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==Overview==
==Overview==
[[SIADH]] may be classified into several sub-types based on the pattern of [[AVP]] ([[arginine vasopressin]]) secretion across a range of plasma osmolalities into type A, type B, type C and type D.
[[SIADH]] may be classified into several sub-types based on the pattern of [[arginine vasopressin|arginine vasopressin (AVP)]] secretion in response to a range of [[plasma osmolality|plasma osmolalities]] into type A, type B, type C, and type D.


==Classification==
==Classification==


[[SIADH]] may be classified in to several sub-types based on the pattern of[[ AVP]][[ secretion]] across a range of [[plasma]] osmolalities:
[[SIADH]] may be classified into several sub-types based on the pattern of [[AVP|arginine vasopressin (AVP)]] [[secretion]] across a range of [[Plasma osmolality|plasma osmolalities]]:<ref name="pmid20164214">{{cite journal |vauthors=Hannon MJ, Thompson CJ |title=The syndrome of inappropriate antidiuretic hormone: prevalence, causes and consequences |journal=Eur. J. Endocrinol. |volume=162 Suppl 1 |issue= |pages=S5–12 |year=2010 |pmid=20164214 |doi=10.1530/EJE-09-1063 |url=}}</ref><ref name="pmid23818806">{{cite journal |vauthors=Yamauchi T, Makinodan M, Nagashima T, Kiuchi K, Noriyama Y, Kishimoto T |title=Type d syndrome of inappropriate antidiuretic hormone secretion in a schizophrenia patient with polydipsia |journal=J Brain Dis |volume=1 |issue= |pages=25–7 |year=2009 |pmid=23818806 |pmc=3676320 |doi= |url=}}</ref><ref name="pmid23148195">{{cite journal |vauthors=Gross P |title=Clinical management of SIADH |journal=Ther Adv Endocrinol Metab |volume=3 |issue=2 |pages=61–73 |year=2012 |pmid=23148195 |pmc=3474650 |doi=10.1177/2042018812437561 |url=}}</ref>
 
This classification scheme includes Fenske's<ref name="pmid24722436">{{cite journal| author=Fenske WK, Christ-Crain M, Hörning A, Simet J, Szinnai G, Fassnacht M | display-authors=etal| title=A copeptin-based classification of the osmoregulatory defects in the syndrome of inappropriate antidiuresis. | journal=J Am Soc Nephrol | year= 2014 | volume= 25 | issue= 10 | pages= 2376-83 | pmid=24722436 | doi=10.1681/ASN.2013080895 | pmc=4178436 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24722436  }} </ref> observation on [[copeptin]] levels, which is "secreted in an equimolar amount to arginine vasopressin (AVP) but can easily be measured in plasma or serum with a sandwich immunoassay."<ref name="pmid31004513">{{cite journal| author=Refardt J, Winzeler B, Christ-Crain M| title=Copeptin and its role in the diagnosis of diabetes insipidus and the syndrome of inappropriate antidiuresis. | journal=Clin Endocrinol (Oxf) | year= 2019 | volume= 91 | issue= 1 | pages= 22-32 | pmid=31004513 | doi=10.1111/cen.13991 | pmc=6850413 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31004513  }} </ref> Normal observations for [[copeptin]] are:
* '''Level during euvolemia: 2 and 38 pmol/L'''"<ref name="pmid24722436"/>. Another view is "Median copeptin levels were significantly higher in the male volunteers compared with the females [median (range): 4.3 (0.4-44.3) compared with 3.2 (1.0-14.8) pmol/l"<ref name="pmid18647134">{{cite journal| author=Bhandari SS, Loke I, Davies JE, Squire IB, Struck J, Ng LL| title=Gender and renal function influence plasma levels of copeptin in healthy individuals. | journal=Clin Sci (Lond) | year= 2009 | volume= 116 | issue= 3 | pages= 257-63 | pmid=18647134 | doi=10.1042/CS20080140 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18647134  }} </ref> and levels are modulated by gender (higher in males), eGFR higher when eGFR lower), left atrial size (higher when LA larger), and longer echocardiographic deceleration times (prolonged ventricular filling)<ref name="pmid18647134"/>.
* '''Slope of change during hypertonic saline infusion: "slope of 0.74 pmol/L''' and mOsM/kg H<sub>2</sub>O ... (95% confidence interval [95% CI], 0.66 to 0.83)"<ref name="pmid24722436"/>
 


