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SODIUM

Disturbances of sodium concentration [Na+] result in most cases from abnormalities of H2O homeostasis, which change the relative ratio of Na+ to H2O. Disorders of Na+ balance per se are, in contrast, associated with changes in extracellular fluid volume, either hypo- or hypervolemia. Maintenance of the “effective circulating volume” is achieved in large part by changes in urinary sodium excretion, whereas H2O balance is achieved by changes in both H2O intake and urinary H2O excretion (Table 2-1). Confusion can result from the coexistence of defects in both H2O and Na+ balance. For example, a hypovolemic pt may have an appropriately low urinary Na+ due to increased renal tubular reabsorption of filtered NaCl; a concomitant increase in circulating arginine vasopressin (AVP)—part of the defense of effective circulating volume (Table 2-1)—will cause the renal retention of ingested H2O and the development of hyponatremia.

TABLE 2-1OSMOREGULATION VERSUS VOLUME REGULATION

HYPONATREMIA

This is defined as a serum [Na+] <135 mmol/L and is among the most common electrolyte abnormalities encountered in hospitalized pts. Symptoms include nausea, vomiting, confusion, lethargy, and disorientation; if severe (<120 mmol/L) and/or abrupt, seizures, central herniation, coma, or death may result (see Acute Symptomatic Hyponatremia, below). Hyponatremia is almost always the result of an increase in circulating AVP and/or increased renal sensitivity to AVP; a notable exception is in the setting of low solute intake (“beer potomania”), wherein a markedly reduced urinary solute excretion is inadequate to support the excretion of sufficient free H2O. The serum [Na+] by itself does not yield diagnostic information regarding total-body Na+ content; hyponatremia is primarily a disorder of H2O homeostasis. Pts with hyponatremia are thus categorized diagnostically into three groups, depending on their clinical volume status: hypovolemic, euvolemic, and hypervolemic hyponatremia (Fig. 2-1). All three forms of hyponatremia share an exaggerated, “nonosmotic” increase in circulating AVP, in the setting of reduced serum osmolality. Notably, hyponatremia is often multifactorial; clinically important nonosmotic stimuli that can cause a release of AVP and increase the risk of hyponatremia include drugs, pain, nausea, and strenuous exercise.

FIGURE 2-1

The diagnostic approach to hyponatremia. See text for details. [From S Kumar, T Berl: Diseases of water metabolism, in Atlas of Diseases of the Kidney, RW Schrier (ed). Philadelphia, Current Medicine, Inc, 1999; with permission.]

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