Parathyroid Hormone: Alterations in Chronic Renal Failure

Nephrology ◽  
1984 ◽  
pp. 1292-1304 ◽  
Author(s):  
Eduardo Slatopolsky ◽  
Kevin J. Martin ◽  
Jeremiah J. Morrissey ◽  
Keith A. Hruska
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic 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

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.

Parathyrin radioimmunoassay: diagnostic utility of antisera produced against carboxyl-terminal fragments of the hormone from the human.

1978 ◽  
Vol 24 (3) ◽  
pp. 451-454 ◽  
Author(s):  
F P Di Bella ◽  
J M Kehrwald ◽  
K Laakso ◽  
L Zitzner
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Guinea Pigs ◽  
Normal Subjects ◽  
Terminal Region ◽  
Diagnostic Utility ◽  
Human Origin ◽  
Widespread Availability ◽  
Carboxyl Terminal

Abstract Antisera directed toward the carboxyl-terminal region of human parathyrin (parathyroid hormone), for use in daignostically applicable radioimmunoassays of the hormone in serum, are scarce, largely because of the lack of suitable immunogens of human origin. We produced four antisera in goats and guinea pigs by immunization with recently discovered carboxyl-terminal fragments of human parathyrin extracted from parathyroid tumors. Here, we report results of radioimmunoassays of nearly 200 normal and pathological sera with one of these antisera; we observed almost complete differentiation between concentrations of parathyrin in serum of healthy normal subjects and patients with primary, secondary (due to chronic renal failure), or "ectopic" hyperparathyroidism (due to nonparathyroid cancer). The availability of a new immunogen should now make possible the deliberate production of large quantities of diagnostically applicable parathyrin antisera directed toward the carboxyl-terminal region of human parathyrin. This should, in turn, lead to more widespread availability of this useful radioimmunoassay.

Effect of chronic renal failure and parathyroid hormone on phospholipid content of brain synaptosomes

1989 ◽  
Vol 256 (4) ◽  
pp. F705-F710
Author(s):  
A. Islam ◽  
M. Smogorzewski ◽  
S. G. Massry
Keyword(s):  
Central Nervous System ◽  
Renal Failure ◽  
Nervous System ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Cholesterol Content ◽  
Phospholipid Content ◽  
Intact Pth ◽  
Central Nervous System Dysfunction ◽  
Brain Synaptosomes

The effects of 21 days of chronic renal failure (CRF) with and without excess parathyroid hormone (PTH) and those of 21 days administration of intact PTH on phospholipids and cholesterol contents of rat brain synaptosomes were examined. CRF and PTH treatment were associated with a significant (P less than 0.01-0.02) reduction in the synaptosomal contents of total phospholipids, phosphatidylinositol (PI), phosphatidylserine (PS), and phosphatidylethanolamine (PE). Parathyroidectomy (PTX) prior to the induction of CRF prevented the decrements in the synaptosomal contents of total phospholipids, PI, PS, and PE. The synaptosomal contents of these phospholipids in CRF-PTX rats were not different from those in normal rats despite CRF. There were no significant changes in the cholesterol content of the synaptosomes in the various experimental groups of animals. The data show that CRF affects synaptosomal metabolism of total phospholipids, PI, PS, and PE, and these derangements are due to the state of secondary hyperparathyroidism of renal failure. The decrements in the content of PI, PS, and PE could be, at least in part, responsible for the previously reported abnormalities in the neurotransmitter functions of brain synaptosomes in CRF and could underlie some of the abnormalities in central nervous system dysfunction in uremia.

Role of uremia, brain calcium, and parathyroid hormone on changes in electroencephalogram in chronic renal failure

1984 ◽  
Vol 246 (5) ◽  
pp. F575-F579
Author(s):  
M. Akmal ◽  
D. A. Goldstein ◽  
S. Multani ◽  
S. G. Massry
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
White Matter ◽  
Blood Levels ◽  
Marked Rise ◽  
Per Se ◽  
Serum Pth ◽  
Electroencephalogram Eeg

Acute uremia is associated with increased calcium (Ca) in brain and changes in electroencephalogram (EEG), and both derangements are related to excess parathyroid hormone (PTH). Also changes in EEG in patients with chronic renal failure (CRF) correlated directly with blood levels of PTH, and fall in PTH was followed by improvement in EEG. We examined whether chronic uremia per se has an effect on brain calcium or EEG. Uremia was produced by 5/6 nephrectomy and maintained for 32-70 wk in seven thyroparathyroidectomized (TPTX) and seven control dogs. There were no differences in creatinine clearance and serum electrolytes except for HCO3, which was lower in control animals (P less than 0.01). Serum PTH was undetectable in TPTX dogs but was significantly elevated in control animals (32.3 +/- 3.3 mu leq /ml). Calcium in gray and white matter was significantly increased in both groups but much higher in control animals. The percent waves of less than 7 Hz in EEG were similar in both groups prior to uremia (TPTX 4.6 +/- 0.8 vs. control 4.2 +/- 0.5%) but remained unchanged in TPTX animals and increased significantly in control dogs (19.0 +/- 1.3%) after uremia. These data suggest that CRF per se is associated with marked rise in Ca in both gray and white matter and increment is higher in the presence of PTH. Disturbance in EEG in a state of CRF requires the presence of excess PTH and is prevented despite increased Ca in brain if hyperparathyroidism is not allowed to develop.

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