Have you considered Gitelmans or Bartters syndromes? Several of the results
are consistent with these syndromes i.e.low serum potassium, high urine
potassium, high bicarbonate, and also high PRA (even though you might expect
the aldosterone to be a little higher). Also the fact that she is
normotensive. Suggest doing serum magnesium (low)and urine
calcium/creatinine and magnesium/creatinine ratios. She appears most likely
to be Gitelmans than Bartters, as this presents typically in adult life
rather than chilhood. Urine Mg/creat ratio will be high in both conditions
(>0.19), whilst calcium/creat ratio is low (<0.10) in Gitelmans and elevated
(>0.20) in Bartters syndrome.
This might be barking completely up the wrong tree, but I think it's worth
looking at.
Avril Owen
Ysbyty Gwynedd
Bangor
North Wales
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-----Original Message-----
From: Phillip Jordan [mailto:[log in to unmask]]
Sent: 09 June 2000 12:55
To: ACB Mailbase
Subject: Puzzling case
Can anyone help with a diagnosis or suggest further investigations on a
patient who is proving to be a problem for the local endocrinologists (and
the laboratory!).
A 36-year-old, non-hypertensive, normally fertile, female patient on no
prescribed medication was initially investigated 1 year ago for "hair loss"
and "fatigue". She has a degree on increased pigmentation, but this is
adjudged to be more typical of chloasma.
Potassium 2.9-3.3 mmol/l (ref 3.5-5.5) on all measurements made over the
last year.
HCO3 = 32-33 mmol/l (ref 23-30)
Urine cortisol 195 mmol/24 h (ref. 40-305)
Random serum cortisol 185 and 266 nmol/l
Short synacthen test - baseline = 571 nmol/l, +30 min = 713 nmol/l
ACTH <10 ng/l
Urine potassium 100-140 mmol/24 h (4 measurements)
Urine sodium 205-360 mmol/24h (4 measurements)
Recumbent -
Plasma renin activity 13.6 nmol/l/h (ref 1.1-2.7)
Aldosterone 130 pmol/l (ref 100-500)
Ambulant -
Plasma renin activity 21.9 nmol/l/h (ref 2.8-4.5)
Aldosterone 205 pmol/l (ref 600-1200)
This pattern of results was reproducible when re-analysed by a different
laboratory, and also consistent with an earlier set of results.
How can the high PRA and low/normal aldosterone be explained in association
with the hypokalaemia?
Phillip Jordan/Maurice Salzmann
Clinical Scientist/Consultant Clinical Chemist
Royal Devon and Exeter Hospital
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