{| style="border: 0px; font-size: 90%; margin: 3px; width: 1000px" align="center"
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! style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|Classification}}
! style="background: #4479BA; width: 100px;" | {{fontcolor|#FFF|Classification}}
! style="background: #4479BA; width: 300px;" | {{fontcolor|#FFF|Features}}
! style="background: #4479BA; width: 400px;" | {{fontcolor|#FFF|Features}}
 
|-
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| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[TypeA]]
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Type A
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
* This type accounts for the most common form which constitutes about 60-70% of SIADH
* Accounts for about 60-70% of [[SIADH]]
* There is excessive, random secretion of AVP, and linear relationship between plasma[[ osmolality]] and plasma[[ AVP]] is lost
* Excessive secretion of [[arginine vasopressin]] ([[AVP]]) is noted
*Commonly seen in [[lung cancer]]
* "Plasma [[copeptin]] consistently >38 pmol/L with a copeptin slope <95% CI for that of healthy persons (i.e., <0.66 pmol/L/mOsM/kg H2O)"<ref name="pmid24722436"/>
* Some studies  have shown that some lung tumours synthesize AVP, and that [[tumour]] tissue stains positive for AVP[[ mRNA]]
* Associated with [[lung cancer]] and [[Nasopharyngeal Carcinoma|nasopharyngeal tumors]]
*Plasma [[AVP]] concentrations in type A SIADH are not suppressed [[physiologically]] by drinking , which makes patients vulnerable to the development of severe [[hyponatremia]]
* Patients are more susceptible to development of severe [[hyponatremia]]
* Studies have also demonstrated a lower[[ osmotic]] threshold for [[thirst]] appreciation in this type of [[SIADH]]
 
* This type of SIADH is also characteristic of [[nasopharyngeal tumours]], which also stain positive for AVP[[ mRNA]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Type B
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Type B
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
*Accounts for (20–40%) of the cases
* Accounts for (20–40%) of the cases
*The[[ osmotic]][[ threshold ]]for AVP release is lowered – a reset osmostat – such that secretion of AVP occurs at lower plasma [[osmolalities]] than normal 
* "Any plasma copeptin concentration with a positive copeptin slope >0.25 pmol/L/mOsM/kg H2O, but a low osmotic threshold <95% CI for that of healthy persons (i.e., <281 mOsM/kg H2O)"<ref name="pmid24722436"/>
*AVP is suppressed at plasma osmolalities below the lower, reset threshold, further over-[[hydration]] leads to suppression of AVP release, which protects against the progression to severe[[ hyponatraemia]]  
* Type B may include [[reset osmostat,]] "characterized by a decline in plasma copeptin levels with increasing saline-stimulated serum osmolality...baseline hypovolemia could not be identified [in these patient]"<ref name="pmid24722436"/>
*Although most tumors manifest type A[[ SIADH]], some also present with type B SIADH, so the[[ pattern]] of [[abnormal]][[ AVP]] (arginine vasopressin) secretion cannot be utilized to predict the [[causation]] of [[SIADH]]
 
* Secretion of [[AVP]] occurs at lower than normal [[Plasma osmolality|plasma osmolalities]]  


|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[TypeC]]
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Type C
| style="padding: 5px 5px; background: #F5F5F5;" |
* Failure to suppress [[AVP]] secretion at [[Plasma osmolality|plasma osmolalities]] below the [[osmotic]] threshold
* "Plasma copeptin concentration between 2 and 38 pmol/L with a copeptin slope between −0.25 and 0.25 pmol/L/mOsM/kg H2O"<ref name="pmid24722436"/>
* [[Reset osmostat]] may be a Type C rather than Type b, "reset osmostat may in part be considered as a less severe variant of the type C defect..., where responsivity to osmotic challenges is completely lost. Copeptin release in this subtype was stable at levels within the normal physiologic range but was not suppressed by hypotonicity or stimulated in response to osmotic stimulation; thus, it deviates from the previously described type C"<ref name="pmid24722436"/>
* Occurs due to dysfunction of inhibitory [[neurons]] in the [[hypothalamus]], leading to persistent low-grade basal [[AVP]] secretion
 
