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

scholarly journals Effects of oral propranolol on parathyroid hormone secretion in chronic renal failure.

BMJ ◽  
1980 ◽  
Vol 281 (6251) ◽  
pp. 1320-1320 ◽  
Author(s):  
K Farrington ◽  
J Hamzeh ◽  
Z Varghese ◽  
J F Moorhead
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Hormone Secretion ◽  
Oral Propranolol

Parathyroid Hormone Secretion: Perturbations in Chronic Renal Failure

2015 ◽  
pp. 16-24 ◽  
Author(s):  
Eduardo Slatopolsky ◽  
Silvia Lopez-Hilker ◽  
Adriana Dusso ◽  
Jeremiah J. Morrissey ◽  
Kevin J. Martin
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Hormone Secretion

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

Pulsatile immunoreactive and bioactive luteinizing hormone secretion in adolescents with chronic renal failure

1991 ◽  
Vol 5 (4) ◽  
pp. 566-571 ◽  
Author(s):  
F. Schaefer ◽  
C. Seidel ◽  
R. Mitchell ◽  
K. Sch�rer ◽  
W. R. Robertson ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Luteinizing Hormone Secretion

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.”

Pregnancy decreases immunoreactive parathyroid hormone level in rats with chronic renal failure

1999 ◽  
Vol 96 (4) ◽  
pp. 427-430 ◽  
Author(s):  
M. BLUM ◽  
Y. WEISMAN ◽  
S. TURGEMAN ◽  
S. CABILI ◽  
Y. WOLLMAN ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Virgin Female ◽  
Normal Pregnancy ◽  
High Serum ◽  
Female Rats ◽  
Pregnant Rats ◽  
Serum Ipth ◽  
Immunoreactive Parathyroid Hormone

Normal pregnancy is associated with an increase in serum parathyroid hormone and 1,25-dihydroxyvitamin D3 (calcitriol). The effect of pregnancy on these hormones in chronic renal failure (CRF) is unknown. The present work was undertaken to study the changes of serum immunoreactive parathyroid hormone (iPTH) and calcitriol in pregnant rats with CRF. The following experimental groups were studied: CRF1 (5/6 nephrectomized virgin female rats), CRF2 (5/6 nephrectomized pregnant rats at day 20–21 of pregnancy), CRF3 (5/6 nephrectomized rats 2 weeks after delivery) and their respective sham-operated control groups: N1, N2 and N3. The 5/6 nephrectomy (CRF1) resulted in renal failure with very high serum iPTH (100±18 pg/ml) and low calcitriol levels (10.6±4.3 pg/ml) compared with normal rats [N1: 14±2.5 pg/ml (P< 0.001) and 18.2±4.2 pg/ml (P< 0.01) respectively]. The pregnancy in CRF rats (CRF2) resulted in normalization of serum iPTH levels (18.2±5.41 pg/ml), which was associated with a parallel increase in serum calcitriol (29.4±8.0 pg/ml) similar to that in pregnancy of normal rats (N2). Two weeks after delivery the CRF rats (CRF3) once again had high serum iPTH (87±17 pg/ml) and low calcitriol levels (9.3±1.2 pg/ml), similar to those observed in non-pregnant uraemic rats (CRF1). It is concluded that pregnancy decreases serum iPTH in 5/6 nephrectomized CRF rats most probably by the increased level of calcitriol synthesized by the feto-placental unit.

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