In chronic renal failure of long standing, hypercalcaemia is usually caused by the use of vitamin D derivatives and phosphate binders, and sometimes by tertiary hyperparathyroidism. [See section on Osteodystrophy]. Usually stopping vitamin D and calcium containing phosphate binders is enough, but be cautious if patient is on a significant dose of vitamin D or has had a parathyroidectomy - calcium may plummet.
In acute renal failure calcium is usually low-normal. A high-normal or high calcium should lead to suspicion that the renal problem is caused by hypercalcaemia itself, or by the same disease as is responsible for hypercalcaemia — e.g., myeloma.
Fluid repletion with saline improves renal impairment caused by hypercalcaemia and has a small effect on calcium level.
Diuretics should be avoided unless adequate volume expansion with normal saline has been achieved. Thereafter loop diuretics can be used with caution, but thiazides tend to increase serum calcium.
Corticosteroids are effective in sarcoidosis, some haematological malignancies and allegedly also in vitamin D poisoning.
Bisphosphonates are effective in all circumstances. Disodium pamidronate can be given as a single dose of 30-90mg over 2-4 hours (maximum infusion rate 20mg/h in renal impairment; maximum concentration 60mg in 250ml 0.9% NaCl). Calcium falls over days, reaching a nadir at 3-5 days, and usually remaining suppressed for several weeks, when the infusion can be repeated. Note that high doses of pamidronate may be nephrotoxic - associated with proteinuria and FSGS.
For dialysis patients, adjusting calcium content of dialysate may be helpful.
Neil
Turner was the main author for this page. It was updated in February 2001 and July 2002 and November 2006, last amended
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