A deficit of calcitriol synthesis may not be the initial factor in the pathogenesis of secondary hyperparathyroidism.
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.
Martinez
I
I
Servicio Nefrologia, Hospital de Galdakao, Vizcaya, Spain.
Saracho
R
R
Montenegro
J
J
Llach
F
F
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002117:Calcitriol / Q000096:biosynthesis*; D002118:Calcium / Q000378:metabolism; D003404:Creatinine / Q000493:pharmacokinetics; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology*; D007676:Kidney Failure, Chronic / Q000378:metabolism; D008297:Male; D008875:Middle Aged
D003404:Creatinine; D002117:Calcitriol; D002118:Calcium