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а уровень 25ОНД3? - в статье замечают что низкий кальций в моче при первичном гиперпаратиреозе может быть связан с сопутствующим дефицитом Д3.

However, simple measurement of urine calcium concentration does not reliably differentiate the two. As discussed previously, some patients with FHH have normal, and even elevated, levels of urine calcium. Conversely, only 40% of patients with primary hyperparathyroidism have frank hypercalciuria defined as a 24-hour urine excretion above 250mg per 24 hours in women or 300mg per 24 hours in men. Confounding factors that can affect urine calcium levels include
concurrent vitamin D deficiency, low dietary calcium intake, renal insufficiency and treatment with a thiazide diuretic or lithium (42).

other indices of renal calcium processing have been proposed to differentiate between FHH and primary hyperparathyroidism, including fractional excretion of calcium, theoretical tubular maximum calcium excretion, the calcium:creatinine excretion ratio, and the calcium:creatinine clearance ratio (CCCR) (15).
Of these indices, the CCCR has demonstrated the clearest delineation between the two diseases. The ratio is calculated as follows: (24-hour urine calcium/plasma total calcium)/ (24-hour urine creatinine/plasma creatinine) with care taken to match/convert the various units of
measurement. Current guidelines recognize this as the biochemical index of choice to differentiate FHH from primary hyperparathyroidism (44). A ratio of less than 0.01 is suggestive of FHH, and a level of 0.02 or higher suggests primary hyperparathyroidism.
The CCCR is obviously limited by the indeterminate range between 0.01 and 0.02. This test provides a sensitivity of 0.80 and a specificity of 0.88 for the diagnosis of FHH, prompting one group to call for a two-step screening process (43). This group proposed CCCR as the initial
screen, with genetic testing of the CaSR gene reserved for those whose CCCR was less than 0.02. The optimum screening strategy has not been clearly defined, but would need to take into account the relative prevalence of primary hyperparathyroidism and FHH, the costs of biochemical and genetic testing, and the costs of misdiagnosis resulting in unnecessary/non-
curative surgery. Of the readily available biochemical tests, the CCCR has gained consensus as the most useful in differentiating FHH from primary hyperparathyroidism in patients with hypercalcemia and normal to elevated PTH levels. Although limited in its sensitivity and specificity, the CCCR
can still alert the clinician to the possible presence of FHH even ith “normal” 24-hour calcium urine excretion.

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