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 “arterial circulatory integrity” is achieved in large part by changes in urinary sodium excretion and vascular tone, whereas H₂O balance is achieved by changes in both H₂O intake and urinary H₂O excretion (Table 1-1). 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 1-1)—will cause the renal retention of ingested H₂O and the development of hyponatremia.