Journal of the American Society of Nephrology
2007 JASN IMPACT FACTOR 7.111 HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP 
    advanced
CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Felsenfeld, A. J.
Right arrow Articles by Rodriguez, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Felsenfeld, A. J.
Right arrow Articles by Rodriguez, M.

Journal of the American Society of Nephrology, Vol 6, 1371-1378, Copyright © 1995 by American Society of Nephrology


REGULAR ARTICLES

Differences in the dynamics of parathyroid hormone secretion in hemodialysis patients with marked secondary hyperparathyroidism

AJ Felsenfeld, A Jara, M Pahl, J Bover and M Rodriguez
Department of Medicine, Wadsworth VA Medical Center, UCLA 90073, USA.

Hemodialysis patients with predialysis intact parathyroid hormone (PTH) levels of more than 500 pg/mL are generally considered to have marked secondary hyperparathyroidism. Because the serum calcium level in these patients varies from low to high, it is not clear whether every hemodialysis patient with a PTH level > 500 pg/mL is part of a uniform group. The dynamics of PTH secretion in 21 hemodialysis patients with predialysis (basal) intact PTH levels > 500 pg/mL (range, 506 to 1978 pg/mL) has been evaluated. The basal/maximal PTH ratio, an indicator of the degree of relative PTH stimulation in the baseline state, was inversely correlated with the maximal PTH (r = -0.71), the basal serum calcium (r = -0.70), and the difference between the serum calcium at basal and maximal PTH (r = 0.81); the latter is the decrement in serum calcium from baseline necessary to maximally stimulate PTH. Because the basal PTH level appeared to be disproportionately influenced by hypocalcemia, the 21 patients were separated into two groups on the basis of the basal serum calcium (Group I < 9 mg/dL and Group II > 9 mg/dL). Basal PTH was not different between the two groups, even though maximally stimulated PTH (1,219 +/- 204 versus 2,739 +/- 412 pg/mL; P < 0.01) as induced by hypocalcemia and maximally suppressed PTH (217 +/- 37 versus 528 +/- 104; P = 0.05) as induced by hypercalcemia were less in Group I with the low basal calcium; moreover, the ratio of basal/maximal PTH was higher (73 +/- 6 versus 47 +/- 5%; P < 0.01) in Group I with the low basal calcium. These results suggest that the reason for a basal PTH > 500 pg/mL may be different among hemodialysis patients. In hypocalcemic patients, the low serum calcium appeared to be a major impetus for the high basal PTH level. In conclusion, (1) the maximally stimulated PTH appears to provide a better means of separating patients with marked secondary hyperparathyroidism than the basal PTH and (2) hemodialysis patients with basal PTH levels > 500 pg/mL may not be a uniform group.


This article has been cited by other articles:


Home page
Nephrol Dial TransplantHome page
A. L. M. de Francisco, M. Izquierdo, J. Cunningham, C. Pinera, R. Palomar, G. F. Fresnedo, J. A. Amado, M. G. Unzueta, and M. Arias
Calcium-mediated parathyroid hormone release changes in patients treated with the calcimimetic agent cinacalcet
Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2895 - 2901.
[Abstract] [Full Text] [PDF]


Home page
CJASNHome page
A. J. Felsenfeld, M. Rodriguez, and E. Aguilera-Tejero
Dynamics of Parathyroid Hormone Secretion in Health and Secondary Hyperparathyroidism
Clin. J. Am. Soc. Nephrol., November 1, 2007; 2(6): 1283 - 1305.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
M. Rodriguez, E. Nemeth, and D. Martin
The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism
Am J Physiol Renal Physiol, February 1, 2005; 288(2): F253 - F264.
[Abstract] [Full Text] [PDF]


Home page
Nephrol Dial TransplantHome page
A. Jara, C. Chacon, A. Valdivieso, L. Aris, R. Jalil, and A. J. Felsenfeld
Effect of calcitriol treatment and withdrawal on hyperparathyroidism in haemodialysis patients with hypocalcaemia
Nephrol. Dial. Transplant., May 1, 2001; 16(5): 1009 - 1016.
[Abstract] [Full Text] [PDF]


Home page
Nephrol Dial TransplantHome page
F. Malberti, M. Farina, and E. Imbasciati
The PTH-calcium curve and the set point of calcium in primary and secondary hyperparathyroidism
Nephrol. Dial. Transplant., October 1, 1999; 14(10): 2398 - 2406.
[Abstract] [Full Text] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
H. Cardinal, J.-H. Brossard, L. Roy, R. Lepage, L. Rousseau, and P. D’Amour
The Set Point of Parathyroid Hormone Stimulation by Calcium Is Normal in Progressive Renal Failure
J. Clin. Endocrinol. Metab., November 1, 1998; 83(11): 3839 - 3844.
[Abstract] [Full Text]




HOME CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP