Hyperparathyroidism, desired phosphate and low or normal calcium

doc_thinkingAssessing the Clinical and Laboratory Parameters 

The parathyroid glands are overactive in the face of a normal phosphate and a normal or low calcium level.

Depending on the level of the calcium, the PT gland may be responding to relative hypocalcemia.  If the calcium level is at the upper end of the normal range the PT gland may be relatively resistant to the calcium signal


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


Therapeutic Options:

{tab=Dialysis Prescription}

Dialysis Prescription

No change in the dialysis prescription is suggested unless 1.00 mmol/L dialysate is being used.  This may be causing frequent episodes of hypocalcemia during dialysis and keeping the PTH level high.  A dialysate calcium concentration of 1.25 mmol/L is recommended.

{tab=Phosphate and Calcium Management}

Phosphate and Calcium Management

No change in phosphate binder is recommended unless the calcium level is low, and a non-calcium containing binder is being used to control phosphate.  Under those circumstances it may be possible to substitute a less expensive calcium containing binder for the non-clacium containing binder. If an aluminum binder is being used and the calcium level is low, consideration should be given to reducing the dose of the aluminum binder and substituting a calcium binder.

Phosphate is normal in this patient.  Ongoing counseling about phosphate in the diet and the timing of binders with respect to meals is required.  

No change in the dose of calcium containing phosphate binder in this patient is needed.  If, however, the calcium level is low, it is possible that the hypocalcemia is driving the PTH.  The introduction of a calcium supplement at a time away from food would be reasonable here.




{tab=PTH Management}

PTH Management

If vitamin D sterols are in use, the PTH is high despite them but the phosphate and calcium are normal. This suggests that the dose of vitamin D sterol used could be increased. This might help reduce the PTH level, but care will have to be taken that this does not increase the calcium or phosphate level (or both).  If vitamin D sterols are not being used, it would be appropriate to introduce them at a low dose and monitor the effect on all parameters of mineral metabolism.

If the patient is not receiving a calcimimetic, consideration should be given to the initiation of such a medication.  The calcimimetic will have an effect to lower the PTH, and is also likely to bring about some reduction in calcium and the phosphate level.  A lowering of the calcium level may may stimulated the pararthyroid glands further, so an increase in the dose of calcium binder, or calcium supplementation at a time away from the ingestion of food could be considered.
If the patient is receiving a calcimimetic, but not a vitamin D sterol, it would be reasonable to start a vitamin D sterol in this case.  
It would be reasonable to increase the calcimimetic dose in this patient if such a medication had already been started, but care is needed since this might lower the calcium and further stimulate the PTH.

This patient has a PTH above the target range.  It may be possible that the hyperparathyroidism is being driven by a low calcium.  If this were the case, increasing the calcium intake, may ameliroate the hyperparathyrodisim. If the PTH is very high, the use of a calcimimetic might bring about control, particularly since this could be combined with more calcium or a vitamin D sterol.  For extremely high PTH levels, or levels unresponsive to medical management, parathyroidectomy should be considered.

{tab=Other Options of Controversies in Management}

Other Options of Controversies in Management

There are very few data examining the role of combining phosphate binders to limit exposure to the potential toxicities of aluminum, calcium, and magnesium. The CSN group acknowledges the lack of evidence in this regard:

“ ..available evidence does not allow the recommendation of one (or several) phosphate binders as superior to any other.”

The KDIGO group makes no mention of combinations of phosphate binders:

Chapter 4.1: Treatment of CKD–MBD targeted at lowering high serum phosphorus and maintaining serum calcium
4.1.4 In patients with CKD stages 3–5 (2D) and 5D (2B), we suggest using phosphate-binding agents in the treatment of hyperphosphatemia. It is reasonable
that the choice of phosphate binder takes into account CKD stage, presence of other components of CKD–MBD, concomitant therapies, and side-effect profile (not graded).

Nonetheless, it seems very reasonable to combine calcium and non-calcium binders in an effort to minimize the cost of using the more expensive calcium binders alone.

    Return to bone and mineral resource home