Turnaround Time: 5 - 7 days
CPT Code:

82030, 82570

Test Type: 10 mL Urine (random), frozen
Stability Time:




14 days

Freeze/thaw cycles

Stable x3


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

The level of urinary cAMP is the result of cAMP released by PTH, action of other hormones and plasma cAMP filtered by the renal glomerulus. “Nephrogenous cAMP” is the urinary excretion of cAMP minus that filtered by the glomerulus and correlates best with the results of plasma PTH levels.5

1. Burtis WJ, Brady TG, Orloff JJ, et al. Immunochemical characterization of circulating parathyroid hormone-related protein in patients with humoral hypercalcemia of cancer. N Engl J Med. 1990 Apr 19; 322(16):1106-1112. PubMed 2320080

2. Mignon M, Bonfils S. Diagnosis and treatment of Zollinger-Ellison syndrome. Baillieres Clin Gastroenterol. 1988 Jul; 2(3):677-698 (review). PubMed 3048457

3. Licata A, Gall D, Gupta M. Monitoring calcium intake in osteoporosis by assay of nephrogenous cyclic AMP. Am J Clin Nutr. 1988 Jun; 47(6):1022-1024. PubMed 2837077

4. Anderson DC, Braidman IP. Hormone receptor disorders. In: Peters TJ, ed. Subcellular Pathology of Systemic Disease. London, England: Chapman and Hall;1987: 229-247.

5. Pollard A, Pritzker KPH, Grynpas MD. Disorders of calcium, magnesium, and bone metabolism. In: Gornall AG, ed. Applied Biochemistry of Clinical Disorders. 2nd ed. Philadelphia, Pa: JB Lippincott Co;1986:408-410.

Arnaud CD. The parathyroid glands, hypercalcemia, and hypocalcemia. In: Wyngaarden JB, Smith LH Jr, eds. Cecil Textbook of Medicine. 18th ed. Philadelphia, Pa: WB Saunders Co;1988:1500-1501.

Stewart AF, Horst R, Deftos LJ, et al. Biochemical evaluation of patients with cancer-associated hypercalcemia: Evidence for humoral and nonhumoral groups. N Engl J Med. 1980 Dec 11; 303(24):1377-1383. PubMed 6253785

Collection Details:

Patient Preparation:

PTH or ADH may be administered as a provocative test. No isotopes administered 48 hours prior to and during collection.

Collection Instructions:

Transport tube.

Transfer the urine into a LabCorp PP transpak frozen purple tube with screw cap (LabCorp No 49482). Freeze immediately and maintain frozen until tested.