Role of Antidiuretic Hormone in Hyponatremia in Patients with Isolated Adrenocorticotropic Hormone Deficiency.

Abstract

Abstract.We found symptomatic hyponatremia in four elderly patients in which serum sodium (Na) levels ranged from 101 to 122 mEq/l. All 4 patients had low levels of plasma adrenocorticotropic hormone (ACTH), serum cortisol, and urinary excretion of 17-OHCS, and poor responses of ACTH to exogenous insulin and antidiuretic hormone (ADH). Other pituitary hormones were all normal. They were therefore diagnosed as having isolated ACTH deficiency. Plasma ADH was relatively high despite hypoosmolality which was associated with the hyponatremia. Water loading test revealed impaired water excretion and poor suppression of plasma ADH. Replacement with 20-30 mg hydrocortisone completely restored the serum Na level and restored the plasma ADH level to the normal range in all 4 patients. Other factors such as decreased glomerular filtration, enhanced urinary Na loss and decreased Na intake were also included. These results indicate that there is marked hyponatremia and that in the presence of hypoosmolality the sustained secretion of ADH is the key factor in causing the impaired water excretion and hyponatremia in isolated ACTH deficiency.

Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency

“…Also, similar results were obtained with hydrocortisone replacement in glucocorticoid-deficient rats and patients with hypopituitarism, i.e. hydrocortisone replacement normalizes AVP secretion, urinary excretion of AQP-2 and water diuresis (4,6,9,10,12,22). Therefore, non-suppressible secretion of AVP plays a crucial role in impaired water excretion in secondary adrenal insufficiency.…”

“…There are several factors that could be involved in the mechanisms for hyponatremia: enhanced secretion of AVP, attenuated renal handling of Na, decreased intake of Na, change in water intake, and others. Enhanced secretion of AVP is closely involved in the mechanism for impaired water excretion and hyponatremia in hypopituitarism, particularly hypofunction of the pituitary and adrenocortical axis (3,9,10). In experimental models of glucocorticoid deficiency non-suppressible release of AVP is found despite hypo-osmolality, which should suppress AVP release to undetectable levels (5 -7).…”

“…There has been an important debate since the 1950s regarding the mechanisms for hyponatremia in adrenal insufficiency, that is, whether water retention or renal deficit of sodium (Na) is more prominent in producing hyponatremia (2 -6). Studies performed in isolated glucocorticoid deficiency showed that impaired water excretion occurred in the patients with hypopituitarism and in experimental models of glucocorticoid deficiency (3,(5)(6)(7)(8)(9)(10). Non-suppressible release of arginine vasopressin (AVP) was found despite hypo-osmolality which should suppress AVP release to undetectable levels (3,6,7,11).…”

Severe chronic hiponatremia: rare cause of adrenal insufficiency

“…Pero el mecanismo es distinto al aceptado para la deficiencia de mineralocorticoides, desde el momento que por la deficiencia de glucocorticoides per se no se genera hipovolemia ni balance negativo de sodio. (8) Es conocido el rol de la vasopresina en la generación de hiponatremia euvolémica, debido a insuficiencia suprarrenal o hipotiroidismo (9,10,11,12,13) Parece claro sin embargo, que existen factores independientes de la vasopresina que también están comprometidos en la excreción alterada del agua que cursa con la deficiencia de glucocorticoides. Así, mientras el componente vasopresina-dependiente puede ser observado en ratas adrenalectomizadas privadas de glucocorticoides por 24 horas, el efecto vasopresina independiente de la excreción de agua ocurre luego de 2 semanas de deficiencia de glucocorticoides, en ratas deficientes en vasopresina.…”

Acute Lymphoblastic Leukemia with Isolated Adrenocorticotropic Hormone Deficiency.

“…This was probably due to the stress and high fever (4), which could stimulate the release of ADH.Another possibility was that the low level of plasma glucocorticoids caused by the ACTH deficiency could induce the release of ADHby a feedback mechanism (5)(6)(7)(8)(9). Considering the rapid improvement in the hyponatremia and plasma hypoosmolality, presumably in response to the prednisolone in the AdVPtherapy, we thought that the hyponatremia and plasma hypoosmolality were due to the ACTHdeficiency.…”