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Secondary hyperparathyroidism is the medical condition of excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels), with resultant hyperplasia of these glands. This disorder is primarily seen in patients with chronic kidney failure.
[30] [31] Tertiary hyperparathyroidism is differentiated from primary hyperparathyroidism by a history of chronic kidney failure and secondary hyperparathyroidism. [citation needed] Hyperparathyroidism can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. [32]
5741 19226 Ensembl ENSG00000152266 ENSMUSG00000059077 UniProt P01270 Q9Z0L6 RefSeq (mRNA) NM_000315 NM_001316352 NM_020623 RefSeq (protein) NP_000306 NP_001303281 NP_065648 Location (UCSC) Chr 11: 13.49 – 13.5 Mb Chr 7: 112.98 – 112.99 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Parathyroid hormone (PTH), also called parathormone or parathyrin, is a peptide hormone secreted ...
High levels of fibroblast growth factor 23 seem to be the most important cause of decreased calcitriol levels in CKD patients. [citation needed] In CKD, the excessive production of parathyroid hormone increases the bone resorption rate and leads to histologic bone signs of secondary hyperparathyroidism. [16]
Signs and symptoms include ectopic calcification, secondary hyperparathyroidism, and renal osteodystrophy. Abnormalities in phosphate metabolism such as hyperphosphatemia are included in the definition of the new chronic kidney disease–mineral and bone disorder (CKD–MBD). [3]
Tertiary hyperparathyroidism is defined by autonomous release of parathyroid hormone while in a hypercalcaemic state. Unlike primary hyperparathyroidism, hypercalcemia in the tertiary form is thought to be the result of resolution of secondary hyperparathyroidism rather than adenoma formation alone. [4] [11] [10]
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