升高（如心力衰竭）或毛细血管通透性增加（如全身炎症反应综合征）的情况下，肾淋巴液流入可能不堪重负。同样，在终末胸导管水平，肾淋巴液流出可能因中心静脉压升高而受损。任何原因引起的肾淋巴管功能障碍都会导致肾间质水肿。超过一定程度的水肿后，肾内集合淋巴管可能会塌陷，进一步损害淋巴引流。此外，在水肿、紧张的肾脏中，通过包膜离开肾脏的淋巴管可能在出口处受阻。肾淋巴管功能障碍和肾间质水肿之间的相互负面影响预计会因包膜内肾脏压力变化而降低肾功能，这种机制在几种常见的肾脏疾病中可能很重要。
