Cellular-level bone resorption in chronic renal failure and primary hyperparathyroidism

1970 ◽  
Vol 5 (1) ◽  
pp. 288-304 ◽  
Author(s):  
A. R. Villanueva ◽  
Z. F. Jaworski ◽  
O. Hitt ◽  
P. Sarnsethsiri ◽  
H. M. Frost
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Bone Resorption ◽  
Primary Hyperparathyroidism ◽  
Cellular Level

BONE RESORPTION IN CHRONIC RENAL FAILURE: A Comparison of Radiological and Histological Assessments

1972 ◽  
Vol 28 (3) ◽  
pp. 225-226 ◽  
Author(s):  
F. H. DOYLE ◽  
THA AUNG ◽  
R. N. P. CARROLL ◽  
E. D. WILLIAMS ◽  
R. SHACKMAN
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Bone Resorption

scholarly journals Parathyroid hormone: what are we measuring and does it matter?

2002 ◽  
Vol 39 (3) ◽  
pp. 169-172 ◽  
Author(s):  
Aubrey Blumsohn ◽  
Amna Al Hadari
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Intact Parathyroid Hormone ◽  
Intact Pth ◽  
Improve Outcome ◽  
Shed Light ◽  
Improved Outcome

Immunometric assays claiming to determine intact parathyroid hormone (PTH) generally cross-react with N-truncated forms such as PTH(7-84). Laboratories need to examine the relevance of new assays with probable PTH(1-84) specificity. It is logical that assays should measure what they state they do. However, it seems unlikely that use of older 'intact' PTH assays will affect the clinical interpretation of results in primary hyperparathyroidism or vitamin D deficiency. It is plausible that appropriate application of new PTH assays could improve outcome in chronic renal failure. However, it has never been suggested that straightforward replacement of existing assays with new PTH(1-84) assays will lead to this improved outcome. A better understanding of PTH fragments and their interaction with PTH receptors may shed light on the relevance of different PTH assays. In the meantime, older technologies will continue to work well for the vast majority of patients.

scholarly journals Primary hyperparathyroidism with chronic renal failure in a Vietnamese pot-bellied pig (Sus scrofa)

2013 ◽  
Vol 33 (4) ◽  
pp. 195-200 ◽  
Author(s):  
S.E. Dumas ◽  
T.M. Grandys ◽  
A.W. Stern ◽  
E.F. Garrett ◽  
M.D. Ridgway
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Sus Scrofa

A Roentgenologic Study of Cortical Bone Resorption in Chronic Renal Failure

Radiology ◽  
1978 ◽  
Vol 126 (1) ◽  
pp. 67-74 ◽  
Author(s):  
H. Erik Meema ◽  
Dimitrios G. Oreopoulos ◽  
Silvia Meema
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Bone Resorption ◽  
Cortical Bone ◽  
Roentgenologic Study

Distribution of Circulating Immunoreactive Components of Parathyroid Hormone in Normal Subjects and in Patients with Primary and Secondary Hyperparathyroidism: The Role of the Kidney and of the Serum Calcium Concentration

1979 ◽  
Vol 57 (5) ◽  
pp. 435-443 ◽  
Author(s):  
M. A. Dambacher ◽  
J. A. Fischer ◽  
W. H. Hunziker ◽  
W. Born ◽  
J. Moran ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Normal Subjects ◽  
Dependent Manner ◽  
Intact Pth ◽  
Calcium Dependent

1. The distribution of intact parathyroid hormone-(1–84) [PTH-(1–84)] and of its COOH-terminal fragments was determined in human serum by column chromatography. In addition to PTH-(1–84) (peak I), COOH-terminal fragments having molecular weights of approximately 4000–7000 (peak II) and immunoreactive components co-eluting with human PTH-(1–12) (peak III) were observed. 2. Mean concentrations of intact PTH-(1–84) and of its COOH-terminal fragments were significantly raised in chronic renal failure as compared with those of normal subjects. Mean amounts of peak II were higher in patients with chronic renal insufficiency than in nutritional vitamin D deficiency, in pseudohypoparathyroidism and in primary hyperparathyroidism, despite comparable amounts of PTH-(1–84). 3. In chronic renal failure as well as in a group of patients with vitamin D deficiency, pseudohypoparathyroidism and primary hyperparathyroidism and in controls, significant linear relations were found between the serum concentrations of calcium and log (peak II/peak I). Our findings suggest that the conversion of intact PTH-(1–84) into COOH-terminal fragments by the parathyroid glands (resulting in a raised secretion of fragments) and/or in peripheral organs may be directly related to the serum concentration of calcium. However, the degradation of the fragments may also be suppressed in a calcium-dependent manner.

Effects of hypercalcemia and parathyroid hormone on blood pressure in normal and renal-failure rats

1986 ◽  
Vol 250 (5) ◽  
pp. F924-F929 ◽  
Author(s):  
K. Iseki ◽  
S. G. Massry ◽  
V. M. Campese
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Mean Arterial Pressure ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Induced Hypertension ◽  
Calcium Infusion ◽  
Permissive Role

Hypertension is common in primary hyperparathyroidism, but the mechanisms are not clear. Significant hypercalcemia induces elevation in blood pressure (BP), whereas excessive parathyroid hormone (PTH) lowers BP. However, in chronic renal failure (CRF) and secondary hyperparathyroidism, the hypercalcemia-induced hypertension is more severe. We examined the interaction between PTH and calcium on BP in normal rats and in those with CRF. Calcium caused a dose-related rise in serum calcium and a rise in mean arterial pressure (MAP). For a comparable rise in serum calcium, the increment in MAP in parathyroidectomized (PTX) rats (7 +/- 3 mmHg) was significantly lower (P less than 0.05) than in sham PTX rats (19 +/- 7.3 mmHg). In PTX rats receiving PTH, the MAP response to calcium infusion (17 +/- 2.4 mmHg) was similar to that in the sham PTX rats. The infusion of similar amounts of calcium in CRF rats caused a greater rise in serum calcium. In CRF-PTX rats, the changes in MAP during calcium infusion were significantly lower (P less than 0.05) than in CRF-sham PTX animals, despite similar rise in serum calcium. For a comparable rise in serum calcium, the rise in MAP in CRF rats was greater than in normal rats. These data suggest that the presence of PTH plays an important permissive role for the hypertensive action of the hypercalcemia.

Renal adenylate cyclase assay for biologically active parathyroid hormone: clinical utility and physiological significance

1986 ◽  
Vol 108 (1) ◽  
pp. 9-15 ◽  
Author(s):  
B. Auf'mkolk ◽  
R.-D. Hesch
Keyword(s):  
Renal Failure ◽  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Renal Stones ◽  
Biologically Active ◽  
Bone Lesions ◽  
Simple Relationship

ABSTRACT The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5′-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4·6 pmol human PTH(1–34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middleand carboxyl-terminal region of the PTH molecule (r = 0·503, P<0·001). A positive correlation (r = 0·572, P<0·05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P<0·01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0·390, P<0·01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied. When comparing the metabolic status of the bones with bioPTH, there was a higher incidence of severe bone lesions in those patients with primary hyperparathyroidism who had extremely raised levels of bioPTH. In osteoporosis no simple relationship was apparent. J. Endocr. (1986) 108, 9–15

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