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.
Keywords: Aldosterone; Hyperkalemia; Hypokalemia; K+ channels.