Hyperkalemia: An adaptive response in chronic renal insufficiency
Hyperkalemia: An adaptive response in chronic renal insufficiency
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DOI：
10.1046/j.1523-1755.2002.00350.x
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发表时间：
2002-07-01
影响因子：
19.6
通讯作者：
Segal, AS
中科院分区：
文献类型：
--
作者：
Gennari, FJ;Segal, AS
背景。高钾血症是慢性肾功能不全的共同特征，通常归因于K+稳态受损。然而，各种实验观察表明，细胞外[K+]的增加实际上以一种稳态的方式起作用。直接刺激肾K+排泄的作用是独立的。方法：我们回顾了在实验动物和人类受试者中有关K+排泄调节及其与血浆[K+]关系的相关研究。研究表明：(1)肾功能不全患者的细胞外[K+]与细胞内K+含量直接相关，(2)高钾血症通过增加根尖和基底外侧膜导率直接促进集管主要细胞的K+分泌。高钾血症的影响不同于醛固酮，因为钾离子电导增加是主要事件。高钾血症引起的主要细胞功能和结构的变化与适应高钾饮食的影响难以区分。我们认为高钾血症通过刺激K+排泄在肾功能不全的钾稳态中起关键作用。在慢性肾功能不全患者中，细胞外[K+]上升到刺激K-排泄所需的水平，使其再次与摄入相匹配，从而形成一个新的稳定状态。当达到这种新的稳定状态时，血浆[K+]保持稳定，除非饮食摄入增加，肾小球滤过率下降。或者药物会破坏新的平衡。
Background. Hyperkalemia is a common feature of chronic renal insufficiency, usually ascribed to impaired K+ homeostasis. However, various experimental observations suggest that the increase in extracellular [K+] actually functions in a homeostatic fashion. directly stimulating renal K+ excretion through an effect that is independent of. and additive to, aldosterone.Methods. We have reviewed relevant studies in experimental animals and in human subjects that have examined the regulation of K+ excretion and its relation to plasma [K+].Results. Studies indicate that (1) extracellular [K+] in patients with renal insufficiency correlates directly with intracellular K+ content, and (2) hyperkalemia directly promotes K+ secretion in the principal cells of the collecting duct by increasing apical and basolateral membrane conductances. The effect of hyperkalemia differs from that of aldosterone in that K+ conductances are increased as the primary event. The changes in principal cell function and structure induced by hyperkalemia are indistinguishable from the effects seen in adaptation to a high K+ diet.Conclusions. We propose that hyperkalemia plays a pivotal role in K- homeostasis in renal insufficiency by stimulating K+ excretion. In patients with chronic renal insufficiency, a new steady state develops in which extracellular [K+] rises to the level needed to stimulate K- excretion so that it again matches intake. When this new steady state is achieved, plasma [K+] remains stable unless dietary intake increases, glomerular filtration rate falls. or drugs are given that disrupt the new balance.