Figure 129

Pathogenesis of hypernatremia. The renal concentrating mechanism is the first line of defense against water depletion and hyper-osmolality. When renal concentration is impaired, thirst becomes a very effective mechanism for preventing further increases in serum osmolality. The components of the normal urine concentrating mechanism are shown in Figure 1-2. Hypernatremia results from disturbances in the renal concentrating mechanism. This occurs in interstitial renal disease, with administration of loop and osmotic diuretics, and with protein malnutrition, in which less urea is available to generate the medullary interstitial tonicity.

Hypernatremia usually occurs only when hypotonic fluid losses occur in combination with a disturbance in water intake, typically in elders with altered consciousness, in infants with inadequate access to water, and, rarely, with primary disturbances of thirst [24]. GFR—glomerular filtration rate; ADH—antidiuretic hormone; DI—diabetes insipidus.

Hypernatremia Algorithm

Diagnostic algorithm for hypernatremia. As for hyponatremia, the initial evaluation of the patient with hypernatremia involves assessment of volume status. Patients with hypovolemic hypernatremia lose both sodium and water, but relatively more water. On physical examination, they exhibit signs of hypovolemia. The causes listed reflect principally hypotonic water losses from the kidneys or the gastrointestinal tract.

Euvolemic hyponatremia reflects water losses accompanied by inadequate water intake. Since such hypodipsia is uncommon, hyperna-tremia usually supervenes in persons who have no access to water or who have a neurologic deficit that impairs thirst perception—the very young and the very old. Extrarenal water loss occurs from the skin and respiratory tract, in febrile or other hypermetabolic states. Very high urine osmolality reflects an intact osmoreceptor-antidiuretic hormone-renal response. Thus, the defense against the development of hyperosmolality requires appropriate stimulation of thirst and the ability to respond by drinking water. The urine sodium (UNa) value varies with the sodium intake. The renal water losses that lead to euvolemic hypernatremia are a consequence of either a defect in vasopressin production or release (central diabetes insipidus) or failure of the collecting duct to respond to the hormone (nephrogenic diabetes insipidus) [23]. (Modified from Halterman and Berl [12]; with permission.)

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