Parathyroid Hyperplasia in Renal Insufficiency

Castleman, Benjamin; Mallory, Tracy B.

doi:10.1097/00005053-193712000-00011

Cited by 51 publications

(18 citation statements)

References 2 publications

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“…99.2 ±0.1 (22) 98.4±0.4 (21) 96.9±0.8 (27) 91.6± 1.2 (18) 87.5± 1.6 (17) 83.9± 1.4 (16) 69.9 ±3.0 (21) 77.3± hyperplastic cells described in humans with secondary hyperparathyroidism (32). The high correlation coefficient of 0.92 between fresh and dry glands indicates that as the glands enlarge in size the cell solids are increasing proportionally, suggesting that weight corresponds to a functional parameter in the glands.…”

Section: Diet Hydrogen Ion Content Variedmentioning

confidence: 99%

The Effects in the Rat of Varying Intakes of Dietary Calcium, Phosphorus, and Hydrogen Ion on Hyperparathyroidism Due to Chronic Renal Failure

Kaye¹

1974

J. Clin. Invest.

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Section: Diet Hydrogen Ion Content Variedmentioning

confidence: 99%

The Effects in the Rat of Varying Intakes of Dietary Calcium, Phosphorus, and Hydrogen Ion on Hyperparathyroidism Due to Chronic Renal Failure

Kaye¹

1974

J. Clin. Invest.

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“…Stereoscopic electron microscopy studies have shown that the parathyroid cells of rats fed a low calcium diet for 3 wk are hypertrophied (7,8), and flow cytometry estimation of parathyroid cell number showed that there was a large increase in PTH gene expression per cell and only a moderate increase in parathyroid cell number (2). However, patients with chronic renal failure are maintained on hemodialysis treatment for years and in this situation the parathyroid cell hyperplasia becomes a major clinical problem resulting in the synthesis of large amounts of PTH (9,10). This excess PTH leads to tremendous bone resorption, osteitis fibrosa cystica, which is a central feature of renal osteodystrophy.…”

Section: Introductionmentioning

confidence: 99%

Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D.

Naveh-Many

Rahamimov²,

Livni³

et al. 1995

J. Clin. Invest.

372

210

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Secondary hyperparathyroidism is characterized by an increase in parathyroid (PT) cell number, and parathyroid hormone (PTH) synthesis and secretion. It is still unknown as to what stimuli regulate PT cell proliferation and how they do this. We have studied rats with dietary-induced secondary hyper-and hypoparathyroidism, rats given 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and rats after 5/6 nephrectomy for the presence of PT cell proliferation and apoptosis. PT cell proliferation has been measured by staining for proliferating cell nuclear antigen (PCNA) and apoptosis by in situ detection of nuclear DNA fragmentation and correlated with serum biochemistry and PTH mRNA levels. A low calcium diet led to increased levels of PTH mRNA and a 10-fold increase in PT cell proliferation. A low phosphate diet led to decreased levels of PTH mRNA and the complete absence of PT cell proliferation. 1,25(OH)2D3 (25 pmol/d x 3) led to a decrease in PTH mRNA levels and unlike the hypophosphatemic rats there was no decrease in cell proliferation. There were no cells undergoing apoptosis in any of the experimental conditions. The secondary hyperparathyroidism of 5/6 nephrectomized rats was characterized by an increase in PTH mRNA levels and PT cell proliferation which were both markedly decreased by a low phosphate diet. The number of PCNA positive cells was increased by a high phosphate diet. Therefore hypocalcemia, hyperphosphatemia and uremia lead to PT cell proliferation, and hypophosphatemia completely abolishes this effect. Injected 1,25(OH)2D3 had no effect.These findings emphasize the importance of a normal phosphate and calcium in the prevention of PT cell hyperplasia. (J. Clin. Invest. 1995. 96:1786-1793.) Key words: parathyroid hormone * apoptosis* hyperplasia * 1,25(OH)2D3 chronic renal failure.

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“…In each instance the glands showed enlargement and hyperplasia of the " secondary " type (23) (Table III), the greatest hypertrophy being found in the patient with renal rickets. In all of these cases the parathyroid function test, performed from 1 to 4 months before death, was negative.…”

Section: Normal Individualsmentioning

confidence: 96%

“…The test was performed in 8 patients with ac- (20,21,22,23). Among the most striking cases of this enlargement are those occurring in patients with renal rickets in whom chronic renal insufficiency is of a marked degree and of long duration (13,24,25,26,27).…”

Section: Other Clinical Conditionsmentioning

confidence: 99%

“…Among the most striking cases of this enlargement are those occurring in patients with renal rickets in whom chronic renal insufficiency is of a marked degree and of long duration (13,24,25,26,27). This enlargement has recently been shown to be due primarily to a chief cell or "secondary " hyperplasia (13,20,23,26,27); this hyperplasia, at times without apparent gross enlargement of the glands, occurs with regularity in all cases with chronic renal insufficiency of long duration (23). Enlargement of the parathyroids and " secondary " hyperplasia has been found in other clinical AAA conditions such as rickets and osteomalacia (28,29,30,31) and occasionally in Paget's disease (23,32,33).…”

Section: Other Clinical Conditionsmentioning

confidence: 99%

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Experience With the Hamilton and Highman Test for Parathyroid Hyperfunction in Chronic Nephritis, Toxic Goiter, and Paget's Disease of Bone

Gilligan¹,

Volk²,

Gargill³

1938

J. Clin. Invest.

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In 1932 Hamilton and Schwartz (1) described a method for the detection of small amounts of parathyroid hormone, three to five units, in preparations of the hormone and in blood. In 1936 Hamilton and Highman (2) presented certain modifications of this test designed to make the method particularly applicable to the detection of abnormally large amounts of parathyroid hormone in the blood of patients suspected of having increased parathyroid function. The test consists, briefly, in measuring the increase in the serum calcium of a rabbit at definite intervals after the rabbit has received an intramuscular injection of the blood or preparation containing parathyroid hormone, the animal being given amounts of calcium chloride solution by stomach tube at definite periods during the experiment.In Highman and Hamilton found abnormally great amounts of parathyroid hormone in the blood of 20 of 23 patients with chronic nephritis and elevated blood urea nitrogen (12). Shelling and Remsen (13) reported a case of renal rickets with elevated concentrations of nitrogen and inorganic phosphorus in the blood, which case showed increased parathyroid hormone in the blood according to the Hamilton and Schwartz test, and at postmortem examination showed four markedly enlarged parathyroid glandules. These authors mention that the results of the Hamilton and Schwartz test were negative in other cases of renal rickets. Bass and Paxter (38) recently performed the "Hamilton test" on two occasions in one patient with renal rickets; on one of these occasions the result was " suggestively positive," on the other trial, negative. 641

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Parathyroid Hyperplasia in Renal Insufficiency

Cited by 51 publications

References 2 publications

The Effects in the Rat of Varying Intakes of Dietary Calcium, Phosphorus, and Hydrogen Ion on Hyperparathyroidism Due to Chronic Renal Failure

The Effects in the Rat of Varying Intakes of Dietary Calcium, Phosphorus, and Hydrogen Ion on Hyperparathyroidism Due to Chronic Renal Failure

Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D.

Experience With the Hamilton and Highman Test for Parathyroid Hyperfunction in Chronic Nephritis, Toxic Goiter, and Paget's Disease of Bone

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