Essential Hypernatremia: Is There such a Thing?

Man S. Oh, MD, Department of Medicine, SUNY, Health Science Center at Brooklyn, 450 Clarkson Ave, Brooklyn, NY 11203 (USA) Louis Welt [1], in an editorial related to the case of a hypematremic child with a thirst defect, first reported by Avioli et al. [2], proposed the term essential hypernatremia. He defined the term as: upward resetting of the osmostat for ADH release, maintenance of the ability to dilute the urine at higher than normal serum sodium concentration, and the absence of volume depletion. Welt reasoned that the only actual abnormality in this condition was regulation of ADH release at higher than usual extracellular osmolality, and that all other functions, especially renal function, were normal. He predicted that effective vascular volume in essential hypernatremia must be normal. A number of investigators doubt the existence of upward resetting of the osmostat, preferring the interpretation that what appears to be the upward resetting of the osmoreceptor actually represents destruction of osmoreceptor cells [3,4]. The purpose of this communication is not to argue whether upward resetting does occur but to propose that even if upward resetting did occur, the absence of volume depletion would not be an expected finding. The argument hinges on the role of serum sodium concentration as a determinant of renal sodium excretion [5, 6], a factor ignored in Welt’s formulation. This discussion will explain why serum sodium concentration is a predictor of effective vascular volume in chronic hyperand hyponatremia. Most observers believe that a patient with diabetes in-sipidus who develops hypernatremia because of inadequate treatment would be dehydrated, and that the degree of dehydration would be positively correlated to the degree of hypernatremia. Yet, in the case of hypematremic patients with upward resetting of the osmostat, these observers predict a normal effective vascular volume [7-11]. The following case illustration will make it clear that volume depletion must accompany any hypernatremia when the kidney is functioning normally. Let us suppose that a patient with combined central diabetes insipidus and defective thirst is being treated with pitressin, and that he maintains normal serum sodium and normal effective vascular volume. Let the patient then develop hypernatremia because of insufficient pitressin dosage, receive pitressin when serum sodium rises to a level above 170 mEq/1, and receive no more drug when serum sodium returns to 170 mEq/1. This situation would be a physiological duplicate of upward resetting of the osmostat, and hypernatremia in both situations would be due initially to water deficit. The patient would be volume depleted, and the kidneys would retain sodium in response to volume depletion. However, renal sodium retention would stop before volume was restored to normal because hypernatremia itself