Fredrick V Osorio Stuart L Linas

Potassium, the most abundant cation in the human body, regulates intracellular enzyme function and neuromuscular tissue excitability. Serum potassium is normally maintained within the narrow range of 3.5 to 5.5 mEq/L. The intracellular-extracellular potassium ratio (Kj/Ke) largely determines neuromuscular tissue excitability [1]. Because only a small portion of potassium is extracellular, neuromuscular tissue excitability is markedly affected by small changes in extracellular potassium. Thus, the body has developed elaborate regulatory mechanisms to maintain potassium homeostasis. Because dietary potassium intake is sporadic and it cannot be rapidly excreted renally, short-term potassium homeostasis occurs via trans-cellular potassium shifts [2]. Ultimately, long-term maintenance of potassium balance depends on renal excretion of ingested potassium. The illustrations in this chapter review normal transcellular potassium homeostasis as well as mechanisms of renal potassium excretion.

With an understanding of normal potassium balance, disorders of potassium metabolism can be grouped into those that are due to altered intake, altered excretion, and abnormal transcellular distribution. The diagnostic algorithms that follow allow the reader to limit the potential causes of hyperkalemia and hypokalemia and to reach a diagnosis as efficiently as possible. Finally, clinical manifestations of disorders of potassium metabolism are reviewed, and treatment algorithms for hypokalemia and hyperkalemia are offered.

Recently, the molecular defects responsible for a variety of diseases associated with disordered potassium metabolism have been discovered [3-8]. Hypokalemia and Liddle's syndrome [3] and hyperkalemia and pseudohypoaldosteronism type I [4] result from mutations at different sites on the epithelial sodium channel in the distal tubules. The hypokalemia of Bartter's syndrome can be accounted for by two separate ion transporter defects in the thick ascending limb of Henle's loop [5]. Gitelman's syndrome, a clinical variant of Bartter's

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