Nephrogenous cyclic adenosine monophosphate as a parathyroid function test.
PDF (1.9M)
Journal: 1977/October - Journal of Clinical Investigation
ISSN: 0021-9738
Abstract:
Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1 degrees HPT), and 10 patients with chronic hypoparathyroidism. In the group with 1 degrees HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium </=10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 ml/min), and 10 patients with moderate renal insufficiency (mean glomerular filtration rate, 43 ml/min). Plasma iPTH was increased in 41 patients (73%). The development of a parametric expression for UcAMP was found to be critically important in the clinical interpretation of results for total cAMP excretion. Because of renal impairment in a large number of patients, the absolute excretion rate of cAMP correlated poorly with the hyperparathyroid state. Expressed as a function of creatinine excretion, UcAMP was elevated in 81% of patients with 1 degrees HPT, but the nonparametric nature of the expression led to a number of interpretive difficulties. The expression of cAMP excretion as a function of glomerular filtration rate was developed on the basis of the unique features of cAMP clearance in man, and this expression, which provided elevated values in 51 (89%) of the patients with 1 degrees HPT, avoided entirely the inadequacies of alternative expressions. Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed the validity of the measurements and the expressions employed.
Open in
PUBMED | DOI | PMC | Google Scholar | Wikipedia
Relations:
Content
Citations
(47)
References
(47)
Diseases
(3)
Conditions
(1)
Chemicals
(3)
Organisms
(1)
Anatomy
(1)
Similar articles
Articles by the same authors
Discussion board
J Clin Invest 60(4): 771-783
PMID: 197123

Nephrogenous Cyclic Adenosine Monophosphate as a Parathyroid Function Test

Abstract

Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1°HPT), and 10 patients with chronic hypoparathyroidism.

In the group with 1° HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium ≤10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 ml/min), and 10 patients with moderate renal insufficiency (mean glomerular filtration rate, 43 ml/min). Plasma iPTH was increased in 41 patients (73%).

The development of a parametric expression for UcAMP was found to be critically important in the clinical interpretation of results for total cAMP excretion. Because of renal impairment in a large number of patients, the absolute excretion rate of cAMP correlated poorly with the hyperparathyroid state. Expressed as a function of creatinine excretion, UcAMP was elevated in 81% of patients with 1° HPT, but the nonparametric nature of the expression led to a number of interpretive difficulties. The expression of cAMP excretion as a function of glomerular filtration rate was developed on the basis of the unique features of cAMP clearance in man, and this expression, which provided elevated values in 51 (89%) of the patients with 1° HPT, avoided entirely the inadequacies of alternative expressions.

Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed the validity of the measurements and the expressions employed.

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.9M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.
icon of scanned page 771
771
icon of scanned page 772
772
icon of scanned page 773
773
icon of scanned page 774
774
icon of scanned page 775
775
icon of scanned page 776
776
icon of scanned page 777
777
icon of scanned page 778
778
icon of scanned page 779
779
icon of scanned page 780
780
icon of scanned page 781
781
icon of scanned page 782
782
icon of scanned page 783
783

