Bone metabolism and disease in chronic kidney disease

https://www.amjmed.com/article/0002-9343(89)90297-0/pdf

Ethanol reduces bone formation and may cause osteoporosis

We studied the natural history of primary hyperparathyroidism in patients in whom the disease was discovered fortuitously by multichannel biochemical screening and who were selected for conservative management because they were asymptomatic, had no renal stone disease or radiographic osteitis fibrosa, and had serum calcium values below 3.00 mmol/L, serum creatinine levels below 133 mumol/L, and forearm bone density not more than 2.5 SD below the mean expected for age, sex, and race. One hundred and seventy-four patients meeting these criteria were encountered during a 10-yr period, of whom 80 (mean age, 61 yr) had adequate follow-up; they did not differ significantly in any initial characteristic from the remaining 94 patients. These 80 patients were followed for 1-11 yr (mean, 46 months; median, 38 months), during which there was no change, mean or individual, in any index of PTH secretion or any of its biochemical effects and no decline in forearm bone density apart from that expected from increased age. There were 4 deaths from causes unrelated to hyperparathyroidism, and the overall death rate was not increased. The data suggest that no change occurred in either the number of parathyroid cells or secretory set-point, the 2 principal determinants of basal PTH secretion. This implies a biphasic course, with a short period of disease progression followed by a long period of disease stability. Our data support the decision to withhold surgical intervention in such patients, but to establish this as the correct policy for all asymptomatic patients will require a controlled clinical trial.

Lack of biochemical progression or continuation of accelerated bone loss in mild asymptomatic primary hyperparathyroidism: evidence for biphasic disease course.

In early chronic renal failure, the state of the bones resembles that of type II primary hyperparathyroidism. Cortical bone becomes thinner and more porous, and there is increased extent of surface remodeling. These changes are followed in turn by osteomalacia and osteitis fibrosa, although sometimes these may be alternate rather than successive stages. Bone turnover is less than would be expected for the elevation of PTH level, probably because of 1,25 (OH)2D3 deficiency. The resorption velocity and lamellar bone appositional rates are depressed, but woven bone appositional rate may be increased, possibly because of hyperphosphatemia. Bone mass reflects the summation of three independent processes: loss of lamellar bone due to hyperparathyroidism (depending on the extent of insulation by osteoid); accumulation of partly mineralized osteoid because of osteomalacia; accumulation of woven bone because of osteitis fibrosa. Osteosclerosis may be growth-related metaphyseal, subchondral or diffuse axial, and periosteal neostosis may also occur. Some patients on hemodialysis lose bone because of planing rather than lacunar or dissecting resorption, combined with depression of both lamellar and woven bone formation. Hyperparathyroid bone disease tends to improve slowly after renal transplantation. Persistent hypocalcemia reflects a defect in the calcium homeostatic system and cannot be explained solely by the known stimuli to secondary hyperparathyroidism. The increment in plasma calcium in response to PTH infusion is subnormal, both in early chronic and in acute renal failure, probably because of 1,25(OH)2D3 deficiency. This is also the most likely explanation for the depressed level of blood-bone equilibrium. The activity of all three of the PTH responsive cell systems in bone is depressed in renal failure, probably because all three require 1,25(OH)2D3 in order to function normally. In pseudohypoparathyroidism, as in chronic renal failure, hypocalcemia results from a defect in the regulation of the blood-bone equilibrium. The bone-remodeling system shows all gradations of response, from slight depression of bone turnover to overt osteitis fibrosa, but bone turnover is never as low as in PTH deficiency. These differences may reflect the presence or absence of resistance to PTH of the osteoprogenitor cell as well as of the calcium homeostatic system, or may be due to varying degrees of 1,25(OH)2D3 deficiency, as in chronic renal failure. An increase in plasma calcium in response to PTH can occur either in the untreated state or after treatment with vitamin D because either the error-correcting or remodeling system remains responsive to PTH. Pseudohypoparathyroidism may be subdivided into three types, depending on whether the urinary cyclic-AMP response to PTH remains defective despite treatment with vitamin D, improves with treatment, or is normal before treatment. Only the former is associated with the genetic syndrome of Albright's hereditary osteodystrophy...

