A 28 year old man of Chinese ethnicity presented to hospital in 2008 with a three week history of generalised and progressive muscle weakness and eventual conscious collapse. This occurred on a background of increased intake of simple carbohydrate foods over the preceding few weeks. Initial arterial blood gas demonstrated severe hypokalemia and mild metabolic alkalosis (K 1.3 mmol/L pH 7.45 HCO3 29.7mmol/L) which was confirmed on venous testing. Electrolytes (mmol/L)- K 1.4, Mg 0.63, Na 135, Cl 90, HCO3 24, Cr 110, Ca (cor) 2.48, PO4 0.72. Spot urine Na 74, K 25. ECG revealed biphasic T waves and prolonged QTc (513ms). TFT and thyroid antibodies were normal. Diuretic and laxative screens were negative. FBG was 14.6mmol/L despite no history of diabetes.

Aggressive potassium (780mmol) and magnesium (70mmol) supplementation was administered with complete symptom resolution despite persistent hypokalemia (K 2.8mmol/L). After potassium replacement, hyper-reninemic hyperaldosteronism was evident (renin 16ng/ml (0.2-2.8), aldosterone 498pmol/L (30-450). 24 hour urine showed hypercalciuria (1.6mmol/d (2.5-6.2)). A working diagnosis of Gitelman’s Syndrome was made. The blood glucose normalised without specific diabetes therapy. Maintenance potassium, magnesium and spironolactone were commenced. Thereafter, the patient was lost to follow-up.  

More recently in December 2011, the patient was admitted to hospital in China with recurrent severe hypokalemia (K 1.5mmol/L) and hyperglycaemia (38.9mmol/L). Despite long-term non-compliance with potassium supplementation, he denied interval symptoms until a change in dietary pattern similar to that which preceded his previous presentation. Potassium, magnesium and insulin were recommenced with rapid resolution of muscle weakness. Despite self ceasing insulin post-discharge, he maintained reasonable glycaemic control (HbA1c 7.2%) while on potassium supplementation and normal diet. 

Glucagon stimulation test was performed to determine beta cell function in the hypokalemic and normokalemic states. In the hypokalemic state (K 3.0mmol/L), C-peptide increased from 0.55 to 1.10nmol/L (50% rise) post 1mg of glucagon, indicative of relative insulin deficiency. Despite administration of 240mmol of potassium over 24 hours, a normokalemic state could not be achieved. Difficulty correcting hypokalemia has been demonstrated in previous small studies involving patients with Gitelman’s Syndrome.

There are no published case studies that demonstrate an association between Gitelman’s Syndrome and diabetes mellitus. However, Gitelman’s Syndrome affects the same element of the distal convoluted tubule as thiazide diuretics, which are strongly linked to new-onset diabetes. We propose that hyperglycaemia causes osmotic diuresis and hence exacerbates renal potassium wasting. Progressive hypokalemia may decrease beta-cell insulin secretion and exacerbate hyperglycaemia although the mechanism is not well understood.