Endocrine Abstracts

GS, Patients have hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria together with normal blood pressure. Most of the patients are clinically asymptomatic, but some patients experience seizures, muscle weakness, cramps, episodic tetany, and paresthesia. The diagnosis is usually made based on clinical features and laboratory blood test. In this study we present a young patient with persistent hypokalaemia. She feels well in herself. She denies any symptoms of hypokalaemia such as muscle weakness and has no medical history other than childhood asthma and chronic tonsillitis for which she had a tonsillectomy. She is not on any regular medications and denies any history of laxative use nor is she on any diuretics. She also denies any history of diarrhoea or vomiting, drinks very occasional alcohol and smokes 6–7 cigarettes a day. No family history of any endocrine disorders. BP in clinic was 108/60. Blood test: K 2.7–3.3 over the last persisting few months. The K of 3.3 was after a two week course of sando-K given by GP. We suspected a rare renal tubular abnormality causing her persistant hypokalaemia. To investigate for renal tubular abnormality such as Gitelman’s syndrome we did further Blood test and 2×24 hr urine collections for electrolytes and calcium. Further blood test: Na 142, K 2.9, Urea 6.7, Creatinine 55, Mg 0.71, PO4 1.24, Adj ca 2.39, TSH 1.04, glucose 4.8. Renin 255.2 mu/L (High) and aldosterone 176 pmol/L, ARR 0.7 pmol/miu²×24 hr urine collection for electrolytes and calcium: urea 361(n), creatinine 12.3(n), urine Na 262 high, ca 0.3 low, K 84(N). Our finding’s of normal BP, hypokalemia, Metabolic alkalosis, loss of Nacl in urine and hypocalciuria confirmed our diagnosis of Gitelman’s syndrome. Timely diagnosis helped us to initiate early treat with long term K replacement and K sparing diuretics and follow up.