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Type D
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
* A rare condition characterized by failure to suppress AVP secretion at plasma osmolalities below the [[osmotic]] threshold
* Low or undetectable [[AVP]] levels and circulating [[AVP]] response is not defective 
* Plasma [[AVP]] concentrations are thus inappropriately high at low plasma osmolalities, but there is a normal relationship between plasma osmolality and plasma AVP at physiological plasma osmolalities
* "Plasma copeptin concentration consistently <2 pmol/L regardless of the copeptin slope"<ref name="pmid24722436"/>
*This variant may be due to dysfunction of inhibitory neurons in the[[ hypothalamus]], leading to persistent low-grade basal AVP secretion
* Nephrogenic SIADH (NSIAD) may be attributed to this condition
* Associated with gain-of-function [[mutations]] in the vasopressin-2 ([[V2 receptor|V2]]) [[V2 receptor|receptor]] leading to a clinical picture of [[SIADH]], with undetectable [[AVP]] levels
* The condition is inherited in an [[X-linked]] manner, although [[heterozygous]] [[females]] may have inappropriate anti-[[diuresis]] of varying degrees.


|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Type D]]
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Type E
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |  
* Is a rare clinical picture of [[SIADH]] with low or undetectable[[ AVP]] levels and no detectable abnormality in circulating AVP response 
* "Any plasma copeptin concentration with a copeptin slope <−0.25 pmol/L/mOsM/kg H<sub>2</sub>O...Theoretically, an alternative explanation of type E could be a reversed osmotic response from stimulation to inhibition"<ref name="pmid24722436"/>
*It is thought that a nephrogenic SIADH (NSIAD) may be responsible for this picture
*Gain-of-function[[ mutations]] in the V2 receptor leading to a clinical picture of SIADH, with undetectable AVP levels, have been described
*The identified mutations had different [[nucleotide]] substitutions causing different levels of V2 receptor activation
*This syndrome appears to be inherited in an X-linked manner,although heterozygous females may have varying degrees of inappropriate antidiuresis. Owing to variable expressivity of the [[gene]] involved,[[ NSIAD]] may be clinically undetectable for years, until other contributing factors in later life lead to clinically significant hyponatraemia<ref name="pmid20164214">{{cite journal |vauthors=Hannon MJ, Thompson CJ |title=The syndrome of inappropriate antidiuretic hormone: prevalence, causes and consequences |journal=Eur. J. Endocrinol. |volume=162 Suppl 1 |issue= |pages=S5–12 |year=2010 |pmid=20164214 |doi=10.1530/EJE-09-1063 |url=}}</ref>  


|}
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==References==
==References==
{{reflist|2}}
{{Reflist|2}}


[[Category:Medicine]]
[[Category:Endocrinology]]
[[Category:Endocrinology]]
[[Category:Nephrology]]
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Latest revision as of 16:35, 2 July 2022

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]

Overview

SIADH may be classified into several sub-types based on the pattern of arginine vasopressin (AVP) secretion in response to a range of plasma osmolalities into type A, type B, type C, and type D.

Classification

SIADH may be classified into several sub-types based on the pattern of arginine vasopressin (AVP) secretion across a range of plasma osmolalities:[1][2][3]

This classification scheme includes Fenske's[4] observation on copeptin levels, which is "secreted in an equimolar amount to arginine vasopressin (AVP) but can easily be measured in plasma or serum with a sandwich immunoassay."[5] Normal observations for copeptin are:

