Parathyroid Disorders. Группа авторов

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      •Calciuria measured on 24-h urine collections (ideally expressed in mg/kg body weight/24 h) represents intestinal absorption of calcium, while the second morning void obtained after an overnight fast, expressed as a ratio to creatininuria, represents an index of bone resorption as the measured calcium may only come from bone. The reference range of urine calcium excretion has been established in normal subjects whose calcium intake was approximately 1,000 mg/day; therefore, calcium intake should be considered and verified concomitantly with urine collection for 24-h calciuria. Questionnaires are freely available online (for example from the International Osteoporosis Foundation, www.iofbonehealth.org/calcium-calculator).

      •Measurement of phosphatemia needs to avoid hemolyzed samples and reference values vary with age: 1.50–2.30 mmol/L in newborns less than 1 month old; 1.50–2.00 mmol/L from 1 month to 2 years; 1.40–1.70 mmol/L from 2 to 12 years; 1.00–1.50 mmol/L from 12 to 16 years, and 0.80–1.40 in adults.

      •Phosphaturia, best calculated as TmP/GFR, should be measured in case of hypophosphatemia to determine whether this anomaly is due to renal leak (tubular acidosis, FGF23 excess) or to another cause. A low TmP/GFR in the presence of hypophosphatemia suggests renal phosphate leak.

•Pregnancy: NPHPT should not be diagnosed in pregnant women. Hypoalbuminemia, increased GFR, transplacental transfer of calcium, and increased levels of estrogen all contribute to lowering gestational serum calcium levels and the masking of HPHPT [27].

      •Vitamin D replacement: subjects with elevated PTH and normal calcium levels and vitamin D insufficiency may fall into 1 of the following 3 categories: (a) they may have HPHPT and their low calcium level is secondary to the impaired vitamin D status: such patients may become hypercalcemic when their vitamin D is replaced; (b) some of these patients may have elevated PTH due to their impaired vitamin D status: such subjects are expected to achieve normal PTH levels when their vitamin D status is replaced, and (c) those with true NPHPT in whom serum calcium remains normal and PTH is not suppressed after replacement with vitamin D.

•Thiazide challenge: in a normocalcemic patient with hypercalciuria and a high serum PTH concentration, a thiazide challenge test has been proposed to help in differentiating SHPT due to a renal calcium leak from normocalcemic [28]. After 2 weeks of thiazide treatment (50 mg/day), a new set of laboratory tests will be performed. If the initial hypercalciuria was due to a renal calcium leak, calciuria and PTH will be significantly reduced (often normalized) without hypercalcemia. If the initial hypercalciuria was due to NPHPT, hypercalcemia may be unmasked with only a moderate decrease in PTH concentration, which usually remains elevated. It must be noted that salt intake must be strictly limited during the thiazide treatment period for the test to be efficient.

•Calcium load test: a calcium loading test has also been proposed; it is a useful tool for this diagnosis if it shows that serum PTH is not sufficiently decreased when calcemia rises starkly above the upper normal limit [29]. Calcium and PTH levels were measured before, 60, 120, and 180 min after oral administration of 1 g of calcium gluconolactate. By calculating the product P, defined as circulating PTH nadir (pg/mL) × peak calcium concentration (mg/dL) (normal threshold 260), and ratio R, defined as relative PTH decline/relative calcium increment (normal threshold 17), the combined parameters diagnose normocalcemic hyperparathyroid patients with 100% sensitivity and 87% specificity [29].

•Kidney function: in the RECORD-IT (Report of Comorbidities in Non-Dialysis Renal Disease Population in Italy) study cohort, 31.5% of nondialysis chronic kidney disease (CKD) patients with KDIGO stage 3b–5 with PTH above this value did not receive any PTH-lowering pharmacologic treatment [30].