|Values are valid only on day of printing.|
Urine calcium is a reflection of dietary intake, bone turnover, and renal excretion mechanisms. At steady-state excretion is usually approximately 30% of the dietary intake.
Patients with renal lithiasis often (35%) have increased urine calcium which may reflect an increased intake or an abnormality in the above mechanisms.
Therapy for hypercalciuria depends on the cause. Increased calcium in diet or increased gastrointestinal absorption usually responds to dietary restriction while hypercalciuria from other mechanisms usually responds to thiazides. Diet restriction is contraindicated in the nonabsorptive groups and thiazides are usually unnecessary or ineffective in the former group.
Differentiating absorptive from nonabsorptive causes of hypercalciuria
If a patient is hypercalciuric and on a 1 g calcium diet, urine calcium results from a 2-hour urine specimen after 14 hours of fasting:
Cause for hypercalciuria
<20 mg/2-hour specimen or
<0.15 calcium/creatinine ratio
Increased gut absorption
>30 mg/2-hour specimen or
Nephrogenic or metabolic indeterminate
20 mg/2 hour to 30 mg/2-hour specimen
Hypercalciuria is markedly dependent on sodium excretion and results may be altered if very low or high sodium diets are allowed.
Patients should drink distilled or deionized water during the test.
Exact timing and volume measurement are essential.
Absorptive hypercalciuria: <20 mg calcium/2-hour specimen or a calcium/creatinine ratio of <0.15
Nonabsorptive hypercalciuria: >30 mg calcium/2-hour specimen or a calcium/creatinine ratio of >0.15
Indeterminate: 20-30 mg calcium/2-hour specimen
Pak CY, Oata M, Lawrence EC, Snyder W: The hypercalciurias. Causes, parathyroid functions, and diagnostic criteria. J Clin Invest 1974;54:387-400