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'Osteouria' the link between osteoporosis and hypercalciuria
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That’s right; your patient might be losing bone with every flush!
The upper limit of urine calcium excretion for both women and men is 4mg/kg body weight — not the 150-250 mg per 24 hours usually listed on lab reports.
A number of important diseases, particularly skeletal metastases and granulomatous diseases can cause hypercalciuria, but it is unlikely that those would be a consideration for most patients you are evaluating for osteoporosis.
Primary hyperparathyroidism is another cause of hypercalciuria but the clue to that diagnosis would be the hypercalcemia.
What I am discussing is “idiopathic” hypercalciuria for which there are two conditions you need to consider:
- Renal leak hypercalciuria which can be recognized in patients with an increased urine calcium excretion and a normal urine sodium excretion. The treatment here is simple, effective and inexpensive — hydrochlorothiazide 25 mg orally daily. There are a number of reports of fracture occurrence being less in patients taking thiazides.
- Sodium-induced hypercalciuria. Yesterday’s salt intake is excreted in today’s urine and takes calcium along with it. The treatment of this situation is seemingly straightforward — reduce the sodium intake. But we all know how difficult that can be for many patients. Just giving thiazides doesn’t work because the urine calcium-sparing effects of thiazides are blocked by a high salt intake.
No patient likes to collect a 24-hour urine sample but I order that in many patients with osteoporosis. The specimen should be analyzed for creatinine (a measure of the adequacy of the collection) as well as calcium and sodium. Not only am I looking for hypercalciuria, but I am also concerned about a low urine calcium output (arbitrarily <100 mg per 24 hours). This should alert you to a low calcium intake, poor calcium absorption or both.