Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia.

Shaw, James W.; Oldham, Susan B.; Rosoff, Leonard; Bethune, John E.; Fichman, Marshal P.

doi:10.1172/jci108611

Cited by 68 publications

(28 citation statements)

References 16 publications

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“…In addition, the influence of sodium restriction on urinary cAMP is unknown. All the interval values for urinary cAMP excretion are within the previously published normal range for humans [26,53,54].…”

Section: Discussionsupporting

confidence: 73%

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

et al. 1981

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To elucidate the relationship between the renal regulation of sodium and calcium excretion at extremes of sodium intake, we studied 6 normal men ingesting a fixed, 400 mg/day calcium intake and four levels of sodium intake from 10 to 1,500 mEq/day. Serum ionized calcium was not influenced by sodium intake. Blood pressure and cardiac index increased modestly. Urinary calcium excretion increased to 262 ± 53 mg/day (mean ± SE). Plasma norepinephrine concentration, serum PTH levels, hematocrit, total serum protein concentrations and CO₂ content decreased with increasing sodium intake. Urinary cAMP increased as sodium intake was raised from 10 to 300 mEq/day, but subsequently decreased to basal values. Urinary calcium and sodium excretion were related (p < 0.001) in a nonlinear fashion as were the fractional excretions of these cations (p < 0.001). The filtered calcium load and the fractional calcium excretion were directly and linearly related (p < 0.001). We conclude that the effect of sodium intake on urinary calcium excretion principally reflects changes in the filtered calcium load rather than changes in renal sodium handling. Calcium homeostasis at extremes of sodium intake does not appear to be critically dependent upon PTH-mediated mechanisms. The data suggest that the proximal tubule has a remarkable capacity to dissociate calcium resorption from that of sodium.

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Section: Discussionsupporting

confidence: 73%

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

et al. 1981

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“…An increase in adenylate cyclase activity and accumulation of intracellular cAMP after PTH administration have been demonstrated (16,26). The intracellular accumulation of cAMP and subsequent leakage from the renal tubular cells is considered to be an explanation for the increase in urinary excretion of CAMP, and thus, the latter change has been used as an indicator of the renal responsiveness to PTH (3,8,22,32). Our study confirms the earlier reports of a phosphaturic response to CT in both humans (1, 2, 7, 19) and rats (24).…”

Section: Resultssupporting

confidence: 88%

“…Studies have shown increased renal formation and urinary excretion of cAMP in response to PTH (1 I, 12). This change in the urinary excretion of cAMP is considered a qualitative indicator of the effect of PTH on the kidney (8,22,32). Some studies also have shown an increase in the formation of cAMP in the kidney after CT administration (20,27).…”

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confidence: 99%

Urinary Excretion of Cyclic Nucleotides and Phosphate in Response to Parathyroid Hormone and Calcitonin in Man

et al. 1981

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SummaryThe response to parathyroid hormone (PTH) and calcitonin (CT) was studied in eight children with various bone diseases by determining the serum calcium (Ca) and phosphate (P) concentration, urinary phosphate excretion rate, renal phosphate clearance, the percentage of filtered phosphate reabsorbed by the renal tubule (%TRP), creatinine clearance (Ccr), urinary cyclic adenosine 3',5' monophosphate excretion rate (UcA~pV), and urinary cyclic guanosine 3',5' monophosphate excretion rate (Ucc~pV). Administration of PTH caused no significant change in serum Ca and P values, whereas CT produced a decrease ih Ca (A Ca, -1.4 + 0.1 mg/100 ml) and P (AP; -1.1 + 0.1 mg/100 ml). There was an increase in U c~~p V ( A U r~~p V ; 437 74 nmoles/min/100 ml Ccr) without any significant change in UcCMpV after administration of PTH. Phosphaturia was produced by both PTH (A TRP, -18 k 3%) and CT (ATRP, -13 -t 2%). However, CT did not elicit any increase in either U c~~p V or U c~~p V . SpeculationParathyroid hormone (PTH) and calcitonin (CT) induce phosphaturia of a similar magnitude whereas PTH alone increased the urinary excretion of cyclic adenosine 3',5' monosphosphate (CAMP). The phosphaturia induced by CT may not be mediated by a similar mechanism involving the adenylate cyclase-CAMP system as demonstrated for PTH.Parathyroid hormone (PTH) and calcitonin (CT) have opposing effects on bone resorption; PTH induces hypercalcemia by stimulating bone resorption whereas CT induces hypocalcemia by inhibiting bone resorption. Despite their opposing effects on bone, they both act on the kidney to produce phosphaturia. The actions of PTH and CT on both bone and kidney are presumably mediated through the adenylate cyclase cyclic adenosine 3',5'-monophosphate (CAMP) system. Studies have shown increased renal formation and urinary excretion of cAMP in response to PTH (1 I, 12). This change in the urinary excretion of cAMP is considered a qualitative indicator of the effect of PTH on the kidney (8,22,32). Some studies also have shown an increase in the formation of cAMP in the kidney after CT administration (20,27). However, few studies have investigated urinary excretion of cAMP after CT administration, and those that are available, report conflicting results. No increase in urinary excretion of cAMP was reported after CT administration in parathyroiaectomized rats, dogs (I I), and in one patient with hypoparathyroidism (28), whereas an increase in cAMP was reported in hamsters (23) and parathyroidectomized rats (24). Some studies in man (1, 2, 28) have shown an increase in urinary cAMP in response to salmon or porcine CT, but the magnitude of rise was insignificant when compared to the rise after PTH. Therefore, to assess the relationship of urinary cAMP excretion and the phosphaturic response to CT in man, we have studied the effect of synthetic human CT on patients with various bone diseases, all of whom had normal phosphaturic and cAMPuric responses to PTH. In view of the possible role of cyclic guanosine 3',Sf-monophosphate (c...

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“…Although the state of hydration (13,29,31,32) or the consumption of methyl xanthines (29,37) do not appear to influence cAMP excretion, physical activity has been reported to increase plasma cAMP (25) Both plasma iPTH (3,38,39) and plasma and urinary cAMP (18,29,37) have been reported to exhibit a diurnal variation, although in each case there is disagreement as to the exact pattern and extent of variation. In 52 patients, plasma cAMP was determined between 8 and 9 a.m. and again between 11 a.m. and 12 noon.…”

Section: Study Protocolmentioning

confidence: 99%

“…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).…”

mentioning

confidence: 99%

Nephrogenous Cyclic Adenosine Monophosphate as a Parathyroid Function Test

Broadus¹,

Mahaffey²,

Bartter³

et al. 1977

J. Clin. Invest.

295

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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Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia.

Cited by 68 publications

References 16 publications

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

Urinary Excretion of Cyclic Nucleotides and Phosphate in Response to Parathyroid Hormone and Calcitonin in Man

Nephrogenous Cyclic Adenosine Monophosphate as a Parathyroid Function Test

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