THE SPECIFICITY OF THE “WATER TEST“ AS A DIAGNOSTIC PROCEDURE IN ADDISON'S DISEASE<sup>1</sup>

Levy, Marvin S.; Power, Marschelle H.; Kepler, Edwin J.

doi:10.1210/jcem-6-9-607

Cited by 69 publications

(9 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies of acute water diuresis were repeated under identical conditions except that Pitressin 1 (vasopressin aqueous) 10 mU or 100 to 200 ,uU per kg per 1 Parke-Davis Lot 184. .t Ratio of 4 hr volume to total volume ingested X 100.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

An Explanation for and Experimental Correction of the Abnormal Water Diuresis in Cirrhosis *

Schedl¹,

Bartter²

1960

J. Clin. Invest.

158

View full text Add to dashboard Cite

It is well established that certain patients with hepatic cirrhosis show impaired water diuresis following water loads (1). With this limitation in free water excretion, hyponatremia may develop on average water intakes. It has been asserted and denied that antidiuretic hormone (ADH), secreted in excess or inadequately inactivated, is responsible for the water retention (2, 3). In this study the role of antidiuretic hormone in cirrhosis is reexamined. The results do not support the concept that it plays the primary role in the retention of water.Since free water is presumably produced by the reabsorption of sodium (4, 5), these patients present a paradox in that they show almost quantitative reabsorption of filtered sodium. The paradox could be resolved by postulating that proximal tubular sodium reabsorption in these subjects is so great as to allow little sodium to pass to the distal site where free water is generated. It follows a) that the defect should be corrected by delivery of proximal tubular fluid into the distal tubules and b) that normal subjects should show a similar "defect" correctable by the same process when depleted of sodium. In the present study these propositions are examined. SUBJECTS AND METHODSEight normal subjects and 8 patients with cirrhosis were maintained in an air-conditioned environment in a metabolic ward. They were fasted, and fluids were withheld after 6:00 p.m. the day prior to the tests. On the day of the study they were weighed at 7:30 a.m. and water loads (20 ml per kg) were drunk in approximately 1 hour, or infused intravenously in 1 to 1.5 hours. Overnight urine specimens were collected from 10:30 p.m. on the previous day to 7:30 a.m. on the day of the study to provide an estimate of the state of hydration of the sub-

show abstract

Section: Methodsmentioning

confidence: 99%

“…(Submitted for publication June 30, 1959; accepted October 1, 1959) It is well established that certain patients with hepatic cirrhosis show impaired water diuresis following water loads (1). With this limitation in free water excretion, hyponatremia may develop on average water intakes.…”

mentioning

confidence: 99%

An Explanation for and Experimental Correction of the Abnormal Water Diuresis in Cirrhosis *

Schedl¹,

Bartter²

1960

J. Clin. Invest.

158

View full text Add to dashboard Cite

show abstract

“…The inability to excrete an oral or parenteral load of water in a normal manner is a characteristic of the adrenalectomized or hypophysectomized animal and of the patient with adrenal or pituitary insufficiency (1)(2)(3)(4)(5)(6)(7)(8)(9). This defect persists in the presence of a normal salt balance, extracellular volume, and an adequate supply of salt-retaining hormone, desoxycorticosterone acetate (DCA) or aldosterone (4,7,8,10,11), but it can usually be corrected by the administration of hydrocortisone-like steroids (3,4,7,9).…”

mentioning

confidence: 99%

Mechanisms of Impaired Water Excretion in Adrenal and Pituitary Insufficiency. I. The Role of Altered Glomerular Filtration Rate and Solute Excretion12

