Control of Renal Tubular Phosphate Reabsorption by Parathyroid Hormone in Man

1977 ◽  
Vol 53 (5) ◽  
pp. 431-438
Author(s):  
D. A. Walker ◽  
S. Joyce Davies ◽  
K. Siddle ◽  
J. S. Woodhead
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Primary Hyperparathyroidism ◽  
Normal Subjects ◽  
Vitamin D Metabolism ◽  
Phosphate Reabsorption ◽  
Important Regulator ◽  
Urinary Cyclic Amp ◽  
Renal Tubular

1. The maximum tubular reabsorption capacity for phosphate relative to glomerular filtration rate (Tm,P/GFR) was found to range from 0·8 to 1·5 mmol/l in 32 normal fasting subjects. In 14 patients with primary hyperparathyroidism and five patients with hyperparathyroidism secondary to vitamin D deficiency or malabsorption values ranged from 0·2 to 0·8 mmol/l. 2. Plasma parathyroid hormone concentrations measured by an immunoradiometric technique ranged from <0·15 to 0·9 ng/ml in the normal subjects and from 0·5 to 10 ng/ml in the patients with hyperparathyroidism. There was no correlation, however, between plasma parathyroid hormone and Tm,P/GFR in either normal or abnormal groups. 3. Plasma parathyroid hormone was lower in 11 out of 13 patients with primary hyperparathyroidism 3 or 4 weeks after tumour removal than immediately before the operation. In all cases there was a rise in Tm,P/GFR, though not all values were normalized. 4. Changes in plasma parathyroid hormone, Tm,P/GFR and plasma and urinary cyclic AMP concentrations were measured during infusion of bovine parathyroid hormone into normal fasting subjects. Phosphate reabsorption fell markedly in response to low doses of parathyroid hormone (0·5 i.u. h−1 kg−1), higher doses (4 i.u. h−1 kg−1) producing little additional change in Tm,P/GFR despite large changes in cyclic AMP excretion. At the highest doses used (8 i.u. h−1 kg−1) apparent saturation of the renal adenylate cyclase occurred. During an infusion of hormone, 0·25 i.u. h−1 kg−1 over 3 h, a fall in Tm,P/GFR was recorded at concentrations of immunoreactive parathyroid hormone within the normal range for endogeneous hormone. At such concentrations it was not possible to detect significant changes in either plasma or urine cyclic AMP. 5. It is concluded that parathyroid hormone is an important regulator of renal phosphate handling under normal physiological conditions. Such a regulatory process has been implicated in the control of vitamin D metabolism.

RENAL TUBULAR LOCALIZATION OF PARATHYROID HORMONE INDUCED URINARY CYCLIC ADENOSINE 3′,5′-MONOPHOSPHATE

1974 ◽  
Vol 77 (2) ◽  
pp. 282-286 ◽  
Author(s):  
Murphy T. Scurry ◽  
George L. Pauk
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Phosphorus Concentration ◽  
Phosphate Reabsorption ◽  
Before And After ◽  
Proximal Tubular ◽  
Urinary Cyclic Amp ◽  
Renal Tubular ◽  
Stop Flow

ABSTRACT Stop-flow studies were done in three dogs before and after a parathyroid hormone (PTH) infusion. The urine cyclic adenosine 3′,5′-monophosphate (cyclic AMP) to inulin U/P ratios did not change during the control stop-flow but with PTH rose sharply and significantly in the proximal tubular samples. The rise in cyclic AMP to inulin U/P ratios was correlated with the fall in phosphorus concentration in the same samples. The PTH induced urinary cyclic AMP enters the tubular fluid in the same proximal area of the tubule in which PTH is known to affect phosphate reabsorption.

Urinary and nephrogenous cyclic AMP and renal phosphate handling in normal subjects and patients with parathyroid dysfunction

1984 ◽  
Vol 106 (2) ◽  
pp. 219-226
Author(s):  
S. Khoury ◽  
J. R. Tucci
Keyword(s):  
Cyclic Amp ◽  
Primary Hyperparathyroidism ◽  
Normal Subjects ◽  
Normal Group ◽  
Permanent Hypoparathyroidism ◽  
Urinary Cyclic Amp ◽  
Parathyroid Dysfunction

Abstract. Studies were performed in 60 patients with proven primary hyperparathyroidism pre-operatively and in 54 of these patients post-operatively, 22 patients with permanent hypoparathyroidism and 34 normal subjects. Urinary and nephrogenous cyclic AMP excretion were increased in the hyperparathyroid patients with an overlap of values with the normal group of 10 and 9%, respectively. Values fell in all patients post-operatively, and were decreased in those with permanent hypoparathyroidism. TmPO4/GFR was decreased in the preoperative hyperparathyroid patients and rose postoperatively while it was increased in the hypoparathyroid patients with an overlap of values with the normal group of 9%. Post-operative hypocalcaemia due to bone hunger was associated with continuing normo- or hypophosphataemia and urinary cyclic AMP that exceeded 4.5 nm/dl GF while those who developed permanent hypoparathyroidism had hyperphosphataemia, increased TmPO4/GFR and urinary cyclic AMP that was less than 3.5 nM/dl G.F. Urinary and nephrogenous cyclic AMP were equally effective in characterizing patients with primary hyperparathyroidism and less effective in distinguishing patients with hypoparathyroidism from normal while TmPO4/GFR estimates were more effective in delineating the hypoparathyroid state.

