A deficit of calcitriol synthesis may not be the initial factor in the pathogenesis of secondary hyperparathyroidism | Zendy

Isabel Martínez | Zendy; Ramón Saracho | Zendy; Jesús Lechuga Montenegro | Zendy; Francisco Llach | Zendy

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A deficit of calcitriol synthesis may not be the initial factor in the pathogenesis of secondary hyperparathyroidism

Author(s) -

Isabel Martínez,

Ramón Saracho,

Jesús Lechuga Montenegro,

Francisco Llach

Publication year - 1996

Publication title -

nephrology dialysis transplantation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.654

H-Index - 168

eISSN - 1460-2385

pISSN - 0931-0509

DOI - 10.1093/ndt/11.supp3.22

Subject(s) - calcitriol , pathogenesis , medicine , endocrinology , secondary hyperparathyroidism , hyperparathyroidism , chronic renal failure , calcium , parathyroid hormone

Secondary hyperparathyroidism (HPT) develops early in chronic renal failure (CRF) at a time when plasma calcitriol levels are normal. At this time, PTH are higher than normal controls and serum phosphorous levels are lower. A decrement in total serum Ca is noted, after an oral phosphate load, only in patients with ERF. These data suggest that factors, other than a decrease in calcitriol synthesis, may be involved in the pathogenesis of HPT. A hypothesis is forwarded suggesting that an alteration in the newly cloned calcium sensor receptor may be the earliest abnormality in the HPT, preceding a decrease in plasma calcitriol levels.

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