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 #e4eaff;" href="https://coo.lumc.nl/trc/linkMap.aspx?linkdomain=FK&subjectID=755&link=https%3A%2F%2Fwww.farmacotherapeutischkompas.nl%2Fbladeren%2Fpreparaatteksten%2Fl%2Flanthaancarbonaat&rnd=177" target="_blank">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 here:
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.