Familial hypocalciuric hypercalcaemia: observations on vitamin D metabolism and parathyroid function

1983 ◽  
Vol 104 (2) ◽  
pp. 210-215 ◽  
Author(s):  
M. Davies ◽  
P. H. Adams ◽  
J. L. Berry ◽  
G. A. Lumb ◽  
P. S. Klimiuk ◽  
...  
Keyword(s):  
Vitamin D ◽  
Serum Concentration ◽  
Primary Hyperparathyroidism ◽  
Calcium Excretion ◽  
Renal Tubules ◽  
Vitamin D Metabolites ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D ◽  
Renal Tubular

Abstract. Serum vitamin D metabolites, the renal tubular maximum reabsorptive rate for phosphate (TMP/GFR) nephrogenic cyclic AMP (NcAMPI, and CaE (urinary calcium excretion per litre of glomerular filtrate) were measured in 14 adults with familial hypocalciuric hypercalcaemia (FHH). The findings were compared with analyses in 14 patients with surgically proven primary hyperparathyroidism matched for serum calcium, creatinine clearance and vitamin D status (assessed by serum concentrations of 25 hydroxyvitamin D). Vitamin D metabolites were also measured in 16 normocalcaemic relatives of patients with FHH. The serum concentration of 24, 25 dihydroxycholecalciferol was appropriate for the prevailing 25 hydroxyvitamin D and no difference was found between groups. The serum concentration of 1, 25 dihydroxycholecalciferol was significantly greater in primary hyperparathyroidism (P < 0.0005) compared with patients with FHH and their normocalcaemic relatives. TMP/GFR was reduced in both primary hyperparathyroidism (0.53 ± 0.12 mmol/l GF, mean ± sem) and FHH (0.86 ±0.14 mmol/l GF). Patients with primary hyperparathyroidism showed an increase in NcAMP output in the urine (38.5 ± 16 mmol/l GF) which was significantly greater (P < 0.0001) than the normal NcAMP (13.5 ± 9.2 nmol/l GF) found in FHH. CaE was low in FHH indicating increased renal tubular reabsorption of calcium. It is concluded that there is no abnormality of vitamin D metabolism in FHH comparable with the changes observed in primary hyperparathyroidism. It is suggested that the biochemical abnormalities in FHH cannot be explained solely upon an increased sensitivity of the renal tubules to the effects of endogenous parathyroid hormone.

Distribution of Circulating Immunoreactive Components of Parathyroid Hormone in Normal Subjects and in Patients with Primary and Secondary Hyperparathyroidism: The Role of the Kidney and of the Serum Calcium Concentration

1979 ◽  
Vol 57 (5) ◽  
pp. 435-443 ◽  
Author(s):  
M. A. Dambacher ◽  
J. A. Fischer ◽  
W. H. Hunziker ◽  
W. Born ◽  
J. Moran ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Normal Subjects ◽  
Dependent Manner ◽  
Intact Pth ◽  
Calcium Dependent

1. The distribution of intact parathyroid hormone-(1–84) [PTH-(1–84)] and of its COOH-terminal fragments was determined in human serum by column chromatography. In addition to PTH-(1–84) (peak I), COOH-terminal fragments having molecular weights of approximately 4000–7000 (peak II) and immunoreactive components co-eluting with human PTH-(1–12) (peak III) were observed. 2. Mean concentrations of intact PTH-(1–84) and of its COOH-terminal fragments were significantly raised in chronic renal failure as compared with those of normal subjects. Mean amounts of peak II were higher in patients with chronic renal insufficiency than in nutritional vitamin D deficiency, in pseudohypoparathyroidism and in primary hyperparathyroidism, despite comparable amounts of PTH-(1–84). 3. In chronic renal failure as well as in a group of patients with vitamin D deficiency, pseudohypoparathyroidism and primary hyperparathyroidism and in controls, significant linear relations were found between the serum concentrations of calcium and log (peak II/peak I). Our findings suggest that the conversion of intact PTH-(1–84) into COOH-terminal fragments by the parathyroid glands (resulting in a raised secretion of fragments) and/or in peripheral organs may be directly related to the serum concentration of calcium. However, the degradation of the fragments may also be suppressed in a calcium-dependent manner.

