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Effects of clodronate in severe hyperparathyroid bone disease in chronic renal failure
N A Hamdy1, E V McCloskey, C B Brown
1Department of Human Metabolism and Clinical Biochemistry, University of Sheffield, UK.
Insights
Intravenous clodronate effectively reduced bone resorption markers in dialysis patients with severe hyperparathyroid bone disease. Further research is warranted for clodronate
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Severe hyperparathyroid bone disease is a complication in patients undergoing hemodialysis.
- Hypercalcemia often precludes the use of vitamin D metabolites in these patients.
Purpose of the Study:
- To investigate the effects of clodronate, a diphosphonate, on bone metabolism in hemodialysis patients with severe hyperparathyroid bone disease.
Main Methods:
- Nine hemodialysis patients received intravenous clodronate (300-600 mg) after dialysis for 5 consecutive occasions.
- Serum calcium, phosphate, hydroxyproline, parathyroid hormone, and alkaline phosphatase were monitored.
Main Results:
- Intravenous clodronate significantly decreased serum calcium, phosphate, and hydroxyproline.
- A concurrent increase in serum parathyroid hormone and alkaline phosphatase activity was observed.
- Treatment cessation led to reversal of changes, while oral supplementation sustained effects.
Conclusions:
- Intravenous clodronate demonstrates potential in inhibiting osteoclast-mediated bone resorption in chronic renal failure.
- Clodronate's therapeutic utility, alone or with vitamin D, warrants further investigation, especially in hypercalcemic patients.
Abstract:
We have examined the effects of the diphosphonate, clodronate, in 9 haemodialysis patients with severe hyperparathyroid bone disease. Clodronate (300-600 mg infused after dialysis on 5 consecutive occasions) significantly decreased mean serum calcium, phosphate and hydroxyproline. This was associated with an increase in serum immunoassayable parathyroid hormone and activity of alkaline phosphatase. These changes reversed 2-4 weeks after stopping treatment but were sustained when treatment with oral clodronate (1.6 g daily) was supplemented for 2 weeks. Our findings suggest that intravenous clodronate is capable of inhibiting osteoclast-mediated bone resorption in chronic renal failure. The therapeutic potential of clodronate alone or with vitamin D derivatives merits further evaluation, particularly in patients with severe hyperparathyroidism, when the use of D metabolites alone is precluded by the presence of hypercalcaemia.