How to treat changes in bone and mineral metabolism seen in progressive kidney disease
What are the therapeutic options to treat the changes in bone and mineral metabolism seen in progressive kidney disease?
The therapeutic options available for a person with derangements in bone and mineral metabolism include normalizing 25 vitamin D levels and dietary counseling to decrease phosphorous intake.
In the setting of persistent hyperphosphatemia, a phosphate binder can be used. These binders are taken with the patient’s meal to bind the phosphorus in the food, preventing absorption.
Phosphate binders include calcium carbonate, calcium acetate, sevelamer, lanthanum, and iron-based binders. Aluminum-containing binders are not recommended due to the increased risk of aluminum toxicity. It should be noted that no studies have demonstrated an improvement in clinical outcomes with the use of phosphate binders.
Indeed, there is concern that the use of calcium-based binders can lead to an increase in vascular calcification. This was demonstrated in a study by Block et al., in which patients treated with binders had increased calcification of the coronary arteries and abdominal aorta compared with placebo.
In addition to treating 25 vitamin D deficiency, active 1,25 vitamin D (calcitriol) or active vitamin D analogues (paricalcitol, ergocalciferol) and the calcimimetic cinacalcet can be used to suppress secondary hyperparathyroidism.
However, similar to phosphate binders, the evidence of the effectiveness of vitamin D analogues on clinical outcomes in CKD is lacking. The relative combination of these agents should be considered on a case-by-case basis following measurement of serum calcium, phosphorus, vitamin D and intact PTH levels.
