Roger,
What about the high cortisol obtained on the previous sample. Could it still be high? and is Pit/Hypothal or Adrenal dysfunction (possible even a Pheo) a consideration here? Suggest further work with those in mind. Of course, also worth investigating the underlying cause of the nephropathy (renal failure; acute vs chronic).
Godfrey
-----Original Message-----
From: Clinical biochemistry discussion list [mailto:[log in to unmask]]On Behalf Of Bertholf, Roger
Sent: Wednesday, July 09, 2008 9:10 PM
To: [log in to unmask]
Subject: Re: Hyponatraemia
Lipids?
I still think this is a pseudohyponatremia due either to volume displacement--hyperlipidemia or hyperproteinemia--or hyperosmolemia from the severe uremia. Direct potentiometric measurement of sodium would verify the former, whereas measurement of serum osmolality by freezing point depression would confirm the latter.
Roger
Roger L. Bertholf, Ph.D.
Professor of Pathology
Director of Clinical Chemistry, Toxicology,
and Point of Care Testing
University of Florida Health Science Center/Jacksonville
-----Original Message-----
From: Clinical biochemistry discussion list on behalf of Mohammad Al-Jubouri
Sent: Wed 7/9/2008 6:03 PM
To: [log in to unmask]
Subject: Re: Hyponatraemia
With limited clinical details, the cause of hyponatraemia is difficult to ascertain form laboratory data only, apart from ruling out Addison's disease as serum cortisol suggests stress response. Details of the present illness including length of history, any GI losses in the form diarrhoea & vomiting, fluid intake history, medications especially diuretics, ACEI, antidepressants, antiepileptics...etc. Volume status assessment is also important, and it seems from the clinical details given that the patient is likely to be dehydrated. Hyponatraemic dehydration can be due to salt loss either renally (e.g Addison's, DI or salt losing nephropathy), or due to GI losses (vomiting & diarrhoea). The low spot urinary sodium suggests extra-renal loss as a likely mechanism and hypovolaemia has led to renal failure due to renal hypoperfusion. Of course the patient may have maintained taking water which can lead to further dilution of the extracellular sodium
concentration. The history of Ca bladder and intravesical installation of Mitomycin C may also be relevant and an associated obstructive uropathy should be ruled out/in.
Sorry, I can't be more specific until further clinical details (history & examination) are furnished.
regards
Mohammad
Dr. M A Al-Jubouri, MB ChB, MSc, FRCP Edin, FRCPath
Consultant Chemical Pathologist
----- Original Message ----
From: Mainwaring-Burton Richard (RGZ) <[log in to unmask]>
To: [log in to unmask]
Sent: Wednesday, 9 July, 2008 5:14:45 PM
Subject: Hyponatraemia
Hyponatraemia
A lady age 73 was sent by the GPwith "tachycardia ? dehydration"for U&E and ECG
On admission :
Sodium 104 mmol/L ( 136 to 145 )
Potassium 7.6 mmol/L ( 3.5 to 5.1 )
Urea 36.2 mmol/L ( 3.5 to 7.2 )
Creatinine 377 umol/L ( 53 to 97 )
Adjusted calcium 2.69 mmol/L ( 2.20 to 2.67 )
Random glucose 8.8 mmol/L ( 3.5 to 7.8 )
Cortisol >1650 nmol/L ( 80 to 480 )
Osmolality 266 mmol/kg ( 285 to 305 )
The ECG was pretty abnormal too, such that the lady was sent to A&E and thence ITU
Today
09/07/2008 14:00serum
Sodium 100 mmol/l ( 136 to 145 )
Potassium 4.7 mmol/l ( 3.5 to 5.1 )
Urea 27.7 mmol/l ( 3.5 to 7.2 )
Creatinine 219 umol/l ( 53 to 97 )
Random glucose 6.1 mmol/l ( 3.5 to 8.0 )
Troponin I 0.10 ug/l ( Up to 1.0 )
09/07/2008 10:30 Mid-stream urine
Sodium <20 mmol/l
Potassium 27 mmol/l
Osmolality 366 mmol/kg
PMH
Ca bladder excised April 2008 -follow-up Mitomycin C bladder infusion
Treated with atenolol and doxazosin for hypertension
U&Es previously:
AG085035Q 28/04/2008 u/k Serum
Specimen ID check ^ID checked
Sodium 137 mmol/l ( 136 to 145 )
Potassium 4.9 mmol/l ( 3.5 to 5.1 )
Urea 5.1 mmol/l ( 3.5 to 7.2 )
Creatinine 86 umol/l ( 53 to 97 )
Any Thoughts please ?
with best wishes
Richard
Richard Mainwaring-Burton
Consultant Biochemist
Queen Mary's Hospital
Sidcup, Kent
020-8308-3084
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