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]], [[Hypertension|hypertensive]] [[intracranial hemorrhage]], and [[bulbar poliomyelitis]] who presented with severe [[dehydration]] and hyponatremia.


==Historical Perspective==
==Historical Perspective ==
 
The historical perspective of hypernatremia is as follows:<ref>{{Cite journal
===Discovery===
* In 1858,Claude Bernard, French physiologist first proposed a direct relationship between the central  nervous system and renal excretion of osmotically active solutes <ref>{{Cite journal


  | author = [[J. Barcroft]] & [[H. Straub]]
  | author = [[J. Barcroft]] & [[H. Straub]]
Line 29: Line 28:
  | pmid = 16993045
  | pmid = 16993045


}}</ref>.
}}</ref><ref>{{cite book | last = Czerny | first = A | title = Ergebnisse der Inneren Medizin und Kinderheilkunde : Achtundvierzigster Band | publisher = Springer Berlin Heidelberg | location = Berlin, Heidelberg | year = 1935 | isbn = 9783642906701 }}</ref><ref>{{Cite journal
* In 1913,Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesioning


*[Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].
| author = [[J. P. PETERS]], [[L. G. WELT]], [[E. A. H. SIMS]], [[J. ORLOFF]] & [[J. NEEDHAM]]


*The association between [important risk factor/cause] and [disease name] was made in/during [year/event].
| title = A salt-wasting syndrome associated with cerebral disease
*In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].
*In [year], [gene] mutations were first implicated in the pathogenesis of [disease name].


==Outbreaks==
| journal = [[Transactions of the Association of American Physicians]]
*There have been several outbreaks of [disease name], which are summarized below:


==Landmark Events in the Development of Treatment Strategies==
| volume = 63
*In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].


==Impact on Cultural History==
| pages = 57–64
 
| year = 1950
 
| month =  
 
| pmid = 14855556
 
}}</ref><ref>{{Cite journal
 
| author = [[L. G. WELT]], [[D. W. SELDIN]], [[W. P. NELSON]], [[W. J. GERMAN]] & [[J. P. PETERS]]
 
| title = Role of the central nervous system in metabolism of electrolytes and water
 
| journal = [[A.M.A. archives of internal medicine]]
 
| volume = 90
 
| issue = 3
 
| pages = 355–378
 
| year = 1952
 
| month = September
 
| pmid = 14952060
 
}}</ref>
===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]], [[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.


==Famous Cases==
*The following are a few famous cases of [[disease name]]:
==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 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

  1. 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)
  2. Czerny, A (1935). Ergebnisse der Inneren Medizin und Kinderheilkunde : Achtundvierzigster Band. Berlin, Heidelberg: Springer Berlin Heidelberg. ISBN 9783642906701.
  3. 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.
  4. 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)

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