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A 25-year-old woman comes to the clinic complaining of increasing fatigue for the past 2 months. She has muscle weakness and frequent muscle cramps. She also noticed that she has to urinate more frequently than usual and has a poor appetite. She takes no medications and doesn't smoke or drink alcohol. The patient is well developed but slim and tired appearing. Her vital signs are normal. The musculoskeletal examination reveals mild bone and muscle tenderness in the lower extremities. She has diminished strength in the lower extremities. Laboratory studies show:
Sodium 140 mEq/L; potassium 2.9 mEq/L; chloride 112 mEq/L; bicarbonate 19 mEq/L; glucose 140 mg/dL; BUN 22 mg/dL; creatinine 1.0 mg/dL; calcium 7.0 mg/dL; albumin 4.0 g/dL.
What is the most accurate diagnostic step in determining the cause of this patient's hypokalemia?
(A) Glucose tolerance test
(B) Vitamin D level
© Urine potassium level
(D) Urinary magnesium level
(E) Urinary phosphorus level
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Answer:
© Urine potassium level
Explanation:
This patient exhibits the signs and symptoms of hypokalemia: fatigue, muscle weakness and pain, polyuria, and diminished motor strength. Three fundamental mechanisms may lead to hypokalemia:
1) Transcellular shift of potassium into cells
2) Reduced potassium intake
3) Excessive potassium loss
Transcellular shift is unlikely in this patient because her glucose is within the normal range, making increased production of insulin unlikely. The bicarbonate level is low, excluding alkalosis. Excessive potassium loss needs to be classified into either renal or extrarenal loss. The urine potassium is the first step. However, the urine potassium concentration may be misleading or simply inadequate when examined by itself because of factors other than potassium homeostasis. The urine potassium concentration may reflect either potassium secretion or aldosterone activity in the tubule. It should, of course, always be done in conjunction with a urinary creatinine. A formula known as the transtubular potassium gradient (TTKG) is designed to take into account factors that might influence a potassium concentration. The TTKG, though, is beyond the scope of this book, and you do not need to learn it to pass your internal medicine boards.
A glucose tolerance test is not indicated because the patient's glucose is within the normal limits. This patient has evidence of Fanconi's syndrome, such as hypocalcemia, metabolic acidosis, and bone tenderness. In this disease, the entire proximal tubule transport function is impaired, resulting in glycosuria, generalized aminoaciduria, proximal RTA, phosphaturia, and uricosuria. There is also an impaired reabsorption of calcium, magnesium, and citrate. As a result of complex disorders of mineral and vitamin D metabolism, the most frequent clinical finding is metabolic bone disease, such as osteomalacia. Other features include polyuria and muscle weakness secondary to potassium depletion, as well as nausea, episodic vomiting, and anorexia.
Vitamin D level measurement would be appropriate in this patient considering her hypocalcemia, bone fractures, and bone tenderness. However, it would not reveal a specific cause of hypokalemia. Magnesium and potassium depletion often go hand in hand, and hypomagnesemia can cause hypokalemia by increasing urinary losses. However, the serum (not urine) magnesium level tests would be appropriate.
The urine phosphorus level would be high in this patient due to Fanconi's syndrome, but it is unrelated to hypokalemia.