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Berson SA, Yalow RS, Aurbach GD, Potts JT. IMMUNOASSAY OF BOVINE AND HUMAN PARATHYROID HORMONE. Proc Natl Acad Sci U S A. 1963 May;49(5):613–617.[PMC free article] [PubMed] [Google Scholar]
  • Potts JT, Jr, Murray TM, Peacock M, Niall HD, Tregear GW, Keutmann HT, Powell D, Deftos LJ. Parathyroid hormone: sequence, synthesis, immunoassay studies. Am J Med. 1971 May;50(5):639–649. [PubMed] [Google Scholar]
  • Reiss E, Canterbury JM. Emerging concepts of the nature of circulating parathyroid hormones: implications for clinical research. Recent Prog Horm Res. 1974;30(0):391–429. [PubMed] [Google Scholar]
  • Segre GV, Habener JF, Powell D, Tregear GW, Potts JT. Parathyroid Hormone in Human Plasma: IMMUNOCHEMICAL CHARACTERIZATION AND BIOLOGICAL IMPLICATIONS. J Clin Invest. 1972 Dec;51(12):3163–3172.[PMC free article] [PubMed] [Google Scholar]
  • Silverman R, Yalow RS. Heterogeneity of parathyroid hormone. Clinical and physiologic implications. J Clin Invest. 1973 Aug;52(8):1958–1971.[PMC free article] [PubMed] [Google Scholar]
  • Arnaud CD, Goldsmith RS, Bordier PJ, Sizemore GW. Influence of immunoheterogeneity of circulating parathyroid hormone on results of radioimmunoassays of serum in man. Am J Med. 1974 Jun;56(6):785–793. [PubMed] [Google Scholar]
  • Chase LR, Aurbach GD. Parathyroid function and the renal excretion of 3'5'-adenylic acid. Proc Natl Acad Sci U S A. 1967 Aug;58(2):518–525.[PMC free article] [PubMed] [Google Scholar]
  • Chase LR, Aurbach GD. Renal adenyl cyclase: anatomically separate sites for parathyroid hormone and vasopressin. Science. 1968 Feb 2;159(3814):545–547. [PubMed] [Google Scholar]
  • Kaminsky NI, Broadus AE, Hardman JG, Jones DJ, Jr, Ball JH, Sutherland EW, Liddle GW. Effects of parathyroid hormone on plasma and urinary adenosine 3',5'-monophosphate in man. J Clin Invest. 1970 Dec;49(12):2387–2395.[PMC free article] [PubMed] [Google Scholar]
  • Scurry MT, Pauk GL. Renal tubular localization of parathyroid hormone induced urinary cyclic adenosine 3',5'-monophosphate. Acta Endocrinol (Copenh) 1974 Oct;77(2):282–286. [PubMed] [Google Scholar]
  • Taylor AL, Davis BB, Pawlson LG, Josimovich JB, Mintz DH. Factors influencing the urinary excretion of 3',5'-adenosine monophosphate in humans. J Clin Endocrinol Metab. 1970 Mar;30(3):316–324. [PubMed] [Google Scholar]
  • Dohan PH, Yamashita K, Larsen PR, Davis B, Deftos L, Field JB. Evaluation of urinary cyclic 3'5'-adenosine monophosphate excretion in the differential diagnosis of hypercalcemia. J Clin Endocrinol Metab. 1972 Dec;35(6):775–784. [PubMed] [Google Scholar]
  • Murad F. Clinical studies and applications of cyclic nucleotides. Adv Cyclic Nucleotide Res. 1973;3:355–383. [PubMed] [Google Scholar]
  • Neelon FA, Birch BM, Drezner M, Lebovitz HE. Urinary cyclic adenosine monophosphate as an aid in the diagnosis of hyperparathyroidism. Lancet. 1973 Mar 24;1(7804):631–633. [PubMed] [Google Scholar]
  • Mallette LE, Bilezikian JP, Heath DA, Aurbach GD. Primary hyperparathyroidism: clinical and biochemical features. Medicine (Baltimore) 1974 Mar;53(2):127–146. [PubMed] [Google Scholar]
  • Debacker M, Manderlier T, Nijs-Dewolf N, Six R, Corvilain J. Urinary cyclic AMP as an aid in the differential diagnosis of hypercalcemia. Biomedicine. 1974 Aug 10;21(8):338–341. [PubMed] [Google Scholar]
  • Pak CY, Kaplan R, Bone H, Townsend J, Waters O. A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. N Engl J Med. 1975 Mar 6;292(10):497–500. [PubMed] [Google Scholar]
  • Shaw JW, Oldham SB, Rosoff L, Bethune JE, Fichman MP. Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia. J Clin Invest. 1977 Jan;59(1):14–21.[PMC free article] [PubMed] [Google Scholar]
