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Hyperkalemia: An adaptive response in chronic renal insufficiency Gennari FJ; Segal ASKidney Int 2002[Jul]; 62 (1): 1-9BACKGROUND: 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.|Adaptation, Physiological[MESH]|Aldosterone/pharmacology[MESH]|Animals[MESH]|Homeostasis[MESH]|Humans[MESH]|Hyperkalemia/*metabolism[MESH]|Kidney Failure, Chronic/*metabolism[MESH]|Kidney/metabolism[MESH]|Potassium/metabolism[MESH]|Sodium-Potassium-Exchanging ATPase/metabolism[MESH] |
