The severity of the infection agrees with the hypercortisolism-induced immunosuppression. This electrolyte alterations combination - hypernatremia, hypokalemia and metabolic alkalosis - is mentioned in very few reports [5,6], but has a pathophysiological basis: hypercortisolism activates mineralocorticoid receptors in renal tubules, inducing an excessive mineralocorticoid activity, leading to increased sodium reabsorption, potassium excretion and increased bicarbonate reabsorption [5]. Here, NR3C2 is linked to Hypokalemia.