The Genesis of Hyponatremia Associated with Marked Overhydration and Water Intoxication

Stormont, James M.; Waterhouse, Christine

doi:10.1161/01.cir.24.2.191

Cited by 45 publications

(16 citation statements)

References 23 publications

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“…Similar discrepancies have been found in healthy individuals given prolonged posterior pituitary extract and fluid (Stormont & Waterhouse, 1961). Thus, there appears to be a shift of water from the intracellular to extracellular compartment, the aetiology of which is not known.…”

supporting

confidence: 55%

Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

Baylis

Thompson

1988

Clinical Endocrinology

135

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supporting

confidence: 55%

Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

Baylis

Thompson

1988

Clinical Endocrinology

135

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“…Several observations on potassium equilibrium during hypotonic expansion in man are consistent with this interpretation, suggesting as they do acceleration of distal cation exchange. In the one study of human subjects made markedly hypotonic by exogenous vasopressin administration, potassium wasting and hypokalemia were commonly encountered (17). Hypokalemia has also been seen with significant frequency among patients with SIADH in whom hypotonicity was of a severity comparable to that which led to potassium wasting in the present studies; analysis of a large group of cases of SIADH (1) indicates that among eight patients in which serum sodium concentration was below 110 mEq/ liter, serum potassium concentration was less than 3.5 mEq/liter in four.…”

Section: Resultsmentioning

confidence: 99%

The effect of chronic hypotonic volume expansion on the renal regulation of acid-base equilibrium

Lowance¹,

Garfinkel²,

Mattern³

et al. 1972

J. Clin. Invest.

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A B S T R A C T Balance studies have been carried out to evaluate the influence of vasopressin-induced volume expansion on acid-base equilibrium in normal dogs and in dogs with steady-state metabolic acidosis induced by the administration of 5-7 mmoles/kg per day of hydrochloric acid.Hypotonic expansion in dogs with metabolic acidosis (mean plasma bicarbonate concentration 14 mEq/liter) produced a marked increase in renal acid excretion that restored plasma bicarbonate concentration to normal (20-21 mEq/liter) despite continued ingestion of acid.When water was restricted during the vasopressin period, and fluid retention thus prevented, no increase in acid excretion or plasma bicarbonate concentration occurred. From these findings we conclude that hypotonic expansion is a potent stimulus to renal hydrogen ion secretion and greatly facilitates the renal removal of an acid load.Normal dogs subjected to expansion demonstrated no change in net acid excretion or in plasma bicarbonate concentration even in the face of a marked diuresis of sodium and chloride and a reduction in plasma sodium concentration to approximately 110 mEq/liter. The animals did, however, regularly lose potassium, a finding that clearly indicates an acceleration of distal sodiumcation exchange. On the basis of these observations, and the findings in the expanded acidotic dogs, we suggest that in the expanded normal dogs acceleration of sodium-hydrogen exchange was responsible for preventing a bicarbonate diuresis and for stabilizing plasma bicarbonate concentration.These studies clearly demonstrate that chronic hypotonic expansion exerts a major influence on the renal A preliminary report of this work was published in abstract form in: 1971. J. Clin. Invest. 50: 62 a. (Abstr.)

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“…Excess natriuresis follows water retention and mainly exceeds the intake when volume expansion is relatively acute. After a few days, the Na balance is reestablished and a decline in the hydroosmotic effect of ADH is observed (vasopressin escape) (1,21).…”

Section: Urine Osmolalitymentioning

confidence: 99%

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Musch²

2008

Clinical Journal of the American Society of Nephrology

145

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Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hypotonicity. Although the differential diagnosis with other causes of hypotonicity such as salt depletion is sometimes challenging, some simple and readily available biologic parameters can be helpful in the diagnosis of SIADH. In SIADH, urea is typically low; this is less specific for elderly patients, for whom lower clearance of urea accounts for higher values. Low levels of uric acid are more often seen in SIADH (70%) compared with salt-depleted patients (40%). Typically, patients with SIADH will show a lower anion gap with nearly normal total CO 2 and serum potassium, this despite dilution. In patients with hyponatremia secondary to hypocorticism, total CO 2 is usually lower than in nonendocrine SIADH despite low urea and uric acid levels. Urine biology can also be helpful in diagnosis of SIADH because patients with SIADH have high urine sodium (Na; >30 mEq/L), and most of them will have a high fractional excretion of Na (>0.5% in 70% of cases), reflecting salt intake. Conversely, low urine Na in patients with SIADH and poor alimentation is not rare. Finally, measurement of urine osmolality is useful for the diagnosis of polydipsia and reset osmostat and could further help in the choice of therapeutic strategy because patients with low urine osmolality will benefit from water restriction or urea, whereas those with high urine osmolality (>600 mOsm/kg) would be good candidates for V 2 antagonist.

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The Genesis of Hyponatremia Associated with Marked Overhydration and Water Intoxication

Cited by 45 publications

References 23 publications

Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

The effect of chronic hypotonic volume expansion on the renal regulation of acid-base equilibrium

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

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