Mayo Test Catalog, (Sorted By Test Name) - Mayo Medical ...

2HCAP
81679
CSRKM
83704
PEAK CALCIUM INFUSION
Males: < or =130 pg/mL
Females: < or =90 pg/mL
Clinical References: 1. Brandi ML, Gagel RF, Angeli A, et al: Guidelines for diagnosis and
therapy of MEN type 1 and type 2. J Clin Endocrinol Metab 2001;86(12):5658-5671 2. Gimm O, Sutter
T, Dralle H: Diagnosis and therapy of sporadic and familial medullary thyroid carcinoma. J Cancer Res
Clin Oncol 2001;127(3):156-165 3. Perdrisot R, Bigorgne JC, Guilloteau D, Jallet P: Monoclonal
immunoradiometric assay of calcitonin improves investigation of familial medullary thyroid carcinoma.
Clin Chem 1990 February;36(2):381-383 4. Weissel M, Kainz H, Tyl E, et al: Clinical evaluation of
new assays for determination of serum calcitonin concentration. ACTA Endocrinol (Copenh) 1991
May;124(5):540-544
Calcium Excretion, 2-Hour Collection, Fasting, Urine
Clinical Information: 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.
Useful For: Differentiating absorptive from nonabsorptive causes of hypercalciuria
Interpretation: 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: Level Cause for hypercalciuria 0.15
calcium/creatinine Nephrogenic or metabolic indeterminate 20 mg/2 hour to 30 mg/2-hour specimen
Reference Values:
Absorptive hypercalciuria: 0.15
Indeterminate: 20-30 mg calcium/2-hour specimen
Clinical References: Pak CY, Oata M, Lawrence EC, Snyder W: The hypercalciurias. Causes,
parathyroid functions, and diagnostic criteria. J Clin Invest 1974;54:387-400
Calcium Sensing Receptor (CASR) Gene, Known Mutation
Clinical Information: The extracellular G-protein-coupled calcium sensing receptor (CASR) is an
essential component of calcium homeostasis. CASR is expressed at particularly high levels in the
parathyroid glands and kidneys. It forms stable homodimeric cell-membrane complexes, which signal
upon binding of extracellular calcium-ions (Ca[++]). In the parathyroid glands, this results in
downregulation of gene expression of the main short-term regulator of calcium homeostasis,
parathyroid hormone (PTH), as well as diminished secretion of already synthesized PTH. At the same
time, renal calcium excretion is upregulated and sodium-chloride excretion is downregulated. Ca(++)
binding to CASR is highly cooperative within the physiological Ca(++) concentration range, leading to
a steep dose-response curve, which results in tight control of serum calcium levels. To date over 100
different alterations in the CASR gene have been described. Many of these cause diseases of abnormal
serum calcium regulation. Inactivating mutations result in undersensing of Ca(++) concentrations and
consequent PTH overproduction and secretion. This leads to either familial hypocalciuric hypercalcemia
(FHH) or neonatal severe primary hyperparathyroidism (NSPHT), depending on the severity of the
functional impairment. Except for a very small percentage of cases with no apparent CASR mutations,
FHH is due to heterozygous inactivating CASR mutations. Serum calcium levels are
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