Chapter 36 - Hyponatremia

Editor

R. J. Alpern, M. J. Caplan, O. W. Moe, & S. E. Quaggin

Department

Medicine

Additional Department

Nephrology

Document Type

Book Chapter

Publication Title

Seldin and Giebisch's The Kidney: Physiology and Pathophysiology

Abstract

Sodium and its accompanying anions are the principal osmotically active solutes in extracellular fluid. Hyponatremia (a low plasma sodium concentration) is usually associated with hypoosmolality and dilution of all body fluids. Because sodium is an effective osmole that does not readily cross cell membranes its concentration in plasma determines plasma tonicity. Hypotonicity makes cells swell and hypertonicity makes them shrink. Hyponatremia is normally prevented by regulation of water exretion. The antidiuretic hormone, arginine vasopressin, controls water excretion by the kidneys. Vasopresin secretion should normally be supressed when plasma sodium falls below 135 mEq/L, allowing excess water to be excreted. Hypotonic hyponatremia can only occur if water excretion is impaired (often because of failure to suppress vasopressin secretion) or overwhelmed. An acute onset of hyponatremia causes cerebral edema which results in severe neurological symptoms and sometimes death from brain herniation. Given time, the brain adapts, minimizing brain cell swelling. As a result of this adaptation, neurological symptoms of chronic hyponatremia (evolving over two days or more) are less severe; correcting chronic hyponatremia too rapidly can result in brain damage due to osmotic demyelination.

First Page

1335

Last Page

1367

DOI

10.1016/B978-0-12-815389-5.00069-1

Publication Date

5-22-2026

Publisher

Academic Press

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