Parathyroid Glands in Chronic Kidney Disease 2020
DOI: 10.1007/978-3-030-43769-5_4
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PTH Receptors and Skeletal Resistance to PTH Action

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Cited by 3 publications
(2 citation statements)
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“…Nevertheless, ∼25% of patients keep elevated iPTH levels after transplantation. This hyperparathyroidism originates either from persistent CKD–MBD characterized by, among others, previous parathyroid hyperplasia associated with an elevated calcium set-point for inhibition of PTH secretion, or from the improved ‘skeletal resistance’, an often unnoticed condition of hyporesponsiveness to PTH effect, resulting from multiple factors, including uremia per se [ 5 ]. Mild hypercalcaemia secondary to persistent hyperparathyroidism is observed in around 30% of KT recipients at 1 year [ 6 ], whether they have been previously treated by cinacalcet or not.…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, ∼25% of patients keep elevated iPTH levels after transplantation. This hyperparathyroidism originates either from persistent CKD–MBD characterized by, among others, previous parathyroid hyperplasia associated with an elevated calcium set-point for inhibition of PTH secretion, or from the improved ‘skeletal resistance’, an often unnoticed condition of hyporesponsiveness to PTH effect, resulting from multiple factors, including uremia per se [ 5 ]. Mild hypercalcaemia secondary to persistent hyperparathyroidism is observed in around 30% of KT recipients at 1 year [ 6 ], whether they have been previously treated by cinacalcet or not.…”
Section: Discussionmentioning
confidence: 99%
“…A different reasonable approach is suggested by some (J. V. Torregrosa et al ., submitted for publication in the Spanish Society of Nephrology journal “Nefrologia”) to avoid an induced and probably inadequate normalization of serum PTH levels in these patients without the need for passive ‘waiting’ until something becomes sufficiently ‘severe’ to consider treatment. Actually, some degree of secondary hyperparathyroidism may be beneficial in CKD patients (PTH is a phosphaturic hormone and is necessary for a normal bone formation rate) due to the presence of PTH hyporesponsiveness (PTH resistance) in CKD [ 52 , 53 ]. Whether these 2017 KDIGO changes will result in a greater number of patients reaching later PTH extremes of risk or real improvement in patient-level outcomes remains to be seen.…”
Section: Kdigo Ckd–mbd Guidelinesmentioning
confidence: 99%