According to its definition (chapter 14.2), the diagnosis of hypervasopressinism rests ultimately on the demonstration that vasopressin is present in plasma and urine in the face of hyponatremia and hypotonicity of body fluids. Consequently if a patient does not have hyponatremia it is impossible to either diagnose or exclude hypervasopressinism. If a patient, in whom excessive AVP secretion is suspected, is given “water loads” and these loads are retained in body fluid compartments producing hyponatremia instead of being normally lost via urine hypervasopressinism is likely. The definitive proof depends on the demonstration that plasma or urinary vasopressin remains inappropriately high for the degree of hypotonicity produced. This approach is adequate to investigate the causes of hypervasopressinism in experimental work as well as in closely controlled clinical investigations. It is obvious however that a similar approach is undesirable in routine clinical practice because of the risk of severe induced hyponatremia. On the other hand, the knowledge derived from animal studies and clinical investigations may have direct therapeutic implications. It increases the ability of the clinician to anticipate vasopressin-mediated. water retention and by judicious administration of free-water and monitoring of serum sodium concentration to prevent the development of severe plasma hypotonicity.
KeywordsSerum Sodium Concentration Body Fluid Compartment Effective Arterial Blood Volume Renal Water Excretion Inappropriate Antidiuresis
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