Hypoparathyroidism, hypophosphatemia and hypercalcemia

Patient Scenario: Hypoparathyroidism, hypophosphatemia and hypercalcemia



Assessing the Clinical and Laboratory Parameters

The phosphate level is low in this patient. Chronically low phosphate levels are unusual in dialysis patients, but may be associated with osteomalacia. The presence of this constellation of parameters in a patient who has received long term aluminum-based phosphate binders is strongly suggestive of aluminum toxicity. Assess both current and previous binder use.

The PTH level is suppressed in this patient. Assess if prior parathyroidectomy, especially total removal, which may cause low PTH levels. Assess if vitamin D sterol use, as current use of vitamin D sterols in an effort to control prior hyperparathyroidism can lead to over suppression by the vitamin D sterol directly, or indirectly by the hypercalcemia.  (Excessive vitamin D sterol therapy usually leads to an elevated phosphate level in addition to the hypercalcemia). Assess if calcimimetics being used, as over suppression of parathyroid glands with a calcimimetic agent is possible. Usually the use of a calcimimetics causes both hypophosphatemia and hypocalcemia.

If there is no history of a prior parathyroidectomy, this patient has hypoparathyroidism in association with high calcium. This is a normal physiologic response to hypercalcemia and suggests that the glands are not functioning autonomously.  PTH levels can be expected to rise as the calcium level is brought under control.

Less than 1% of all patients are in this category.

{tab=Dialysis Prescription}

Dialysis Prescription

Lowering the dialysis calcium concentration may help correct the hypercalcemia quickly, particularly if the patient is symptomatic from the hypercalcemia.  This will provide a stimulus to PTH formation and secretion. Dialysate Calcium of 1 mM is available and could be used instead of the usual 1.25 or 1.5 mM Ca.

{tab=Phosphate and Calcium Management}

Phosphate and Calcium Management

In the presence of a prior parathyroidecotmy, this constellation of biochemical findings suggests an imbalance between the vitamin D sterol replacement and the dose of calcium-based phosphate binders.  A decrease in the dose of ingested calcium will allow the phosphate to rise and help correct the hypercalcemia.

A reduction in the calcium containing phosphate binder is required in this patient with hypercalcemia and low phosphate levels. This should allow the phosphate to rise and remove the inhibitory signal to PTH formation and release. If the phosphate rises too much, use of a non-calcium based binder may be helpful.

The aluminum binder should be discontinued in favor of a non-calcium, non-aluminum binder.  A DFO challenge test to diagnose significant aluminum accumulation may be indicated here, but care must be taken to avoid precipitation of acute neurologic sequelae.


{tab=PTH Management}

PTH Management

Excessive vitamin D sterol doses usually usually lead to hyperphosphatemia in addition to the hypercalcemia.  However, if a vitamin D sterol is being used, the dose should be reduced.

Calcimimetic use should be reviewed and the dose be dropped or consideration be given to withdrawal of the agent.  Sudden discontinuation of a calcimimetic has been associated with a rapid rise in PTH with loss of prior good control


{tab=Other Options of Controversies in Management}

Other Options of Controversies in Management

There have been very few studies examining the use impact of dialysate calcium level on calcium balance and serum levels. Most programs would consider 1.25 mM and 1.5 mM as standard dialysate calcium levels. Acid concentrates with 1 mM Ca are available and could be used to correct the high calcium and potentially stimulate an increase in PTH level.

{tab=Suggested References}

Suggested References

1. Spasovski G et al. Improvement of Bone and Mineral Parameters Related to Adynamic Bone Disease by Diminishing Dialysate Calcium. Bone 2007; 41: 698–703.

2. Lezaic V, Pejanovic S, Kostic S et al. Effects of lowering dialysate calcium concentration on mineral metabolism and parathyroid hormone secretion: a multicentric study. Ther Apher Dial 2007

3. Molina Vila P, Sanchez Perez P, Garrigos Almerich E et al. Marked improvement in bone metabolism parameters after increasing the dialysate calcium concentration from 2.5 to 3 mEq/L in nonhypercalcemic hemodialysis patients. Hemodial Int 2008; 12: 73–79

4. Seyffart G, Schulz T, Stiller S. Use of two calcium concentrations in hemodialysis—report of a 20-year clinical experience. Clin Nephrol 2009; 71: 296–305

5. Toussaint N, Cooney P, Kerr PG. Review of dialysate calcium concentration in hemodialysis. Hemodial Int 2006; 10: 326–337

Return to bone and mineral resource home