A Trial of Calcitonin Therapy in Renal Osteodystrophy

Delano, Barbara G.; Baker, R.; Gardner, Bernard; Wallach, Stanley

doi:10.1159/000180236

Cited by 10 publications

(2 citation statements)

References 7 publications

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“…It seems probable that the rise in alkaline phosphatase in our patients was due to an increase in osteoblastic activity, since we and others have noted a strong positive correlation between osteoblastic surfaces and plasma alkaline phosphatase in chronic renal failure (Table 3) [14, 30, 331. The question arises whether the rise in alkaline phosphatase reflected an increase in bone turnover (increased osteoblastic bone formation plus increased bone resorption) or a net increase in bone formation (increased osteoblastic bone formation without increased bone resorption). A previous report has suggested that daily administration of salmon calcitonin in chronic renal failure may increase net bone resorption [34], but several of our observations suggest at least a transient uncoupling between the rates of bone formation and resorption. Hypocalcaemia was noted in many of the patients throughout treatment even though plasma calcium was measured 48-72 h after each dose of calcitonin.…”

Section: Iacontrasting

confidence: 68%

Responses to salmon calcitonin in chronic renal failure: relation to histological and biochemical indices of bone turnover

Cundy

Heynen

Gaspar

et al. 1981

Eur J Clin Investigation

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Twenty-one patients with chronic renal failure and bone disease or hypercalcaemia were studied before and following single (twenty patients) or repeated (fourteen patients) intravenous injection of synthetic salmon calcitonin. Significant correlations were noted before treatment between bone surfaces occupied by osteoblasts or osteoclasts and plasma levels of immunoreactive parathyroid hormone, alkaline phosphatase and hydroxyproline. Following a single injection of 2--200 i.u. salmon calcitonin, plasma levels of calcium and phosphate fell for 6--8 h, but rose subsequently to pre-injection levels at 24 h. The magnitude and duration of the hypocalcaemic response was not clearly dose-dependent, but correlated with measured indices of bone cell activity. Repeated administration of calcitonin (10--200 i.u. thrice weekly for up to 2 months) lowered plasma calcium in the majority of patients and restored plasma calcium to normal in four previously hypercalcaemic patients. Mean levels of alkaline phosphatase increased but no significant changes in plasma phosphate, immunoreactive parathyroid hormone and calcitonin, or hydroxyproline occurred. Calcium absorption (six studies) did not change during treatment. We conclude that synthetic salmon calcitonin is an effective short-term inhibitor of bone resorption in patients with chronic renal failure. Its use as a possible treatment for hypercalcaemia and hyperparathyroid bone disease in chronic renal failure is discussed.

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Section: Iacontrasting

confidence: 68%

Responses to salmon calcitonin in chronic renal failure: relation to histological and biochemical indices of bone turnover

Cundy

Heynen

Gaspar

et al. 1981

Eur J Clin Investigation

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“…In a bone histomorphometric study, no correlation was found between bone activity and CT levels while correlations were observed with PTH [ 75 ]. Finally, several studies from many years ago showed that treatment with CT failed to improve renal osteodystrophy [ 76 – 78 ].…”

Section: Calcitonin and Renal Failurementioning

confidence: 99%

Calcitonin, the forgotten hormone: does it deserve to be forgotten?

Felsenfeld

Levine

2015

Clinical Kidney Journal

109

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Calcitonin is a 32 amino acid hormone secreted by the C-cells of the thyroid gland. Calcitonin has been preserved during the transition from ocean-based life to land dwellers and is phylogenetically older than parathyroid hormone. Calcitonin secretion is stimulated by increases in the serum calcium concentration and calcitonin protects against the development of hypercalcemia. Calcitonin is also stimulated by gastrointestinal hormones such as gastrin. This has led to the unproven hypothesis that postprandial calcitonin stimulation could play a role in the deposition of calcium and phosphate in bone after feeding. However, no bone or other abnormalities have been described in states of calcitonin deficiency or excess except for diarrhea in a few patients with medullary thyroid carcinoma. Calcitonin is known to stimulate renal 1,25 (OH)2 vitamin D (1,25D) production at a site in the proximal tubule different from parathyroid hormone and hypophosphatemia. During pregnancy and lactation, both calcitonin and 1,25D are increased. The increases in calcitonin and 1,25D may be important in the transfer of maternal calcium to the fetus/infant and in the prevention and recovery of maternal bone loss. Calcitonin has an immediate effect on decreasing osteoclast activity and has been used for treatment of hypercalcemia. Recent studies in the calcitonin gene knockout mouse have shown increases in bone mass and bone formation. This last result together with the presence of calcitonin receptors on the osteocyte suggests that calcitonin could possibly affect osteocyte products which affect bone formation. In summary, a precise role for calcitonin remains elusive more than 50 years after its discovery.

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Renal Osteodystrophy

Llach¹

Replacement of Renal Function by Dialysis

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A Trial of Calcitonin Therapy in Renal Osteodystrophy

Cited by 10 publications

References 7 publications

Responses to salmon calcitonin in chronic renal failure: relation to histological and biochemical indices of bone turnover

Responses to salmon calcitonin in chronic renal failure: relation to histological and biochemical indices of bone turnover

Calcitonin, the forgotten hormone: does it deserve to be forgotten?

Renal Osteodystrophy

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