“Essential” hypernatremia due to ineffective osmotic and intact volume regulation of vasopressin secretion

DeRubertis, Frederick R.; Michelis, Michael F.; Beck, Nama; Field, James B.; Davis, Bernard B.

doi:10.1172/jci106489

Cited by 82 publications

(15 citation statements)

References 63 publications

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“…In the past, some hyperosmolal syndromes have been attributed to resetting of the osmostat and referred to as 'essential hypernatremia' [57,59]. Unfortunately, in only two cases has the 'shift to the right' of the AVP/plasma osmolality curve been documented [87,102].…”

Section: Complete Defect1mentioning

confidence: 99%

Severe Hypernatremia with Impaired Thirst

Pérez

Oster²,

Robertson³

1989

Am J Nephrol

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Section: Complete Defect1mentioning

confidence: 99%

Severe Hypernatremia with Impaired Thirst

Pérez

Oster²,

Robertson³

1989

Am J Nephrol

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“…The occurrence of hypernatraemia, hyperosmolality and neurologic disorders have been reported previously (Alford et al 1973;Avioli et al 1962; Blank & Farnsworth 1974;DeRubertis et al 1971;Fyhrquist et al 1977;Halter et al 1977;Hays et al 1963; Lascelles & Lewis 1972;Mahoney & Good¬ man 1966;). These complex disorders have certain common clinical features: sustained hypernatraemia is not secondary to a significant extracellular fluid volume deficit, spon¬ taneous fluid intake is low inspite of elevated plasma osmotic pressure indicating defective thirst stimuli, antidiuretic hormone (ADH) response to various stimuli appears impaired, endogenous ADH production is partially intact since urine can be concentrated under several circumstances, and hyperosmolality cannot be completely corrected by fluid repair.…”

mentioning

confidence: 75%

Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide

AvRuskin

Tang

Juan

1981

Acta Endocrinologica

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An adolescent boy with essential hypernatreamia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with 'inappropriate' ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism; however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.

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“…Chlorpropamide has been used to restore drinking behavior in individuals with hypodipsia and diabetes insipidus [1,2]. These individuals invariably had essential hypernatremia, a condition with dysregulation of osmotic vasopressin release but normal vasopressin response to baroreceptor stimulation [31,32], rather than brain tumors. This patient's baroreflex-mediated vasopressin release was not formally tested, but he was not able to concentrate his urine and developed hypernatremia despite relative hypotension and volume depletion at the time of admission.…”

Section: Discussionmentioning

confidence: 99%

Central diabetes insipidus and adipsia due to astrocytoma: diagnosis and management

2012

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Adipsia and/or diabetes insipidus is rarely a direct complication of astrocytoma. We report a young man with recurrence of anaplastic astrocytoma who presented as severe hypernatremia. This case highlights key diagnostic and therapeutic challenges: (1) the interpretation of the response to exogenous vasopressin in a patient with steroid-induced hyperglycemia and (2) the potential risk of brain edema and herniation if excess water is prescribed along with vasopressin supplementation. The patient was successfully managed with prescribed fluid replacement, daily weights, and regular electrolyte monitoring but no exogenous vasopressin for 8 months until he succumbed to his tumor.

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“Essential” hypernatremia due to ineffective osmotic and intact volume regulation of vasopressin secretion

Cited by 82 publications

References 63 publications

Severe Hypernatremia with Impaired Thirst

Severe Hypernatremia with Impaired Thirst

Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide

Central diabetes insipidus and adipsia due to astrocytoma: diagnosis and management

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