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

1999 ◽  
Vol 96 (4) ◽  
pp. 427 ◽  
Author(s):  
M. BLUM ◽  
Y. WEISMAN ◽  
S. TURGEMAN ◽  
S. CABILI ◽  
Y. WOLLMAN ◽  
...  
2005 ◽  
Vol 28 (4) ◽  
pp. 117-121 ◽  
Author(s):  
E. Vigo Gago ◽  
C. Cadarso-Suárez ◽  
R. Perez-Fernandez ◽  
R. Romero Burgos ◽  
J. Devesa Mugica ◽  
...  

1999 ◽  
Vol 96 (4) ◽  
pp. 427-430 ◽  
Author(s):  
M. BLUM ◽  
Y. WEISMAN ◽  
S. TURGEMAN ◽  
S. CABILI ◽  
Y. WOLLMAN ◽  
...  

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.


BMJ ◽  
1982 ◽  
Vol 284 (6318) ◽  
pp. 776-778 ◽  
Author(s):  
C K Biswas ◽  
R S Arze ◽  
J M Ramos ◽  
M K Ward ◽  
J H Dewar ◽  
...  

Author(s):  
Chiranjee Lal Dayma ◽  
Devendra Ajmera ◽  
Shiv Charan Jelia ◽  
Pankaj Jain

Background: Secondary hyperparathyroidism is known and early complication of chronic renal failure patients. Aim of this study was to assess the prevalence of secondary hyperparathyroidism and correlation between serum parathyroid hormone level with biochemical parameters in renal failure patients in tertiary care hospital in Kota, Rajasthan.Methods: A cross sectional observational study was carried out in 50 patients who had creatinine clearance of 30ml/min/1.73m2 or less for greater than 6 weeks attended the OPD of department of General Medicine, New Medical College hospital, Kota, Rajasthan from May 2018 to November 2018. Investigations like complete blood count, renal function test, urine routine microscopy and USG abdomen with serum parathyroid hormone, serum phosphorus, serum calcium levels were done. Serum parathyroid hormone level was done by calorimetric method.Results: The prevalence of secondary hyperparathyroidism in our study was 72%.In hyperparathyroidism patient’s serum calcium level was low and the difference was highly significant (p<0.001). There is negative correlation between S.PTH and S. calcium level (r=-0.536). Mean serum calcium level in our study is 1.6mmol/l. In hyperparathyroidism patient’s serum phosphate level was high and the difference was highly significant (p<0.001). There was positive correlation between S.PTH and S.PO4 level (r=0.402). Mean serum phosphorus level in our study is 5.7 mg/dl. Prevalence of hyperparathyroidism was high among CRF patients with normal BP than hypertensive patients and with normal sugar than diabetics but the difference in proportion was not significant (p=0.87, p=0.98 respectively). 90% patients were on haemodialysis while 10% patients were on conservative management.Conclusions: Early detection of secondary hyperparathyroidism in chronic renal failure patients can reduce its complications like bone fracture and cardiovascular complications.


1985 ◽  
Vol 75 (3) ◽  
pp. 1037-1044 ◽  
Author(s):  
M Akmal ◽  
S G Massry ◽  
D A Goldstein ◽  
P Fanti ◽  
A Weisz ◽  
...  

1996 ◽  
Vol 50 (5) ◽  
pp. 1700-1705 ◽  
Author(s):  
Jesper C. Madsen ◽  
Anne Q. Rasmussen ◽  
Søren D. Ladefoged ◽  
Peter Schwarz

1980 ◽  
Vol 239 (1) ◽  
pp. F1-F12 ◽  
Author(s):  
E. Slatopolsky ◽  
K. Martin ◽  
K. Hruska

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.”


Nephrology ◽  
1984 ◽  
pp. 1292-1304 ◽  
Author(s):  
Eduardo Slatopolsky ◽  
Kevin J. Martin ◽  
Jeremiah J. Morrissey ◽  
Keith A. Hruska

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