TRC: Secondary hyperparathyroidism

Secondary hyperparathyroidism

Chronic kidney disease: secondary hyperparathyroidism

In chronic kidney disease (CKD) PTH production and secretion is stimulated by vitamin D deficiency hyperphosphatemia and hypocalcemia.

Secondary hyperparathyreoidism is usually asymptomatic but may result in symptoms such as pain in the bones and spontaneous fractures. Increased bone turnover may contributes to vascular calcifications.

Treatment aims at prevention of high and low bone formation rates by maintaining slightly elevated PTH levels. Control of the phosphate levels by dietary phosphate restriction and phosphate binders like calcium carbonate or calcium acetate is essential in this respect.

If this is not sufficient, sevelamer or lanthanum carbonate could be used. Cholecalciferol (early CKD), alfacalcidol or paricalcitol (in hemodialysis patients) can be given in order to treat vitamin D deficiency and thereby control PTH secretion. Treatment resistant hyperparathyroidism might be treated by the calcimimetic, cinacalcet which stimulates the calcium sensing receptor.

The normal physiological regulation of PTH, vitamin D and calcium is depicted in the illustration above.

What is NOT happening in a normal kidney?

Extra info: Hydroxylation of 25-hydroxycholechalciferol into its active form occurs in the kidney. Remember this CONVERSION is impaired EARLY in chronic renal failure (not late). So renal bone disease is almost always seen in established uremias.

Option explanation:

EPO is secreted by peritubular cells in response to hypoxia

hydroxylation of 1-hydroxycholecalciferol into its active form

renin is secreted from the juxta glomerular apparatus

locally produced prostaglandins have a very important role in maintaining renal perfusion

Secondary hyperparathyroidism

Chronic kidney disease: secondary hyperparathyroidism

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