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CYCLIC AMP, URINE
Message"PTH or ADH may be administered as a provocative test. No isotopes administered 48 hours prior to and during collection.
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Test Code
4903
Alias/See Also
cAMP, Urine
CPT Codes
82030; 82570
Preferred Specimen
"Urine (random),
10 mL
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10 mL
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Minimum Volume
"0.5 mL (Note: This volume does not allow for repeat testing.)
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Instructions
"Transfer the urine into a LabCorp PP transpak frozen purple tube with screw cap (LabCorp No 49482). Freeze immediately and maintain frozen until tested.
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Transport Container
"Transport tube
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Transport Temperature
Frozen
Specimen Stability
Freeze
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
"Specimen not received frozen; recently administered radioisotopes
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Methodology
"Radioimmunoassay (RIA) "
Limitations
"There is some overlap between results of patients with hyperparathyroidism and those of normal subjects. Not all patients with hyperparathyroidism have abnormal urinary cAMP results. Urinary cAMP is reported increased in hypercalcemic cancer patients.
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Clinical Significance
"Differential diagnosis of hyperparathyroidism. In hyperparathyroidism there is increased cAMP in urine. Increased levels are also found in humoral hypercalcemia of malignancy and vitamin D deficiency. The plasma concentrations of immunoreactive parathyroid hormone-related protein correlate with levels of excreted cyclic AMP.1
There is a role for cAMP excretion measurement in the evaluation of Zollinger-Ellison syndrome and differentiation of sporadic cases from those of multiple endocrine neoplasia type I.2 Assay of nephrogenous cyclic AMP has been applied to the monitoring of calcium intake in cases of osteoporosis.3
A target of parathyroid hormone (PTH) action is the renal tubule. The result is release of cAMP into the urine. Cyclic AMP output in the urine is thus an indirect measure of parathyroid action. PTH utilizes cyclic AMP to exert its effect on cells. Upon binding of PTH to its receptor, the latter undergoes a confirmational change which increases its affinity (through a second binding site) for a linking protein (Ns) which also binds guanosine triphosphate.
Type I pseudohypoparathyroidism (autosomal dominant inheritance), mimics hypoparathyroidism with hypocalcemia resistant to vitamin D and high serum phosphate and PTH levels. This condition appears to be due to a defect in linking protein (Ns) structure. Type I is characterized by defective renal tubular response to PTH and increased circulating and urinary cyclic AMP. Type II pseudohypoparathyroidism (autosomal dominant inheritance) has a normal cyclic AMP response.4
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There is a role for cAMP excretion measurement in the evaluation of Zollinger-Ellison syndrome and differentiation of sporadic cases from those of multiple endocrine neoplasia type I.2 Assay of nephrogenous cyclic AMP has been applied to the monitoring of calcium intake in cases of osteoporosis.3
A target of parathyroid hormone (PTH) action is the renal tubule. The result is release of cAMP into the urine. Cyclic AMP output in the urine is thus an indirect measure of parathyroid action. PTH utilizes cyclic AMP to exert its effect on cells. Upon binding of PTH to its receptor, the latter undergoes a confirmational change which increases its affinity (through a second binding site) for a linking protein (Ns) which also binds guanosine triphosphate.
Type I pseudohypoparathyroidism (autosomal dominant inheritance), mimics hypoparathyroidism with hypocalcemia resistant to vitamin D and high serum phosphate and PTH levels. This condition appears to be due to a defect in linking protein (Ns) structure. Type I is characterized by defective renal tubular response to PTH and increased circulating and urinary cyclic AMP. Type II pseudohypoparathyroidism (autosomal dominant inheritance) has a normal cyclic AMP response.4
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