Lack of Relationship between Parathyroid Hormone and 1,25-Dihydroxyvitamin D in Chronic Renal Failure

Nephron ◽  
1991 ◽  
Vol 58 (2) ◽  
pp. 144-149 ◽  
Author(s):  
Martin Rudnicki ◽  
Peter McNair ◽  
Ib Transbøl ◽  
Bent Nielsen
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Determinants of Intact Parathyroid Hormone and Free 1,25-Dihydroxyvitamin D Levels in Mild and Moderate Renal Failure

Nephron ◽  
1992 ◽  
Vol 61 (4) ◽  
pp. 422-427 ◽  
Author(s):  
Andrew St. John ◽  
Mark B. Thomas ◽  
Charmian P. Davies ◽  
Brian Mullan ◽  
Ian Dick ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Intact Parathyroid Hormone ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Moderate Renal Failure

scholarly journals Serum levels of 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D, and 25-hydroxyvitamin D in nondialyzed patients with chronic renal failure

1999 ◽  
Vol 55 (3) ◽  
pp. 1019-1027 ◽  
Author(s):  
Eiji Ishimura ◽  
Yoshiki Nishizawa ◽  
Masaaki Inaba ◽  
Naoki Matsumoto ◽  
Masanori Emoto ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Serum Levels ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
25 Hydroxyvitamin D

scholarly journals Influence of Glomerular Filtration Rate on Non-(1-84) Parathyroid Hormone (PTH) Detected by Intact PTH Assays

2000 ◽  
Vol 46 (5) ◽  
pp. 697-703 ◽  
Author(s):  
Jean-Hugues Brossard ◽  
Raymond Lepage ◽  
Héloïse Cardinal ◽  
Louise Roy ◽  
Louise Rousseau ◽  
...  
Keyword(s):  
Renal Failure ◽  
Glomerular Filtration Rate ◽  
Parathyroid Hormone ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Molecular Form ◽  
Healthy Individuals ◽  
Progressive Renal Failure ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Abstract Background: Commercial intact parathyroid hormone (I-PTH) assays detect molecular form(s) of human PTH, non-(1-84) PTH, different from the 84-amino acid native molecule. These molecular form(s) accumulate in hemodialyzed patients. We investigated the importance of non-(1-84) PTH in the interpretation of the increased I-PTH in progressive renal failure. Methods: Five groups were studied: 26 healthy individuals, 12 hemodialyzed patients, and 31 patients with progressive renal failure subdivided according to their glomerular filtration rate (GFR) into 11 with a GFR between 60 and 100 mL · min−1 · 1.73 m−2, 12 with a GFR between 30 and 60 mL · min−1 · 1.73 m−2, and 8 with a GFR between 5 and 30 mL · min−1 · 1.73 m−2. We evaluated indicators of calcium and phosphorus metabolism and creatinine clearance (CrCl) in the progressive renal failure groups, and the HPLC profile of I-PTH and C-terminal PTH in all groups. Results: Only patients with a GFR <30 mL · min−1 · 1.73 m−2 and hemodialyzed patients had decreased Ca2+ and 1,25-dihydroxyvitamin D, and increased phosphate. In patients with progressive renal failure, I-PTH was related to Ca2+ (r = −0.66; P <0.0001), CrCl (r = −0.61; P <0.001), 1,25-dihydroxyvitamin D (r = −0.40; P <0.05), and 25-hydroxyvitamin D (r = −0.49; P <0.01) by simple linear regression. The importance of non-(1-84) PTH in the composition of I-PTH increased with each GFR decrease, being 21% in healthy individuals, 32% in progressive renal failure patients with a GFR <30 mL · min−1 · 1.73 m−2, and 50% in hemodialyzed patients, with PTH(1-84) making up the difference. Conclusions: As I-PTH increases progressively with GFR decrease, part of the increase is associated with the accumulation of non-(1-84) PTH, particularly when the GFR is <30 mL · min−1 · 1.73 m−2. Concentrations of I-PTH 1.6-fold higher than in healthy individuals are necessary in hemodialyzed patients to achieve PTH(1-84) concentrations similar to those in the absence of renal failure.

scholarly journals Role of parathyroid hormone in the glucose intolerance of chronic renal failure.

1985 ◽  
Vol 75 (3) ◽  
pp. 1037-1044 ◽  
Author(s):  
M Akmal ◽  
S G Massry ◽  
D A Goldstein ◽  
P Fanti ◽  
A Weisz ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Glucose Intolerance

scholarly journals Parathyroid hormone secretion in chronic renal failure

1996 ◽  
Vol 50 (5) ◽  
pp. 1700-1705 ◽  
Author(s):  
Jesper C. Madsen ◽  
Anne Q. Rasmussen ◽  
Søren D. Ladefoged ◽  
Peter Schwarz
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Hormone Secretion

The Interrelationships among Prolactin, 1,25-Dihydroxyvitamin D, and Parathyroid Hormone in Humans*

1979 ◽  
Vol 49 (4) ◽  
pp. 628-630 ◽  
Author(s):  
NANCY D. ADAMS ◽  
THOMAS L. GARTHWAITE ◽  
RICHARD W. GRAY ◽  
THAD C. HAGEN ◽  
JACOB LEMANN
Keyword(s):  
Parathyroid Hormone ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

scholarly journals Vitamin D Status among Thai School Children and the Association with 1,25-Dihydroxyvitamin D and Parathyroid Hormone Levels

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e104825 ◽  
Author(s):  
Lisa A. Houghton ◽  
Andrew R. Gray ◽  
Michelle J. Harper ◽  
Pattanee Winichagoon ◽  
Tippawan Pongcharoen ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
School Children ◽  
Vitamin D Status ◽  
Hormone Levels ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Parathyroid hormone metabolism and its potential as a uremic toxin

1980 ◽  
Vol 239 (1) ◽  
pp. F1-F12 ◽  
Author(s):  
E. Slatopolsky ◽  
K. Martin ◽  
K. Hruska
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Biological Effects ◽  
Uremic Toxin ◽  
Terminal Portion ◽  
Single Chain ◽  
Biochemical Alterations ◽  
Amino Terminal ◽  
Carboxy Terminal

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a “uremic toxin” responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant “uremic toxin.”

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