The actions of parathyroid hormone on bone: relation to bone remodeling and turnover, calcium homeostasis, and metabolic bone disease. Part IV of IV parts: The state of the bones in uremic hyperaparathyroidism--the mechanisms of skeletal resistance to PTH in renal failure and pseudohypoparathyroidism and the role of PTH in osteoporosis, osteopetrosis, and osteofluorosis.

We measured lumbar spine, femoral neck, and forearm bone mineral (BMD) in 24 women (14 premenopausal and 10 postmenopausal) who had been treated with total thyroidectomy and 131 Iodine ablation therapy for nonanaplastic thyroid carcinoma and 24 case controls. At the time of the study, all patients were free of cancer (negative 131 Iodine whole body scan and serum thyroglobulin levels < 0.3 μg/L) and all were receiving doses of T4 sufficiently high to preventa rise in a serum thyroid-stimulating hormone concentration after an iv bolus of TRH. Femoralneck BMD were significantly reduced in both the premenopausal women (89 ± 3.8% of case controls, 95% CI, 81 to 98) and postmenopausal women (77 ± 3.9% of case controls; 95% CI, 68 to 86)receiving T4. Lumbar spine BMDand forearm BMD were unaffected in the premenopausal women, but significantly reduced in the postmenopausal women receiving T4 (lumbar spine BMD = 84 ± 6.2% of case controls; 95% CI, 70 to 98 and forearm BMD = 89 ± 5.6%of case controls; 95%...

A therapeutic dilemma: suppressive doses of thyroxine significantly reduce bone mineral measurements in both premenopausal and postmenopausal women with thyroid carcinoma.

A radioimmunoassay is described for parathyroid hormone in human serum, in which commercially available reagents are used almost exclusively. This assay can be done by any laboratory with experience in radloimmunoassay. Thirty-two of thirty-three patients with surgically proven primary hyperparathyroidism had detectable concentrations of parathyroid hormone in their serum, and concentrations of the hormone exceeded the normal range in 24 of them. Significant positive correlations were found between pre-operative serum calcium, pre-operative serum parathyroid hormone, and the weight of parathyroid tissue removed at operation. These three parameters were also significantly correlated with severity of the skeletal changes as assessed by semiquantitative histological methods.

Parathyroid Hormone Assay in Primary Hyperparathyroidism: Experiences with a Radioimmunoassay Based on Commercially Available Reagents

A radioimmunoassay is described for parathyroid hormone in human serum, in which commercially available reagents are used almost exclusively. This assay can be done by any laboratory with experience in radloimmunoassay. Thirty-two of thirty-three patients with surgically proven primary hyperparathyroidism had detectable concentrations of parathyroid hormone in their serum, and concentrations of the hormone exceeded the normal range in 24 of them. Significant positive correlations were found between pre-operative serum calcium, pre-operative serum parathyroid hormone, and the weight of parathyroid tissue removed at operation. These three parameters were also significantly correlated with severity of the skeletal changes as assessed by semiquantitative histological methods. Additional Keyphrases: indexes to hyperparathyroidism #{149} diagnostic aid #{149} calculous disease #{149} parathyroid adenoma e normal values

Parathyroid HormoneAssayinPrimary Hyperparathyroidism: Experiences witha Radioimmunoassay Basedon Commercially Available Reagents

Renal transplantation reduced circulating parathyroid hormone in recipients of renal allografts. Nevertheless, biochemical and histological evidence of mild hyperparathyroidism persisted up to eight years after renal transplantation despite good graft function.

https://www.bmj.com/content/bmj/3/5985/680.full.pdf

Hyperparathyroidism after renal transplantation.

Corticotrophin in cerebrospinal fluid of patients with nelson's syndrome

With the increasing availability of parathyroid hormone (PTH) assays'-7the clinician must ask himself what decisions, if any, he is likely to base on the results of this investigation. What surgical operations will be performed or deferred ? What treatment will be given or withheld because of a particular PTH concentration ? We attempt here to answer these questions by analysing several clinical conditions and individual case reports. Whenever results of PTH estimations are quoted they have been obtained by the method of Kleerekoper et a17, which, though not as sensitive as some other methods, has the advantage of using commercially available reagents. The antibody used \"sees\" both the intact PTH molecule and C-terminal fragments. The clinical conclusions are valid for most other diagnostic assays.

https://www.bmj.com/content/bmj/1/6000/16.full.pdf

Parathyroid hormone assay in clinical desicion-making.

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M. Kleerekoper

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