A Specific Water Diuresis Test for Adrenocortical Insufficiency

Oleesky, S.

doi:10.1016/s0140-6736(53)91895-9

Cited by 57 publications

(8 citation statements)

References 12 publications

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“…Hypoosmolar syndrome with impaired water diuresis by the kidney is sometimes associated in patients with primary or secondary adrenal insufficiency (Bethune and Nelson, 1965;Schambelan et al, 1969;Agus and Goldberg, 1971), which is quickly improved by glucocorticoid replacement (Oleesky, 1953), Hypoosmolar syndrome is also observed in hypothyroid patients (Goldberg and Reivich, 1962;Pettinger et al, 1965). The glucocorticoid replacement normalized her serum Na concentration before levothyroxine replacement.…”

Section: Discussionmentioning

confidence: 99%

A case of Hyponatremia in Panhypopituitarism Caused by the Primary Empty Sella Syndrome

et al. 1987

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Section: Discussionmentioning

confidence: 99%

A case of Hyponatremia in Panhypopituitarism Caused by the Primary Empty Sella Syndrome

et al. 1987

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“…In most of the studies in the literature, the dose of glucocorticoid given to correct the impaired water diuresis was larger than the normal daily secretion of steroid by the adrenal cortex. It is interesting to note that this physiologic amount of glucocorticoid, at times, may not ade quately correct the defect in water excretion in adrenal insufficiency and that larger doses may be required for complete restoration of water diuresis [42,47,65).…”

Section: Sodium and Potassium Excretionmentioning

confidence: 99%

Kidney and Adrenocortical Hormones

Kleeman¹,

Levi²,

Better³

1975

Nephron

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We have presented a review of the interrelationship between the kidney and the adrenocortical steroids, aldosterone and cortisol, primarily in the regulation of water and electrolyte metabolism. The presentation is divided into three parts: (1) the influence of cortisol and aldosterone on renal structure and function; (2) the effect of kidney disease on secretion and metabolism of these steroids, and (3) the role of the kidneys in the plasma clearance of these steroids and their metabolites. There is no evidence that an excess or deficit of these steroids have a direct effect on renal structure, but both are necessary to maintain normal GFR and RPF. Glucocorticoids augment renal hemodynamics in pharmacologic doses. The phenomenon of ‘escape’ by the kidney from the sodium-retaining effect of adrenocortical steroids is discussed in detail, as well as the ability of glucocorticoid to antagonize the sodium retaining activity of any adrenal steroid of analogue with lesser glucocorticoid noperties. It is included that the impaired water dunesis of glycocorticoid deficiency is due to the absence of the permissive action of these steroids on the kidney, augmented at times by enhanced ADH secretion in response to sustained nonosmotic stimuli. The effect of gluco and mineralocorticoids on the renal excretion of divalentions and uric acid is also discussed. While progressive chronic renal failure (CRF) does not seem to significantly after the secretion or metabolism of cortisol it is possible that CRF causes a state of chronic hyperaldosteronism that is essential to maintain normal excretion (secretion) of potassium per nephron as renal mass progressively decreases. A direct or an indirect effect of potassium ion may be responsible for the hypersecretion or aldosterone rather than the renin-angiotensin system.

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“…Although the defect in water excretion in adrenal insufficiency previously has been shown to be improved by replacement of glucocorticoid hormone, supraphysiological doses of the hormone have been used in these previous studies (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). In this regard, Oleesky (27) did not observe improvement in diluting capacity in humans with adrenal insufficiency who were treated with physiological doses of glucocorticoid hormone and improvement required the administration of amounts of the hormone in excess of that normally produced by the adrenal gland. Moreover, the administration of large doses of glucocorticoid hormone to normal subjects with intact adrenal glands has been shown to enhance renal diluting capacity (28).…”

Section: V0mentioning

confidence: 99%

Importance of sodium intake and mineralocorticoid hormone in the impaired water excretion in adrenal insufficiency

Ufferman¹,

Schrier²

1972

J. Clin. Invest.

100

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A B S T R A C T The response of trained, conscious dogs to an acute water load was studied before adrenalectomy and under five conditions of hormonal replacement and sodium intake after adrenalectomy. Before adrenalectomy, with the dogs drinking isotonic saline, the minimal urinary osmolality (Uosm) was 47±7 (SEM) mOsm and free-water clearance (CH2o) was 8.6±1 ml/min. These values were not different after adrenalectomy with or without deoxycorticosterone (DOCA) if the animals continued to drink saline and receive dexamethasone. Moreover, after adrenalectomy in the presence of saline drinking both dexamethasone and DOCA could be withdrawn for up to 4 days without impairment of diluting ability (Uosm, 544+7 mOsm and CH20, 7.3±1 ml/min).In contrast, when the dogs drank tap water (Na intake 30 mEq/day), water loading in the absence of dexamethasone and DOCA was associated with a significantly higher Uosm (127±28,mOsm) and lower CH20 (2.7+0.3 ml/min). Replacing DOCA alone in the presence of this limited Na intake returned diluting ability to normal (Uosm 31±7 mOsm, CH2o 7.7±0.5 ml/min). Glomerular filtration rate for each animal was the same under each condition except for a significant diminution which occurred when dexamethasone and DOCA were withdrawn while the animals were on a 30 mEq sodium intake. In contrast to previous conclusions, the present results indicate that in the absence of adrenal hormones normal renal diluting ability may occur, indicating both maximal suppression of vasopressin release and maximal distal tubular impermeability to water.

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A Specific Water Diuresis Test for Adrenocortical Insufficiency

Cited by 57 publications

References 12 publications

A case of Hyponatremia in Panhypopituitarism Caused by the Primary Empty Sella Syndrome

A case of Hyponatremia in Panhypopituitarism Caused by the Primary Empty Sella Syndrome

Kidney and Adrenocortical Hormones

Importance of sodium intake and mineralocorticoid hormone in the impaired water excretion in adrenal insufficiency

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