Urine Calcium: Laboratory Measurement and Clinical Utility

Kevin F. Foley, PhD, DABCC; Lorenzo Boccuzzi, DO

Disclosures

Lab Med. 2010;41(11):683-686. 

In This Article

Use in FHH and Primary Hyperparathyroidism

The prognosis and treatments differ significantly between FHH and primary hyperparathyroidism (PH). Familial hypocalciuric hypercalcemia is typically a benign disease requiring no treatment, whereas surgical intervention is required to treat PH in order to prevent long-term complications of hypercalcemia.[7] Can urine calcium measurement help differentiate PH from FHH? Guidelines have been suggested stating that a CCCR of <0.010 implicates FHH, whereas a CCCR of >0.020 is highly suspicious of PH.[9,11] Christensen and colleagues compared CCCR measurement with CE and CR in 54 patients with FHH (all with mutations in the CASR gene), and 97 hypercalcemic patients with histological confirmation of PH.[7] They found the CCCR measurement was marginally better than CE or CR at differentiating the 2 diseases. At a cut-off point of <0.020, the CCCR index in their population included 98% of all patients with FHH but still included 35% of patients with PH. Although this cut-off still included some PH patients, the CCCR misclassified fewer PH patients than CR or CE. The authors concluded CCCR might be useful as an initial screening test for FHH, followed by CASR gene analysis for patients <0.020 to rule in/out FHH.

Urinary calcium measurements may also play a role in identifying certain patients with osteoporosis who form kidney stones. Patients at risk for stone formation typically follow different treatment options for their osteoporosis. Giannini and colleagues determined that measuring urinary CE in osteoporotic patients may help identify those patients with idiopathic hypercalciuria and calcium nephrolithiasis.[12] As pointed out in their study, there are data to support the association between low bone density in nephrolithiasic patients with hypercalciuria but not in those without hypercalciuria. More importantly, the author points out a number of retrospective and prospective studies showing thiazides (which decrease urine calcium), have been associated with a reduction in fracture incidence,[13–16] and an increase in bone density.[17–21] Giannini and colleagues suggest the majority of the patients in their study may suffer from a diet-independent form of hypercalciuria similar to that seen in patients with kidney stones and low bone density.[12] They conclude that urinary CE should be measured in osteoporotic patients in order to identify this group of patients.

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