Urine diuretic screening is appropriate for this patient. The first step when assessing a patient with metabolic alkalosis is to clinically assess the patient's volume status. This patient has metabolic alkalosis as implied by the elevated serum bicarbonate and is hypovolemic as evidenced by the orthostatic blood pressure and pulse changes. Such a patient would be expected to have low urine concentrations of sodium and chloride. However, this patient's urine electrolytes show increased excretion of sodium and chloride despite the evident hypovolemia. These findings suggest the presence of active diuretic use or a renal tubular defect that impairs handling of sodium and chloride, such as Bartter and Gitelman syndromes. These rare autosomal recessive genetic disorders of renal sodium and chloride transporters clinically mimic loop diuretic and thiazide diuretic use, respectively, but should be considered only after diuretic use has been eliminated with negative urine diuretic screening.

Measurement of 24-hour urine free cortisol excretion is a standard test for diagnosing Cushing syndrome, which is characterized by proximal muscle weakness, hypokalemia, hypertension, and diabetes mellitus. These findings are not present in this patient.

Plasma aldosterone-plasma renin ratio is unlikely to be helpful in this situation. Although primary hyperaldosteronism is characterized by hypokalemia and metabolic alkalosis, the absence of hypertension makes this diagnosis unlikely. Finally, diuretics and Gitelman and Bartter syndromes are associated with various degrees of volume contraction and secondary hyperaldosteronism. Plasma aldosterone and renin activity levels will not differentiate these disorders.

Thyroid dysfunction is not associated with acid-base abnormalities and may be associated with hypokalemia only in rare and severe cases such as thyrotoxic periodic paralysis, in which attacks of profound generalized weakness occur suddenly with preserved consciousness.