Syndrome of inappropriate antidiuretic hormone classification

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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 AVP (arginine vasopressin) secretion across a range of plasma osmolalities into type A, type B, type C and type D.

Classification

SIADH may be classified in to several sub-types based on the pattern ofAVPsecretion across a range of plasma osmolalities:

Classification	Features
TypeA	Accounts for about 60-70% of SIADH Excessive secretion of ADH is noted Associated with lung cancer and nasopharyngeal tumors Patients are more susceptible to development of severe hyponatremia
Type B	Accounts for (20–40%) of the cases Theosmoticthreshold for AVP release is lowered – a reset osmostat – such that secretion of AVP occurs at lower plasma osmolalities than normal 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 severehyponatraemia Although most tumors manifest type ASIADH, some also present with type B SIADH, so thepattern of abnormalAVP (arginine vasopressin) secretion cannot be utilized to predict the causation of SIADH
TypeC	A rare condition characterized by failure to suppress AVP secretion at plasma osmolalities below the osmotic threshold 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 This variant may be due to dysfunction of inhibitory neurons in thehypothalamus, leading to persistent low-grade basal AVP secretion
Type D	Is a rare clinical picture of SIADH with low or undetectableAVP levels and no detectable abnormality in circulating AVP response It is thought that a nephrogenic SIADH (NSIAD) may be responsible for this picture Gain-of-functionmutations 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