Intact Parathyroid Hormone, Ionized Calcium and Calcium Infusion Test in the Evaluation of Hyperparathyroidism in Chronic Renal Failure

Pietilä, K; Mörsky, Pertti; Pasternack, Amos; Mustonen, Jukka; Koivula, Timo

doi:10.1159/000184525

Cited by 16 publications

(6 citation statements)

References 16 publications

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“…In agreement with several previous studies, our results indicate that the concentration of ionized calcium still regulates PTH secretion in chronic renal failure (group 1) [1][2][3][4], The direct correlation between the concentration of ionized calcium and Ccr supports the earlier finding that development of hypocalcemia in chronic renal failure may in part be responsible for the development of hyper parathyroidism [2], However, as only 51-74% of the varia tion in PTH seem to be explained by variations in ionized calcium concentration, other factors such as parathyroid cell mass and differences in the setpoint of the cells may be of importance in regulating the circulating level of PTH in such patients [19,20]. Although the level of l,25(OH)2D3 has been proposed to be involved in the regulation of PTH, we did not find any correlation be tween these two variables using the intact PTH or the midregion/C-terminal PTH assays [8][9][10][11].…”

Section: Discussionsupporting

confidence: 93%

“…However, a certain degree of correlation between the concentrations of intact PTH and ionized calcium was anticipated due to the short half-life of intact PTH (less than 5 min) [27]. That no correlation was found may depend on marked differ ences in glandular masses and setpoint [19,20], In a recent study, intact PTH concentration fell during calcium infu sion, indicating that calcium modified the secretion of PTH in patients on hemodialysis [4], Due to the rather long half-life of l.25(OH):D-" 11-16 h [26], compared to the short half-life of PTH one would not expect any correlation between the concentrations of 1,25(0H)2D3 and PTH, ionized calcium and phosphate, as rapid changes in these variables have been found during hemo dialysis [4,29,30], Another factor which may blunt the interreaction between l,25(OH)2D3 and phosphate is the varying degree and duration of hyperphosphatemia. Fur thermore, in patients on hemodialysis, who have the poorest renal mass compared to nondialyzed patients, a relatively larger proportion of l,25(OH)2D3 may derive from extrarenal hydroxylation of 25(OH)D3 [17,18].…”

Section: Discussionmentioning

confidence: 98%

“…The relationship between parathyroid hormone (PTH), 1,25-dihydroxyvitamin D [l,25(OH)2D3], ionized calcium and phosphate in chronic renal failure is com plex [I], Although ionized calcium is a modifier of PTH secretion in such patients [2][3][4], recent work suggests an important role for l,25(OH)2D3 as a down-regulator of PTH at the level of transcription [5], In hemodialysis patients, it seems that in addition to the calcemic effects, l,25(OH)2D3 per se modifies the secretion of PTH [6. 7], However, concerning the correlation between these two variables different results have been obtained in patients with renal failure [8][9][10][11], The disparity between these studies may be related to the use of PTH assays directed against different regions of PTH.…”

Section: Introductionmentioning

confidence: 99%

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Lack of Relationship between Parathyroid Hormone and 1,25-Dihydroxyvitamin D in Chronic Renal Failure

Rudnicki¹,

McNair

Transbøl

et al. 1991

Nephron

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In the present study, concentrations of parathyroid hormone (PTH), determined by an intact PTH assay and a midregion/C-terminal PTH assay, 1,25-dihydroxyvitamin D [1,25(OH)₂D₃], ionized calcium and phosphate were measured in 15 patients with a stable creatinine clearance (C_cr) of 21.2 ± 14.4 ml/min (mean ± SD; group 1) and in 10 patients with a C_cr regularly undergoing hemodialysis (group 2, C_cr not measured). In group 1, the mean concentration of 1,25(OH)₂D₃ was significantly increased compared with the level in group 2, whereas no differences were found concerning the concentrations of intact PTH, midregion/C-terminal PTH, ionized calcium and phosphate. In group 1, the PTH concentration correlated inversely with ionized calcium concentration and C_cr, which in turn, was directly correlated. The concentration of 1,25(OH)₂D₃ correlated inversely with phosphate concentration, but did not correlate with either PTH or ionized calcium concentrations. In group 2 no correlation was found between any of the biochemical variables. The data demonstrate that in patients with stable renal failure, the concentration of ionized calcium still regulates PTH secretion but other variables such as parathyroid cell mass and setpoint may interfere with the interrrelation. The elevated concentration of phosphate in renal failure may override PTH as a regulator of the renal 1,25(OH)₂D₃ formation. The lack of correlations in the hemodialyzed patients may be attributed to extrarenal production of 1,25(OH)₂D₃, reduced binding of 1,25(OH)₂D₃ to parathyroid tissue or the major changes in calcium homeostasis caused by the hemodialysis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Lack of Relationship between Parathyroid Hormone and 1,25-Dihydroxyvitamin D in Chronic Renal Failure