Parathyroid Function in Primary Osteoporosis

1979 ◽  
Vol 57 (2) ◽  
pp. 167-171 ◽  
Author(s):  
R. Bouillon ◽  
P. Geusens ◽  
J. Dequeker ◽  
P. De Moor
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Normal Subjects ◽  
Primary Osteoporosis ◽  
Vitamin D Binding Protein ◽  
Parathyroid Function ◽  
25 Hydroxy Vitamin D ◽  
Nutritional Vitamin

1. Parathyroid hormone and 25-hydroxy-vitamin D concentrations were measured in patients with severe primary osteoporosis and the results were compared with those found in normal subjects and in patients with primary hyperparathyroidism of vitamin D deficiency. 2. The parathyroid hormone concentrations in 19 patients with primary osteoporosis were within the normal range, both in the basal state (215 ± 85 ng/l, mean ± sd) and during a maximal stimulation (460 ±154 ng/l) induced by the infusion of disodium EDTA (70 mg/kg body weight). Increased serum concentrations of parathyroid hormone were found in patients with primary hyperparathyroidism (821 ± 323 ng/l, n = 33) and nutritional vitamin D deficiency (565 ± 144 ng/l, n = 11). 3. Serum 25-hydroxy-vitamin D concentrations (16·8 ± 7·7 μg/l) were found to be normal in patients with primary osteoporosis. Slightly (9·1 ± 2·1 μg/l) or markedly lower (2·2 ± 1·1 μg/l) 25-hydroxy-vitamin D concentrations were found respectively in patients with primary hyperparathyroidism and secondary hyperparathyroidism due to vitamin D deficiency. The serum concentration of the vitamin D-binding protein was normal in all groups. 4. A clearcut separation was therefore obtained between osteoporotic subjects (normal parathyroid hormone and normal 25-hydroxy-vitamin D concentrations) and patients with either primary hyperparathyroidism (increased parathyroid hormone and normal 25-hydroxy-vitamin D) or vitamin D deficiency (high parathyroid hormone and very low 25-hydroxy-vitamin D).

Reversible Resistance to the Renal Action of Parathyroid Hormone in Human Vitamin D Deficiency

1982 ◽  
Vol 62 (4) ◽  
pp. 381-387 ◽  
Author(s):  
I. G. Lewin ◽  
S. E. Papapoulos ◽  
G. N. Hendy ◽  
S. Tomlinson ◽  
J. L. H. O'riordan
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Urinary Excretion ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Normal Subjects ◽  
Cyclic Monophosphate ◽  
Renal Action ◽  
Plasma Adenosine

1. The response to exogenous parathyroid hormone (PTH) was tested in normal subjects and patients with osteomalacia due to vitamin D deficiency; 200 MRC units of bovine PTH were administered intravenously. 2. The rise in plasma adenosine 3′:5′-cyclic monophosphate (cyclic AMP) and the increase in urinary excretion of cyclic AMP were reduced in the patients with vitamin D deficiency. After treatment with vitamin D the responses returned to normal. 3. It is suggested that this reversible resistance is due to the secondary hyperparathyroidism associated with vitamin D deficiency.

scholarly journals Plasma 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone in familial hypocalciuric hypercalcemia and primary hyperparathyroidism

2008 ◽  
Vol 159 (6) ◽  
pp. 719-727 ◽  
Author(s):  
Signe Engkjær Christensen ◽  
Peter H Nissen ◽  
Peter Vestergaard ◽  
Lene Heickendorff ◽  
Lars Rejnmark ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Plasma Levels ◽  
Familial Hypocalciuric Hypercalcemia ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
25 Hydroxyvitamin D

IntroductionFamilial hypocalciuric hypercalcemia (FHH) is a lifelong, benign, inherited condition caused by inactivating mutations in the calcium-sensing receptor (CASR) gene. Both FHH and primary hyperparathyroidism (PHPT) are characterized by elevated P-calcium, normal or elevated plasma-parathyroid hormone (P-PTH), and typically normal renal function. In PHPT, vitamin D metabolism is typically characterized by low plasma levels of 25-hydroxyvitamin D (25OHD), and high plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D). In FHH, the vitamin D metabolism is not very well known.ObjectiveTo compare and evaluate plasma 25OHD, 1,25(OH)2D, and PTH in FHH and PHPT.DesignCross-sectional study.MaterialsAbout 66 FHH patients with mutations in the CASR gene, 147 patients with surgically verified PHPT, and 46 controls matched to FHH patients according to age (±5 years), sex, and season. All patients had a P-creatinine <140 μmol/l.MethodsWe measured P-calcium, P-Ca2+, P-albumin, P-creatinine, P-phosphate, P-magnesium, and P-PTH by standard laboratory methods. P-25OHD and P-1,25(OH)2D were measured by RIA or enzyme immunoassay. In FHH, all protein-coding exons in the CASR gene were sequenced and aligned to GenBank reference sequence .ResultsPHPT patients had higher body mass index (2p<0.01), together with higher P-PTH (2p<0.01) and P-1,25(OH)2D (2p<0.01) compared with FHH patients. The groups had similar levels of P-Ca2+ and of P-25OHD. The phenotypic expression of the CASR mutations (as determined by the degree of hypercalcemia) did not influence the levels of P-1,25(OH)2D.ConclusionEven though P-calcium and P-25OHD were comparable, P-1,25(OH)2D and P-PTH differed between FHH and PHPT.

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