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Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations
Insights
Hypercalcemia in dialysis patients is linked to increased bone aluminum and severe osteomalacia. Treatment with 24,25-dihydroxyvitamin D effectively lowered serum calcium levels in these patients.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Renal osteodystrophy is a common complication in dialysis patients.
- Hypercalcemia in this population is associated with significant morbidity.
Purpose of the Study:
- To investigate the relationship between hypercalcemia and bone disease in dialysis patients.
- To evaluate the efficacy of 24,25-dihydroxyvitamin D in managing hypercalcemia.
Main Methods:
- Comparison of 10 hypercalcemic dialysis patients with 30 non-hypercalcemic controls.
- Bone histomorphometry, including mineralization defects and aluminum staining.
- Measurement of intact parathyroid hormone (PTH) levels.
- Assessment of serum calcium levels before and after treatment with 24,25-dihydroxyvitamin D.
Main Results:
- Hypercalcemic patients exhibited greater disability and more severe osteomalacia with increased bone aluminum staining.
- Intact PTH levels did not differentiate bone disease types in hypercalcemic patients, unlike in controls.
- 24,25-dihydroxyvitamin D treatment significantly reduced serum calcium levels in hypercalcemic patients.
Conclusions:
- Hypercalcemia in dialysis patients correlates with elevated bone aluminum and worsened osteomalacia.
- Intact PTH is a reliable predictor of bone histomorphometry only in the absence of hypercalcemia.
- 24,25-dihydroxyvitamin D is an effective therapeutic option for reducing serum calcium in dialysis-associated hypercalcemia.
Abstract:
Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.