Hyponatremia historical perspective: Difference between revisions
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{{Hyponatremia}} | {{Hyponatremia}} | ||
{{CMG}}; {{AE}} {{Saeedeh | {{CMG}}; {{AE}} {{Saeedeh}} | ||
==Overview== | ==Overview== | ||
In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes. In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion. In 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and | In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the [[central nervous system]] and [[renal]] excretion of osmotically active solutes. In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through [[medullary]] lesion. In 1950, Peters, Welt, and co-workers described few patients with [[encephalitis]], [[Hypertension|hypertensive]] [[intracranial hemorrhage]], and [[bulbar poliomyelitis]] who presented with severe [[dehydration]] and hyponatremia. | ||
==Historical Perspective == | ==Historical Perspective == | ||
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}}</ref> | }}</ref> | ||
===Discovery=== | ===Discovery=== | ||
* In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the [[central nervous system]] and renal excretion of osmotically active [[solutes]]. | * In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the [[central nervous system]] and [[renal]] excretion of osmotically active [[solutes]]. | ||
* In 1913, Jungmann and Meyer in Germany induced [[polyuria]] and increased urinary salt excretion in animals through [[medullary]] lesion. | * In 1913, Jungmann and Meyer in Germany induced [[polyuria]] and increased urinary salt excretion in animals through [[medullary]] lesion. | ||
* in 1950, Peters, Welt, and co-workers described few patients with [[encephalitis]], hypertensive [[intracranial hemorrhage]], and bulbar [[poliomyelitis]] who presented with severe [[dehydration]] and [[hyponatremia]]. | * In 1920, cerebral edema from water toxication was recognized. | ||
* In 1936, first successful treatment of severe hyponatremia was published. | |||
* in 1950, Peters, Welt, and co-workers described few patients with [[encephalitis]], [[Hypertension|hypertensive]] [[intracranial hemorrhage]], and bulbar [[poliomyelitis]] who presented with severe [[dehydration]] and [[hyponatremia]]. | |||
* In 1952, Welt and colleagues presented patients with cerebral lesions (including [[trauma]], [[tumor]], and [[infection]]) and severe hyponatremia with clinical [[dehydration]] but no [[potassium]] retention. | |||
* In 1967, Bartter and Schwartz introduced SIAD. | |||
* In 1970s, the complications of rapid treatment of hyponatremia were first described. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Latest revision as of 08:01, 30 May 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Saeedeh Kowsarnia M.D.[2]
Overview
In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes. In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion. In 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and hyponatremia.
Historical Perspective
The historical perspective of hypernatremia is as follows:[1][2][3][4]
Discovery
- In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes.
- In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion.
- In 1920, cerebral edema from water toxication was recognized.
- In 1936, first successful treatment of severe hyponatremia was published.
- in 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and hyponatremia.
- In 1952, Welt and colleagues presented patients with cerebral lesions (including trauma, tumor, and infection) and severe hyponatremia with clinical dehydration but no potassium retention.
- In 1967, Bartter and Schwartz introduced SIAD.
- In 1970s, the complications of rapid treatment of hyponatremia were first described.
References
- ↑ J. Barcroft & H. Straub (1910). "The secretion of urine". The Journal of physiology. 41 (3–4): 145–167. PMID 16993045. Unknown parameter
|month=ignored (help) - ↑ Czerny, A (1935). Ergebnisse der Inneren Medizin und Kinderheilkunde : Achtundvierzigster Band. Berlin, Heidelberg: Springer Berlin Heidelberg. ISBN 9783642906701.
- ↑ J. P. PETERS, L. G. WELT, E. A. H. SIMS, J. ORLOFF & J. NEEDHAM (1950). "A salt-wasting syndrome associated with cerebral disease". Transactions of the Association of American Physicians. 63: 57–64. PMID 14855556.
- ↑ L. G. WELT, D. W. SELDIN, W. P. NELSON, W. J. GERMAN & J. P. PETERS (1952). "Role of the central nervous system in metabolism of electrolytes and water". A.M.A. archives of internal medicine. 90 (3): 355–378. PMID 14952060. Unknown parameter
|month=ignored (help)