What is the pathophysiology of secondary hyperparathyroidism?

Updated: Dec 24, 2020
  • Author: Lawrence Kim, MD, FACS, FACE; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Answer

Answer

Calcium and phosphorous homeostasis is tightly regulated between bone, the kidney, and the parathyroid gland. Key modulators of calcium and phosphorous include FGF-23, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone. FGF-23 is released from bone due to increasing serum phosphorus levels and acts in the kidney to increase phosphorous excretion and decrease 1 alpha hydroxylation of 25-hydroxyvitamin D. FGF-23, along with serum phosphorous, also decreases parathyroid hormone secretion, to maintain calcium and phosphorous balance. In CKD, stages 3-5 (eGFR < 59 mL/min), FGF-23 levels increase, initially leading to phosphaturia and decreased parathyroid hormone excretion. As the CKD progresses, there is a resistance in the kidney and parathyroid gland to FGF-23 and a deficiency in the kidney of 1 alpha hydroxylation of vitamin D, both of which contribute to reduced phosphorous excretion. The deficiency of 1,25-dihydroxyvitamin D, along with the decreased phosphorus excretion, results in hypocalcemia and hyperphosphatemia, thereby maintaining stimulation of parathyroid hormone synthesis and parathyroid gland hyperplasia.


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