Rudnicki¹,

McNair

Transbøl

et al. 1991

Nephron

View full text Add to dashboard Cite

show abstract

“…However, the values of N-PTH and intact PTH were not suitable for the comparative study with morphometrical analysis, because these results were changeable to serum Ca level and medication as vitamin Dj, etc. [23,24]. So we examined relationships between morphometrical param eters and serum C-PTH.…”

Section: Discussionmentioning

confidence: 99%

Oxyphil Cells of Parathyroid Glands in Chronic Renal Failure May Not Secrete Parathyroid Hormone

Suzuki

Suzuki²,

Hirasawa³

et al. 1990

Nephron

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To evaluate the function of parathyroid oxyphil cell in chronic renal failure, we studied the histopathological findings of 148 parathyroid glands of 42 patients (29 males, 13 females) on maintenance hemodialysis. The individual and total weights of resected parathyroid specimens in each patient were recorded. Using the morphometrical analyzing system, we measured the oxyphil cell area and total area in each excised section taken through the maximum diameter, to estimate them in each patients. According to the fractional ratio (R:oxyphil cell area/total area), patients were divided into four groups: group I (R < 1%), group II (1%≤ < 5%), group III (5% ≤ R < 10%) and group IV (10% ≤ R). There were no differences in age, duration of hemodialysis and serum C-PTH level among the different groups. There was a positive correlation not only between total glandular weight and serum C-PTH level, but also between total glandular weight and total area, and also a positive correlation was found between serum C-PTH level and total area. No tendency was found between oxyphil cell area and serum C-PTH level. However, in 15 patients whose oxyphil cell area was more than 10 mm², there was a negative correlation between the area and serum C-PTH level. Also, in 16 patients whose R was more than 5%, there was a negative correlation between the rate and serum C-PTH level. These results suggested that oxyphil cell in chronic renal failure might not secrete PTH.

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“…an intravenous calcium infusion test [7] was made to study the suppressibility of parathyroid function.…”

Section: Co-citratementioning

confidence: 99%

Acute Effects of Calcium Carbonate and Citrate on Secondary Hyperparathyroidism in Chronic Renal Failure

Saha

Pietilä²,

Mustonen³

et al. 1991

Am J Nephrol

Self Cite

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Two grams of elemental calcium as carbonate or citrate were given after an overnight fast to 14 patients with advanced renal failure (serum creatinine 759 ± 365 µmol/l, mean ± SD). The suppressibility of their hyperparathyroidism was confirmed with a calcium infusion test. Both calcium citrate and carbonate increased significantly plasma ionized calcium (6.8 and 4.5%, respectively) and total calcium (9.3 and 6.0%), p < 0.001. In the majority of the patients, calcium citrate but not carbonate increased plasma calcium sufficiently to induce the suppression of hyperparathyroidism. The decrease of plasma intact parathyroid hormone was 35.9 ± 24.8% (mean ± SD); p < 0.001) after calcium citrate and 9.2 ± 18.9% (mean ± SD; NS) after calcium carbonate.

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Intact Parathyroid Hormone, Ionized Calcium and Calcium Infusion Test in the Evaluation of Hyperparathyroidism in Chronic Renal Failure

Cited by 16 publications

References 16 publications

Lack of Relationship between Parathyroid Hormone and 1,25-Dihydroxyvitamin D in Chronic Renal Failure

Lack of Relationship between Parathyroid Hormone and 1,25-Dihydroxyvitamin D in Chronic Renal Failure

Oxyphil Cells of Parathyroid Glands in Chronic Renal Failure May Not Secrete Parathyroid Hormone

Acute Effects of Calcium Carbonate and Citrate on Secondary Hyperparathyroidism in Chronic Renal Failure

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