  • von Lilienfeld-Toal H, Hesch RD, Hüfner M, McIntosh C. Excretion of cyclic 3',5'-adenosine monophosphate in renal insufficiency and primary hyperparathyroidism after stimulation with parathyroid hormone. Horm Metab Res. 1974 Jul;6(4):314–318. [PubMed] [Google Scholar]
  • Beck N, Singh H, Reed SW, Davis BB. Direct inhibitory effect of hypercalcemia on renal actions of parathyroid hormone. J Clin Invest. 1974 Mar;53(3):717–725.[PMC free article] [PubMed] [Google Scholar]
  • Ball JH, Kaminsky NI, Hardman JG, Broadus AE, Sutherland EW, Liddle GW. Effects of catecholamines and adrenergic-blocking agents on plasma and urinary cyclic nucleotides in man. J Clin Invest. 1972 Aug;51(8):2124–2129.[PMC free article] [PubMed] [Google Scholar]
  • Broadus AE, Kaminsky NI, Northcutt RC, Hardman JG, Sutherland EW, Liddle GW. Effects of glucagon on adenosine 3',5'-monophosphate and guanosine 3',5'-monophosphate in human plasma and urine. J Clin Invest. 1970 Dec;49(12):2237–2245.[PMC free article] [PubMed] [Google Scholar]
  • Fichman MP, Brooker G. Deficient renal cyclic adenosine 3'-5' monophosphate production in nephrogenic diabetes insipidus. J Clin Endocrinol Metab. 1972 Jul;35(1):35–47. [PubMed] [Google Scholar]
  • Bell NH, Clark CM, Jr, Avery S, Sinha T, Trygstad CW, Allen DO. Demonstration of a defect in the formation of adenosine 3',5'-monophosphate in vasopressin-resistant diabetes insipidus. Pediatr Res. 1974 Apr;8(4):223–230. [PubMed] [Google Scholar]
  • Hamet P, Kuchel O, Fraysse J, Genest J. Plasma adenosine 3',5'-cyclic monophosphate in human hypertension. Can Med Assoc J. 1974 Aug 17;111(4):323–328.[PMC free article] [PubMed] [Google Scholar]
  • Lin T, Kopp LE, Tucci JR. Urinary excretion of cyclic-3',5'-adenosine monophosphate in hyperthyroidism. J Clin Endocrinol Metab. 1973 May;36(5):1033–1036. [PubMed] [Google Scholar]
  • Carter DJ, Heath DA. Proceedings. Urinary cyclic AMP excretion in thyroid disease. Clin Sci Mol Med. 1974 Nov;47(5):19P–20P. [PubMed] [Google Scholar]
  • Broadus AE, Kaminsky NI, Hardman JG, Sutherland EW, Liddle GW. Kinetic parameters and renal clearances of plasma adenosine 3',5'-monophosphate and guanosine 3',5'-monophosphate in man. J Clin Invest. 1970 Dec;49(12):2222–2236.[PMC free article] [PubMed] [Google Scholar]
  • ORLOFF J, HANDLER JS. THE CELLULAR MODE OF ACTION OF ANTIDIURETIC HORMONE. Am J Med. 1964 May;36:686–697. [PubMed] [Google Scholar]
  • Butlen D, Jard S. Renal handling of 3'-5'-cyclic AMP in the rat. The possible role of luminal 3'-5'-cyclic AMP in the tubular reabsorption of phosphate. Pflugers Arch. 1972;331(2):172–190. [PubMed] [Google Scholar]
  • Hardman JG, Davis JW, Sutherland EW. Effects of some hormonal and other factors on the excretion of guanosine 3',5'-monophosphate and adenosine 3',5'-monophosphate in rat urine. J Biol Chem. 1969 Dec 10;244(23):6354–6362. [PubMed] [Google Scholar]
  • Schmidt-Gayk H, Röher HD. Urinary excretion of cyclic adenosine monophosphate in the detection and diagnosis of primary hyperparathyroidism. Surg Gynecol Obstet. 1973 Sep;137(3):439–444. [PubMed] [Google Scholar]
  • Babka JC, Bower RH, Sode J. Nephrogenous cyclic AMP levels in primary hyperparathyroidism. Arch Intern Med. 1976 Oct;136(10):1140–1144. [PubMed] [Google Scholar]
  • Drezner MK, Neelon FA, Curtis HB, Lebovitz HE. Renal cyclic adenosine monophosphate: an accurate index of parathyroid function. Metabolism. 1976 Oct;25(10):1103–1112. [PubMed] [Google Scholar]
  • Bilezikian JP, Doppman JL, Powell D, Wells SA, Heath DA, Ketcham AS, Monchik J, Mallette LE, Potts JT, Jr, Aurbach GD. Preoperative localization of abnormal parathyroid tissue. Cumulative experience with venous sampling and arteriography. Am J Med. 1973 Oct;55(3):505–514. [PubMed] [Google Scholar]
  • Murad F, Pak CY. Urinary excretion of adenosine 3',5'-monophosphate and guanosine 3',5'-monophosphate. N Engl J Med. 1972 Jun 29;286(26):1382–1387. [PubMed] [Google Scholar]
