Cerebral Salt Wasting

Cort, J. H.

doi:10.1016/s0140-6736(54)92715-4

Cited by 168 publications

(41 citation statements)

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“…Both patients had increased urine sodium loss and dehydration inspite of high sodium diet. In 1952, Cort [3] in Yale described another similar patient as having Cerebral salt wasting syndrome.…”

Section: Discussionmentioning

confidence: 99%

“Hyponatremia in Stroke: Cerebral Salt Wasting Versus Syndrome of Inappropriate Anti-Diuresis”

Natarajan¹,

Prasad²

2016

IOSR

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Section: Discussionmentioning

confidence: 99%

“Hyponatremia in Stroke: Cerebral Salt Wasting Versus Syndrome of Inappropriate Anti-Diuresis”

Natarajan¹,

Prasad²

2016

IOSR

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“…Such a center might become hyperactive in arterial hypertension, exerting a more pronounced effect on renal functioii. The literature contains reports of salt-losing syndromes associated with cerebral lesions.23 24 In a patient carefully studied by Cort24 interruption of the hypothalamic tracts by a pleomnorphic glioma produced excessive loss of sodium from the body. This could not be explained by renal disease or abnormal pituitary-adrenal function.…”

Section: Effect Of Chavges Inmentioning

confidence: 99%

Renal Excretion of Sodium in Arterial Hypertension

et al. 1959

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Patients with arterial hypertension excrete a sodium load more rapidly than do individuals with normal blood pressure. The relationship of this abnormal sodium excretory response to blood pressure and such extrarenal factors as the central nervous system, dietary salt intake, body fluid volume and sodium content, and the adrenal glands has been studied. On the basis of this and other evidence, it is suggested that the exaggerated natriuresis is the result of a renal tubular defect which occurs after the development of hypertension.IT HAS been recognized since the studies of Farnsworth and Barker' that there is an abnormally high renal excretion of chloride in hypertensive individuals. Most subsequent research has been concerned with sodium rather than chloride. There have been several reports2-7 in which subjects with essential hypertension were observed to excrete an intravenous sodium load more rapidly than individuals with normal blood pressure. The explanation has been offered that this excretory derangement is related to alterations in renal function and that the high salt excretors were those hypertensive subjects whose renal plasma flow was reduced and filtration fraction elevated.8 Others,5' 6 however, have failed to observe such a relationship between increased sodium output and renal hemodynainics. The parallelism of the sodium clearance with both the level of the blood pressure2 4-6 9, 10 and renal vascular resistance6 suggested to The present study was undertaken to characterize further the hypertensive pattern of sodium excretion and the factors contributing to it. Consideration was given to the followinig: (1) the relationship of sodium excretion to blood pressure in subjects with labile, essential, and secondary hypertension; (2) the influence of extrarenal factors, such as the central nervous system, dietary salt intake, body fluid volume and sodium content, and the adrenal glands. MATERIALS AND METHODSThe studies were performed on the following subjects: 16 with essential hypertension of varying severity, 4 with labile hypertension, 4 with secondary hypertension, and 11 with normal blood pressure. In the presentation of the data, the subjects with essential hypertension have been grouped in order of increasing blood pressure as follows: for 2 patients with severe essential hypertension and diminished glomerular filtration there was no evidence of renal functional impairment. Cardiac decompensation was absent in all patients. The degree of retinopathy in the subjects with elevated blood pressure was grade II or less. There was no dietary restriction except when the effect of salt intake was being studied. No patient was receiving antihypertensive drugs.Procedures, except when noted, were carried out at approximately the same time in the morning. Water and food were withheld from the preceding midnight until the completion of the study. The subjects were in the supine position. Whenever possible urines were collected through a soft rubber, nmultiholed, indwelling urethral catheter. In the remai...

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“…On a severely sodium-restricted diet, his patient continued to excrete sodium in her urine; however, despite negative sodium balance, she remained normotensive. 3,4 In 1953, Leaf et al 5 demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain. This was not "salt wasting"; it was a physiologic response to an expanded intraPublished online ahead of print.…”

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confidence: 99%