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Iatrogenic hypercalcemia in hemodialysis patients
M A Muhammedi1, B Piraino, R Rault
1Department of Medicine, University of Pittsburgh, Presbyterian University Hospital, PA 15213.
Insights
Hypercalcemia is common in hemodialysis patients using calcitriol and calcium carbonate. Lower calcitriol doses increased hypercalcemia risk, suggesting careful dosing is crucial for managing phosphorus and calcium levels.
Area of Science:
- Nephrology
- Mineral and Bone Disorder
Background:
- Calcium carbonate is a common phosphorus binder for hemodialysis patients.
- Hypercalcemia is a frequent side effect of high-dose calcium carbonate therapy.
- The interaction between calcitriol and calcium supplements regarding hypercalcemia risk is not well-established.
Purpose of the Study:
- To investigate the relationship between serum calcium levels, calcitriol use, calcium therapy, and parathyroid hormone (PTH) levels in hemodialysis patients.
- To assess the risk of hypercalcemia in hemodialysis patients receiving both calcitriol and calcium supplements.
Main Methods:
- Retrospective chart review of 74 hemodialysis patients (119 patient-dialysis years).
- Analysis of serum calcium, calcitriol dosage, calcium therapy, and PTH levels.
- Statistical analysis to determine the association between variables and hypercalcemia.
Main Results:
- 38% of patients experienced hypercalcemia at some point.
- Calcitriol therapy significantly increased hypercalcemia risk, independent of calcium therapy (p = 0.032).
- Patients on lower calcitriol doses had a higher risk of hypercalcemia and lower PTH levels, indicating less severe hyperparathyroidism.
Conclusions:
- Hypercalcemia is a common complication in hemodialysis patients treated with calcitriol and calcium carbonate.
- Lower calcitriol doses may increase hypercalcemia risk, necessitating careful dose titration.
- Further research is needed to determine optimal dialysate calcium levels to mitigate hypercalcemia without exacerbating hyperparathyroidism.
Abstract:
Calcium carbonate is frequently used in large doses as a phosphorus binder in hemodialysis patients, which often results in hypercalcemia. In most studies in which calcium carbonate is prescribed to control serum phosphorus levels the patients are not given calcitriol. However, calcitriol may be necessary for suppression of parathyroid hormone. The risk of hypercalcemia when calcium supplements are used in conjunction with calcitriol has not previously been examined in detail. We reviewed the charts of 74 hemodialysis patients (119 patient dialysis years) to determine the relationship of serum calcium to calcitriol, calcium therapy, and PTH levels. Twenty-eight patients (38%) were hypercalcemic at some point. Calcitriol therapy significantly increased the risk of hypercalcemia, independently of calcium therapy (p = 0.032). However, patients on a low dose of calcitriol were more than twice as likely to be hypercalcemic than patients on higher doses. Mean PTH levels were lower in the patients on the lower doses of calcitriol, indicating less severe hyperparathyroid disease. We conclude that hypercalcemia is a common complication in hemodialysis patients on calcitriol and calcium carbonate. Whether lowering the dialysate calcium, as suggested by other investigators, will successfully decrease the risk of hypercalcemia without worsening hyperparathyroidism remains to be determined.