Demonstration of a Defect in the Formation of Adenosine 3′, 5′-Monophosphate in Vasopressin-resistant Diabetes Insipidus

Bell, Norman H.; Clark, Charles M.; Avery, Susan; Sinha, Tushar; Trygstad, Carl W.; Allen, Donald O.

doi:10.1203/00006450-197404000-00002

Cited by 37 publications

(14 citation statements)

References 9 publications

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“…Finally, there are two reports that patients with hereditary nephrogenic DI showed reduced urinary excretion of cyclic AMP in response to exogenous vasopressin (42,43). This finding is at least compatible with the view that in such patients the formation of cyclic AMP may be impaired.…”

Section: Resultssupporting

confidence: 72%

Cellular Action of Antidiuretic Hormone in Mice with Inherited Vasopressin-Resistant Urinary Concentrating Defects

Douša¹,

Valtin²

1974

J. Clin. Invest.

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A B S T R A C T Previous workand decreased to a lesser extent in DI +/+ nonsevere animals. A significant correlation was found between the activity of adenylate cyclase maximally stimulated by AVP in a given genotype, and the urine osmolality in the same animals. There were no significant differences in maximal stimulation of renal medullary adenylate cyclase in control experiments: not when stimulated nonspecifically by sodium fluoride, nor when stimulated by AVP in tissues from rats with induced water diuresis as compared to antidiuretic rats. Nor were there significant differences between VII +/+ and DI +/+ severe mice in the activity of renal cortical adenylate Preliminary reports of this work have appeared in abstract form:

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Section: Resultssupporting

confidence: 72%

Cellular Action of Antidiuretic Hormone in Mice with Inherited Vasopressin-Resistant Urinary Concentrating Defects

Douša¹,

Valtin²

1974

J. Clin. Invest.

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“…Based on these findings, a number of laboratories have attempted to use measurements of cAMP excretion (UcAMP) diagnostically in patients with parathyroid disease, with varying success (11)(12)(13)(14)(15)(16)(17)(18). The fact that this analysis has not gained widespread acceptance as a valid index of parathyroid function can be attributed principally to three aspects of the data base currently available: (a) the lack of a demonstrably parametric expression for total cAMP excretion, (b) the description of several clinical and (or) experimental circumstances, including renal impairment (11,12,19) and high extracellular calcium concentrations (20), 1Abbreviations used in this paper: cAMP, cyclic AMP; which might interfere with the cAMP analyses or their interpretation, and (c) the alterations in plasma and (or) urinary cAMP which have been reported after pharmacologic doses of a number of agents (11,(21)(22)(23)(24) and the apparent increases in UcAMP which have been noted in several disorders other than primary hyperparathyroidism (1°HPT) (13,(25)(26)(27). Thus, there has been reasonable doubt concerning the clinical specificity of in vivo measurements of cAMP.…”

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confidence: 99%

Nephrogenous Cyclic Adenosine Monophosphate as a Parathyroid Function Test

Broadus¹,

Mahaffey²,

Bartter³

et al. 1977

J. Clin. Invest.

294

112

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A B S T R A C T 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 (10 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 c 10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 mllmin), 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 10 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%) ofthe patients with 10 HPT, avoided entirely the inadequacies of alternative expressions.Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed An abstract ofthis work appeared in 1976. Clin. Res. 24: 456A.

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“…In type I form of NDI, renal cyclic AMP production was deficient after administration of ADH (Fichman and Brooker 1972;Bell et al 1974). In type II form of NDI, remarkable increment of urinary cyclic AMP (609-1984% increase) in response to ADH was reported (Ohzeki et al 1984).…”

Section: Discussionmentioning

confidence: 99%

“…The primary type is inherited as an x-linked disease with carriers showing partial response to ADH (Bode and Crawford 1969; Uttley and Thistlethwaite 1972). Some authors have demonstrated deficient renal cyclic 3', 5'-adenosine monophosphate (AMP) production in NDI after administration of ADH and interpreted that as being defect in the adenylate cyclase system in NDI (Fichman and Brooker 1972;Bell et al 1974). Others have reported that urinary cyclic AMP increased after ADH administration in their patients of NDI and entitled that newly described defect as a type II form of NDI (Zimmerman and Green 1975).…”

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confidence: 99%