  • Level during euvolemia: 2 and 38 pmol/L"[4]. Another view is "Median copeptin levels were significantly higher in the male volunteers compared with the females [median (range): 4.3 (0.4-44.3) compared with 3.2 (1.0-14.8) pmol/l"[6] and levels are modulated by gender (higher in males), eGFR higher when eGFR lower), left atrial size (higher when LA larger), and longer echocardiographic deceleration times (prolonged ventricular filling)[6].
  • Slope of change during hypertonic saline infusion: "slope of 0.74 pmol/L and mOsM/kg H2O ... (95% confidence interval [95% CI], 0.66 to 0.83)"[4]
Classification Features
Type A
Type B
  • Accounts for (20–40%) of the cases
  • "Any plasma copeptin concentration with a positive copeptin slope >0.25 pmol/L/mOsM/kg H2O, but a low osmotic threshold <95% CI for that of healthy persons (i.e., <281 mOsM/kg H2O)"[4]
  • Type B may include reset osmostat, "characterized by a decline in plasma copeptin levels with increasing saline-stimulated serum osmolality...baseline hypovolemia could not be identified [in these patient]"[4]
Type C
  • Failure to suppress AVP secretion at plasma osmolalities below the osmotic threshold
  • "Plasma copeptin concentration between 2 and 38 pmol/L with a copeptin slope between −0.25 and 0.25 pmol/L/mOsM/kg H2O"[4]
  • Reset osmostat may be a Type C rather than Type b, "reset osmostat may in part be considered as a less severe variant of the type C defect..., where responsivity to osmotic challenges is completely lost. Copeptin release in this subtype was stable at levels within the normal physiologic range but was not suppressed by hypotonicity or stimulated in response to osmotic stimulation; thus, it deviates from the previously described type C"[4]
  • Occurs due to dysfunction of inhibitory neurons in the hypothalamus, leading to persistent low-grade basal AVP secretion
Type D
  • Low or undetectable AVP levels and circulating AVP response is not defective
  • "Plasma copeptin concentration consistently <2 pmol/L regardless of the copeptin slope"[4]
  • Nephrogenic SIADH (NSIAD) may be attributed to this condition
  • Associated with gain-of-function mutations in the vasopressin-2 (V2) receptor leading to a clinical picture of SIADH, with undetectable AVP levels
  • The condition is inherited in an X-linked manner, although heterozygous females may have inappropriate anti-diuresis of varying degrees.
Type E
  • "Any plasma copeptin concentration with a copeptin slope <−0.25 pmol/L/mOsM/kg H2O...Theoretically, an alternative explanation of type E could be a reversed osmotic response from stimulation to inhibition"[4]

References

  1. ↑ Hannon MJ, Thompson CJ (2010). "The syndrome of inappropriate antidiuretic hormone: prevalence, causes and consequences". Eur. J. Endocrinol. 162 Suppl 1: S5–12. doi:10.1530/EJE-09-1063. PMID 20164214.
  2. ↑ Yamauchi T, Makinodan M, Nagashima T, Kiuchi K, Noriyama Y, Kishimoto T (2009). "Type d syndrome of inappropriate antidiuretic hormone secretion in a schizophrenia patient with polydipsia". J Brain Dis. 1: 25–7. PMC 3676320. PMID 23818806.
  3. ↑ Gross P (2012). "Clinical management of SIADH". Ther Adv Endocrinol Metab. 3 (2): 61–73. doi:10.1177/2042018812437561. PMC 3474650. PMID 23148195.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 4.9 Fenske WK, Christ-Crain M, Hörning A, Simet J, Szinnai G, Fassnacht M; et al. (2014). "A copeptin-based classification of the osmoregulatory defects in the syndrome of inappropriate antidiuresis". J Am Soc Nephrol. 25 (10): 2376–83. doi:10.1681/ASN.2013080895. PMC 4178436. PMID 24722436.
  5. ↑ Refardt J, Winzeler B, Christ-Crain M (2019). "Copeptin and its role in the diagnosis of diabetes insipidus and the syndrome of inappropriate antidiuresis". Clin Endocrinol (Oxf). 91 (1): 22–32. doi:10.1111/cen.13991. PMC 6850413 Check |pmc= value (help). PMID 31004513.
  6. ↑ 6.0 6.1 Bhandari SS, Loke I, Davies JE, Squire IB, Struck J, Ng LL (2009). "Gender and renal function influence plasma levels of copeptin in healthy individuals". Clin Sci (Lond). 116 (3): 257–63. doi:10.1042/CS20080140. PMID 18647134.
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