Not understood as far as I know, not that common
and usually mild.
Mostly in an acute crisis, so hard to study.
At least part is renal, I guess predominantly
simply due to the low GFR (fluid replacement
brings the calcium down), though some increased
tubular reabsorption may be down to other
mechanisms. There may also be increased bone
resorption.
Isolated ACTH deficiency can cause it as well as
glucocorticoid withdrawal with surgical
treatment of Cushings.
AB
DMS> Dear colleagues,
DMS> A nephrologist stopped by to ask the
DMS> following question: "What is the
DMS> formal pathogenesis of hypercalcaemia in Addison's crisis ?"
DMS> I hardly knew that this may happen (in some
DMS> 5% according to a textbook)
DMS> let alone the pathomechanism behind it ...
DMS> Thank you for your input.
DMS> Mike
DMS> Dr Michael Steiner
DMS> University of Rostock
DMS> Institute of Clinical Chemistry & Laboratory Medicine
DMS> D-18057 Rostock
DMS> GERMANY
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Regards
Aubrey Blumsohn
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