Maxwell¹,

Rockney²

1958

J. Clin. Invest.

View full text Add to dashboard Cite

The inability to excrete an oral or parenteral load of water in a normal manner is a characteristic of the adrenalectomized or hypophysectomized animal and of the patient with adrenal or pituitary insufficiency ( 1-9). This defect persists in the presence of a normal salt balance, extracellular volume, and an adequate supply of salt-retaining hormone, desoxycorticosterone acetate (DCA) or aldosterone (4,7,8,10,11), but it can usually be corrected by the administration of hydrocortisone-like steroids (3,4,7,9).The basic mechanisms responsible for impaired water tolerance in these diseases have not been adequately clarified, nor have the processes by which hydrocortisone causes a normal water diuresis to occur.Gaunt, Birnie and Eversole (8) and others (7, 12) have suggested that a homeostatic "balance" exists between the antidiuretic hormone (ADH) of the neurohypophysis and the 11, 17 hydroxylated steroids of the adrenal cortex. They suggest that in the absence of these steroids, a relative or absolute excess of ADH exists, preventing a normal water diuresis. To prove this hypothesis, a sustained level of secretion of ADH should be demonstrated after the adrenal or anterior pituitary deficient animal has been water loaded, a procedure which ordinarily inhibits ADH secretion. To date, no such sustained activity has been observed using a generally acceptable and specific assay technique (6,13,14). Furthermore, the patient with adrenal or pituitary insufficiency normally inactivates and is not hypersensitive to exogenous antidiuretic hormone (Pitressin®) (6). Recent studies have stressed the importance of nonhormonal factors in determining the characteristics of water diuresis in normal subjects. The rate of glomerular filtration and solute excretion, and the distribution of the reabsorbed solutes between the proximal and distal tubules can profoundly alter the diuretic response to water in the absence of circulating ADH (15-21). Reduced glomerular filtration and renal blood flow are usually present in subjects with pituitary and adrenal insufficiency. In the latter, and occasionally in the former group, tubular reabsorption of sodium is impaired. Welt (22) postulated that the impaired water diuresis of these states is related primarily to alterations in the nonhormonal factors rather than to any disturbance in the secretion, metabolism, or action of ADH. If this theory is correct, it should be possible, while these subjects are under the influence of a sustained water load, to improve considerably their response to water loading by techniques which increase glomerular filtration rate and alter the distribution of solute (sodium) reabsorption between the proximal and distal tubule.This approach formed the basis of the present study. Aminophyllin was used to increase glomerular filtration acutely and alter the tubular reabsorption of solute. Its effect was compared in the same subject with the subsequent administration of hydrocortisone. The results indicate that the marked improvement in the execretion of water which...

show abstract

“…Observations in patients with Addison's disease and in individuals receiving cortisone therapy indicate that the adrenal cortical hormones may modify the diurnal excretory rhythm (20)(21)(22). Sirota, Baldwin, and Villarreal have demonstrated that the small nocturnal decrease in glomerular filtration rate is of insufficient magnitude to account for nocturnal oliguria, which must therefore depend upon increased tubular reabsorption of water ( 11 ).…”

mentioning

confidence: 99%

Diurnal Variation in the Diuretic Response to Ingested Water

Papper¹,

Rosenbaum²

1952

J. Clin. Invest.

View full text Add to dashboard Cite

THE SPECIFICITY OF THE “WATER TEST“ AS A DIAGNOSTIC PROCEDURE IN ADDISON'S DISEASE¹

Cited by 69 publications

References 0 publications

An Explanation for and Experimental Correction of the Abnormal Water Diuresis in Cirrhosis *

An Explanation for and Experimental Correction of the Abnormal Water Diuresis in Cirrhosis *

Mechanisms of Impaired Water Excretion in Adrenal and Pituitary Insufficiency. I. The Role of Altered Glomerular Filtration Rate and Solute Excretion12

Diurnal Variation in the Diuretic Response to Ingested Water

Contact Info

Product

Resources

About

THE SPECIFICITY OF THE “WATER TEST“ AS A DIAGNOSTIC PROCEDURE IN ADDISON'S DISEASE1

Cited by 69 publications

References 0 publications

An Explanation for and Experimental Correction of the Abnormal Water Diuresis in Cirrhosis *

An Explanation for and Experimental Correction of the Abnormal Water Diuresis in Cirrhosis *

Mechanisms of Impaired Water Excretion in Adrenal and Pituitary Insufficiency. I. The Role of Altered Glomerular Filtration Rate and Solute Excretion12

Diurnal Variation in the Diuretic Response to Ingested Water

Contact Info

Product

Resources

About

THE SPECIFICITY OF THE “WATER TEST“ AS A DIAGNOSTIC PROCEDURE IN ADDISON'S DISEASE¹