Hypo-osmolar syndromes secondary to impaired water excretion.

Abstract

Impaired water diuresis, or the inability to excrete free water generated from endogenous or exogenous sources, is one of the commonest metabolic defects observed in the hospitalized patient. This defect is responsible for most of the hypo-osmolar or hyponatremic syndromes we observe. Excluding patients with chronic renal failure in whom impaired water excretion may re­ sult simply from the marked reduction in renal mass (1), we are left with the patient who fails to excrete water in adequate amounts despite a structurally intact kidney. This failure could be due to (a) an alteration in renal func­ tion which prevents the delivery of an adequate volume of water to the dilut­ ing segments of the nephron (ascending limb of the loop of Henle, distal con­ voluted and collecting tubules) (Table 1); (b) an abnormal permeability of these segments to water despite the absence of circulating antidiuretic hor­ mone (ADH, vasopressin), or a substance such as oxytocin (2,3) which, in high concentration, can mimic the effect of ADH on the nephron (such an ab­ normal permeability may be present in patients or animals with a deficiency of adrenal glucocorticoids, i.e., Cp F); (c) a sustained level of circulating anti­ diuretic material which causes an increased permeability to water of the dis­ tal convoluted tubule and collecting duct. Each of the above (a, b, and c) could make the urine more concentrated and low in volume than appropriate for given solute and water intake. thus resulting in abnormal water retention and hypo-osmolality of body fluids. While (b) may be confined to adrenal cortical insufficiency (4,5), (a) and (c) may frequently be present together and result in a greater impairment in water excretion than either alone (4, 6-8). In fact, all three may at times con­ tribute to the defect in water excretion almost invariably present in primary or secondary adrenal insufficiency (4,6--8). The abnormalities in renal func­ tion mentioned could prevent a necessary water diuresis, the urine being relatively low in volume and less hypotonic than it should be, and even mod­ erately hypertonic. Confronted with this situation one would be unable to determine whether the impaired diuresis was the result of an inappropriate circulating level of ADH or some other antidiuretic material [oxytocin (2,3),