4.5 Review

Potassium: From Physiology to Clinical Implications

Journal

KIDNEY DISEASES
Volume 2, Issue 2, Pages 72-79

Publisher

KARGER
DOI: 10.1159/000446268

Keywords

Hypokalemia; Hyperkalemia; K+ channels; Aldosterone

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Background: Potassium (K+) is the major intracellular cation, with 98% of the total pool being located in the cells at a concentration of 140-150 mmol/l, and only 2% in the extracellular fluid, where it ranges between 3.5 and 5 mmol/l. A fine regulation of the intracellular-extracellular gradient is crucial for life, as it is the main determinant of membrane voltage; in fact, acute changes of K+ plasma levels may have fatal consequences. Summary: An integrated system including an 'internal' and 'external' control prevents significant fluctuations of plasma levels in conditions of K+ loading and depletion. The internal control regulates the intra-extracellular shift, a temporary mechanism able to maintain a constant K+ plasma concentration without changing the total amount of body K+. The external control is responsible for the excretion of the ingested K+, and it has the kidney as the major player. The kidney excretes nearly 90% of the daily intake. Along the proximal tubule and the thick ascending limb on Henle's loop, the amount of K+ reabsorption is quite fixed (about 80-90%); conversely, the distal nephron has the ability to adjust K+ excretion in accordance with homeostatic needs. The present review analyzes: (1) the main molecular mechanisms mediating K+ reabsorption and secretion along the nephron; (2) the pathophysiology of the principal K+ derangements due to renal dysfunction, and (3) the effect of ingested K+ on blood pressure and renal electrolyte handling. Key Messages: Maintaining plasma K+ levels in a tight range is crucial for life; thus, multiple factors are implicated in K+ homeostasis, including kidney function. Recent studies have suggested that K+ plasma levels, in turn, affect renal salt absorption in animal models; this effect may underlie the reduction of blood pressure observed in hypertensive subjects under K+ supplementation. (C) 2016 S. Karger AG, Basel

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