  • Arnaud CD, Tsao HS, Littledike T. Radioimmunoassay of human parathyroid hormone in serum. J Clin Invest. 1971 Jan;50(1):21–34.[PMC free article] [PubMed] [Google Scholar]
  • Sinha TK, Miller S, Feming J, Khairi R, Edmondson J, Johnston CC, Jr, Bell NH. Demonstration of a diurnal variation in serum parathyroid hormone in primary and secondary hyperparathyroidism. J Clin Endocrinol Metab. 1975 Dec;41(06):1009–1013. [PubMed] [Google Scholar]
  • Gilman AG. A protein binding assay for adenosine 3':5'-cyclic monophosphate. Proc Natl Acad Sci U S A. 1970 Sep;67(1):305–312.[PMC free article] [PubMed] [Google Scholar]
  • Berson SA, Yalow RS. Parathyroid hormone in plasma in adenomatous hyperparathyroidism, uremia, and bronchogenic carcinoma. Science. 1966 Nov 18;154(3751):907–909. [PubMed] [Google Scholar]
  • Hamet P, Stouder DA, Ginn HE, Hardman JG, Liddle GW. Studies of the elevated extracellular concentration of cyclic AMP in uremic man. J Clin Invest. 1975 Aug;56(2):339–345.[PMC free article] [PubMed] [Google Scholar]
  • Guttler RB, Shaw JW, Otis CL, Nicologg JT. Epinephrine-induced alterations in urinary cyclic AMP in hyper- and hypothyroidism. J Clin Endocrinol Metab. 1975 Oct;41(4):707–711. [PubMed] [Google Scholar]
  • Llach F, Massry SG, Singer FR, Kurokawa K, Kaye JH, Coburn JW. Skeletal resistance to endogenous parathyroid hormone in pateints with early renal failure. A possible cause for secondary hyperparathyroidism. J Clin Endocrinol Metab. 1975 Aug;41(2):339–345. [PubMed] [Google Scholar]
  • Streeto JM. Renal cortical adenyl cyclase: effect of parathyroid hormone and calcium. Metabolism. 1969 Nov;18(11):968–973. [PubMed] [Google Scholar]
  • Popovtzer MM, Robinette JB, McDonald KM, Kuruvila CK. Effect of Ca++ on renal handling of PO4 identical to: evidence for two reabsorptive mechanisms. Am J Physiol. 1975 Oct;229(4):901–906. [PubMed] [Google Scholar]
  • Marx SJ, Spiegel AM, Brown EM, Aurbach GD. Family studies in patients with primary parathyroid hyperplasia. Am J Med. 1977 May;62(5):698–706. [PubMed] [Google Scholar]
  • Foley TP, Jr, Harrison HC, Arnaud CD, Harrison HE. Familial benign hypercalcemia. J Pediatr. 1972 Dec;81(6):1060–1067. [PubMed] [Google Scholar]
Hypertension-Endocrine Branch, National Heart and Lung Institute, Bethesda, Maryland 20014
Endocrine Division, Massachusetts General Hospital, Boston, Massachusetts 02114
Copyright notice
Abstract
Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1°HPT), and 10 patients with chronic hypoparathyroidism.
In the group with 1° HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium ≤10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 ml/min), and 10 patients with moderate renal insufficiency (mean glomerular filtration rate, 43 ml/min). Plasma iPTH was increased in 41 patients (73%).
The development of a parametric expression for UcAMP was found to be critically important in the clinical interpretation of results for total cAMP excretion. Because of renal impairment in a large number of patients, the absolute excretion rate of cAMP correlated poorly with the hyperparathyroid state. Expressed as a function of creatinine excretion, UcAMP was elevated in 81% of patients with 1° HPT, but the nonparametric nature of the expression led to a number of interpretive difficulties. The expression of cAMP excretion as a function of glomerular filtration rate was developed on the basis of the unique features of cAMP clearance in man, and this expression, which provided elevated values in 51 (89%) of the patients with 1° HPT, avoided entirely the inadequacies of alternative expressions.
Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed the validity of the measurements and the expressions employed.
Collaboration tool especially designed for Life Science professionals.Drag-and-drop any entity to your messages.