Unexplained hypokalaemia?
Hi, I was treated in the ER for hypokalaemia with IV potassium and then on K+ supplements in the hospital for a few days. Also had slightly raised creatinine (no treatment needed it resolved itself) I also had ECG changes (T wave inversion). No explanation for hypokalaemia…had not had any vomiting/diarrhoea, not on medication, no excessive vomiting or sweating, don’t have an eating disorder or use diuretics, and apart from the slightly rasied creatinine, urine was fine.
Had stress testand echo which were both ok.
Any ideas?
edit: was told by ER drs that potassium level was too low to have been caused by dietary insufficiency.
Filed under: Potassium and Being Sick
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A rare cause of hypokalaemia
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A 26 year old lady presented to her general practitioner complaining of fatigue. Investigations showed serum potassium of 2.5 mmol/l, (reference range 3.3–4.7 mmol/l). This was repeated on two more occasions and was 2.6 and 2.8 mmol/l. An ECG showed no features of hypokalaemia. She was seen in Endocrine clinic with serum potassium of 2.5 mmol/l. There was no history of an eating disorder, laxative or diuretic abuse. Her father had type 2 diabetes. Her height was 1.56 m and she weighed 50 kg. Blood pressure was 102/60 mmHg.
Further investigation revealed chloride 97 mmol/l (98–109), magnesium 0.64 mmol/l (0.74–1.03), renin 2.0 pmol/ml/h (0.5–3.1), aldosterone 160 pmol/l (100–800), and urinary calcium 1.1 mmol/24 h (2.5–7.5). The findings of hypokalaemia, hypochloraemia, hypomagnesaemia and hypocalciuria are consistent with a diagnosis of Gitelman’s syndrome (GS). The patient was treated with amiloride.
Gitelman’s syndrome:
GS is a hypokalaemic renal tubulopathy characterised by metabolic alkalosis with hypocalcuria and hypomagnesaemia. GS can be distinguished clinically from Bartter’s syndrome because GS is milder and tends to present at a later age. Patients are less likely to be short or to have polyuria and polydipsia. They typically present with fatigue, muscle weakness and symptoms of neuromuscular irritability. GS is also diagnosed in asymptomatic adults who present with unexplained hypokalaemia. Joint pain secondary to chondrocalcinosis has been described in a subset of patients and attributed to hypomagnesaemia.
GS is autosomal recessive, caused by mutations in the SLC12A3 gene, which encodes the thiazide sensitive sodium-chloride co-transporter, located in the distal convoluted tubules of the kidney. Management is directed towards potassium and magnesium replacement and long-term prognosis is excellent. GS should be considered in the differential diagnosis of normotensive or hypotensive adults who present with hypokalaemia.
This article is for patient information only, for sensible diagnosis and treatment, consult your professional healthcare provider.
i have some ideas..
stop stressing..
what about dietary deficiency….
possible
You have carefully excluded all known medical causes in your question. Perhaps you should have stayed in hospital a day extra - and found out the answer there…
THE PREVIOUS RESPONSE REGARDING GITELMANS SYNDROME, THOUGH ITS RARE, IS IN THE RIGHT BALL PARK. THE FACT YOUR CREATININE WAS ELEVATED AND YOU POTASSIUM DROPPED SUGGESTS THERE WAS SOMETHING OCCURING WITH YOUR KIDNEYS, THOUGH FROM THE TOP OF MY HEAD, I CANNOT THINK OF SOMETHING SO TRANSIENT THAT THE CREATININE WOULD CORRECT ITSELF. THE ECG CHANGES ARE MORE LIKELY RELATED TO THE EFFECT OF THE LOW POTASSIUM RATHER THAN ITS CAUSE.
IF YOU’RE IN AMERICA (WHICH I GUESS YOU ARE FROM THE USE OF ER RATHER THAN A+E) I ASSUME THAT YOU WOULD HAVE TO PAY FOR FURTHER INVESTIGATION. THE CHOICE IS YOURS, BUT PERSONALLY, I WOULD HAVE MY KIDNEYS LOOKED BEFORE DECIDING NOT TO INVESTIGATE IT ANY FURTHER.
HOPE THAT HELPS!