Hyperparathyroidism, hypophosphatemia & low or normal calcium


Assessing the Clinical and Laboratory Parameters


This is an unusual combination, with several possibilities;

  1. True vitamin D deficiency (i.e. measure serum 25 OH D).
  2. Diet and phosphate binder dosing are associated with malnutrition.
  3. Consider direct suppression of PT glands with either active vitamin D analogues or calcimimetics (expensive)


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


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Dialysis Prescription

If technically simple, consider increasing dialysate calcium by 0.25 – 0.50 mmol/L (0.50-1.00 mEq/L).




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Phosphate and Calcium Management

Counseling about phosphate in the diet and the timing of binders with respect to meals is required

Phosphate Binders

Therapeutic avenues;

  • If managed with non-calcium binders, switch to calcium based binder.
  • If managed solely with calcium based binder, a reduced dose will allow normalization of serum phosphate levels, and potential to increase dose of vitamin D analogue (see below)


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PTH Management

Vitamin D Sterols

This constellation of parameters strongly suggests active vitamin D deficiency; measure serum 25 OH D. Therapeutic avenues;

  • If vitamin D “deficiency” confirmed (serum 25 OH D <25 nmol/L), supplement with 1000-2000 units/day.
  • If active vitamin D analogues not in use, start calcitriol or 1-alpha
  • If already on active vitamin D analogues, increase the dose.


An expensive alternative, if the only reason for starting cinecalcet is the high serum PTH (see above). If already on cinecalcet, increase the dose, or add treatment with a vitamin D analogue to achieve normal serum calcium levels.

Suggested Guidelines include;


7. Vitamin D sterols can be used in the treatment of secondary hyperparathyroidism, but should be discontinued when PTH levels decrease below target levels, or if calcium or phosphate levels increase above target levels.(Grade C)


4.2.1 In patients with CKD stages 3–5 not on dialysis, the optimal PTH level is not known. However, we suggest that patients with levels of intact PTH (iPTH) above the upper normal limit of the assay are first evaluated for hyperphosphatemia, hypocalcemia, and vitamin D deficiency (2C). It is reasonable to correct these abnormalities with any or all of the following: reducing dietary phosphate intake and administering phosphate binders, calcium supplements, and/or native vitamin D (not graded).

4.2.3 In patients with CKD stage 5D, we suggest maintaining iPTH levels in the range of approximately two to nine times the upper normal limit for the assay (2C). We suggest that marked changes in PTH levels in either direction within this range prompt an initiation or change in therapy to avoid progression to levels outside of this range (2C).

4.2.4 In patients with CKD stage 5D and elevated or rising PTH, we suggest calcitriol, or vitamin D analogs, or calcimimetics, or a combination of calcimimetics and calcitriol or vitamin D analogs be used to lower PTH (2B).

a) It is reasonable that the initial drug selection for the treatment of elevated PTH be based on serum calcium and phosphorus levels and other aspects of CKD–MBD (not graded).

b) It is reasonable that calcium or non-calcium-based phosphate binder dosage be adjusted so that treatments to control PTH do not compromise levels of phosphorus and calcium (not graded).

e) We suggest that, in patients with hypocalcemia, calcimimetics be reduced or stopped depending on severity, concomitant medications, and clinical signs and symptoms (2D).

f) We suggest that, if the intact PTH levels fall below two times the upper limit of normal for the assay, calcitriol, vitamin D analogs, and/or calcimimetics be reduced or stopped (2C).

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Other Options or Controversies in Management



There is no indication for parathyroidectomy. The high serum PTH is more likely to be secondary to nutritional issues (see above), rather than autonomous hyperparathyroidism

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