Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines

Abstract

Hyponatremia is a common water balance disorder that often poses a diagnostic or therapeutic challenge. Therefore, guidelines were developed by professional organizations, one from within the United States (2013) and one from within Europe (2014). This review discusses the diagnosis and treatment of hyponatremia, comparing the two guidelines and highlighting recent developments. Diagnostically, the initial step is to differentiate hypotonic from nonhypotonic hyponatremia. Hypotonic hyponatremia is further differentiated on the basis of urine osmolality, urine sodium level, and volume status. Recently identified parameters, including fractional uric acid excretion and plasma copeptin concentration, may further improve the diagnostic approach. The treatment for hyponatremia is chosen on the basis of duration and symptoms. For acute or severely symptomatic hyponatremia, both guidelines adopted the approach of giving a bolus of hypertonic saline. Although fluid restriction remains the first-line treatment for most forms of chronic hyponatremia, therapy to increase renal free water excretion is often necessary. Vasopressin receptor antagonists, urea, and loop diuretics serve this purpose, but received different recommendations in the two guidelines. Such discrepancies may relate to different interpretations of the limited evidence or differences in guideline methodology. Nevertheless, the development of guidelines has been important in advancing this evolving field.

Keywords: cerebral edema; copeptin; osmotic demyelination syndrome; urea; vasopressin; vasopressin receptor antagonist.

Copyright © 2017 by the American Society of Nephrology.

Figures

Figure 1.

Diagnostic algorithm for hyponatremia. Based on the European guideline. ECF, extracellular fluid.

Figure 2.

Copeptin-based classification of five subtypes of the syndrome of inappropriate antidiuresis (SIAD). The shaded gray area and the black dashed line show the normal physiologic relationship between serum osmolality and plasma copeptin (as surrogate marker for vasopressin). In SIAD type B this relationship is intact, but the osmotic threshold for vasopressin release has decreased. In SIAD types A and C vasopressin release is no longer regulated by serum osmolality. In SIAD type D plasma copeptin levels are undetectable. In SIAD type E the normal relationship between serum osmolality and copeptin has reversed. This phenomenon has been coined “barostat reset,” as it may indicate increased sensitivity of baroreceptors to increased vasopressin release. Percentages indicate how often each subtype was present in one study of 50 patients. Data on the basis of Fenske et al. and figure modified from Fenske et al. with permission.