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At least 19 recordsLinked to original sources
PubMed1979

Parathyroid autotransplantation in renal osteodystrophy.

Severe renal osteodystrophy with metaphyseal fractures developed in two children with hypoplastic-dysplastic kidneys and chronic renal failure despite therapy with vitamin D, CaCO3, phosphate-binding agents, and protein restriction. Serum immunoreactive parathyroid hormone (iPTH) levels were elevated to 709 and 1,537 pg/mL (N = 255 +/- 92 pg/mL). Total parathyroidectomy and then autotransplantation of a small portion of parathyroids into the left brachioradialis muscle resulted in complete healing of renal osteodystrophy with the same dose of vitamin D. Serum iPTH and histological studies have demonstrated functioning parathyroid autotransplants, 19 and 20 months postoperatively in these two patients. Advantage of such a procedure over 3 3/4 parathyroidectomy is that this transplanted parathyroid tissue is easily accessible for partial removal in case of recurrence of uncontrollable hyperparathyroidism. We believe that total parathyroidectomy and autotransplantation can be successfully performed even in small children.

Child, Preschool↗
PubMed1979

Effect of 1 alpha-hydroxyvitamin D3 in rats with experimental renal osteodystrophy.

A model of experimental renal osteodystrophy was established in the rats with chronic renal failure induced by partial nephrectomy and therapeutic effects of 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3) were studied. Male Wistar rats weighing 180 g were 5/6 nephrectomized and fed a normal diet (Ca and P : 1%) for 6 months. After the surgery, serum creatinine levels increased 60% and thereafter continued to rise gradually with their growth for 4 to 5 months, followed by rapid increase. The serum phosphorus levels were also elevated concomitantly and the serum calcium concentrations were normal. Marked bone resorption accompanied with hypertrophy of parathyroid glands was observed by histological examinations (Tetrachrome-Fuchsin stain, contact microradiography and H-E stain). The bone resorption seemed to be due to secondary hyperparathyroidism. Treatment with 0.25 micrograms/kg/day p.o. of 1 alpha-OH-D3 for 10 days in the uremic state resulted in remarkable new bone formation which was confirmed by histological examinations. These results clearly demonstrated that the reduction of nephron mass play a critical clue of renal osteodystrophy and 1 alpha-OH-D3 appears to have a good potential for clinical use in patients with renal failure and metabolic bone diseases.

Animals↗
PubMed1978

The effect of 1alpha(OH)D3 and 1alpha,25(OH)2D3 on the bone in patients with renal osteodystrophy.

Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1alpha,25-dihydroxyvitamin D3 (1alpha25(OH)D3) or 1alpha,hydroxyvitamin D3 (1alpha(OH)D3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1alpha,25(OH)2D3 or 1alpha(OH)D3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1alpha,25(OH)2D3, play a role in regulating bone formation and/or mineralization.

Aged↗
PubMed1977

Renal osteodystrophy--a radiological review.

Renal osteodystrophy is an amalgam of a number of distinct pathological conditions, in particular, hyperparathyroidism and osteomalacia. In addition, there may be a change in the guantity of bone, i.e., osteopenia (osteoporosis) or osteosclerosis. While bone biopsy may be the most reliable method for detecting these lesions, it is not yet a routine procedure in many centers. Radiological assessment of the bones, therefore, is the most widely used method for assessing the type and severity of the bone lesions in patients with chronic renal failure. This article reviews the world literature and pays attention to conventional radiological techniques as well as macroradiography. In addition, studies in which radiological appearances are correlated with histological appearances are described. Mention is also made of the effects on radiological bone disease of dialysis and transplantation. Consideration is also given to the manifestations of soft-tissue calcification, both of the vascular and subcutaneous type, and to the effects of treatment.

Alveolar Process↗
PubMed1977

The effect of 1alpha-hydroxyvitamin D3 on calcium and mineral content of bone in renal osteodystrophy.

Ten patients with renal osteodystrophy were treated with 1alpha-hydroxyvitamin D3 for 18 months. The effect of treatment was measured by a number of different methods and bone mass assessed by mineral and neutron activation analysis. In the majority of patients, raised serum levels of parathyroid hormone and alkaline phosphatase, histological features and radiological changes returned to normal. These effects were inconsistent in patients with a raised serum calcium level before starting treatment. In general, in patients without evidence of severe hyperparathyroidism there was a reduction in the rate of fall or an increase in the mineral and calcium content of the bone.

Alkaline Phosphatase↗
PubMed1977

Is renal osteodystrophy reversible?

In order to investigate the possible reversibility of renal osteodystrophy, eleven necrograft recipients were investigated six years after transplantation, when treatment with prednisone had been withdrawn for 1.5 years. Serum ionised calcium, phosphorus, alkaline phosphatases, PTH, skeletal radiography, Technetium polyphosphate (Tc-PP) bone scintigraphy and radial bone mineral content (BMC) were studied. Normal blood biochemistry, radiography and Tc-PP scintigraphy were found in nine (82%) of the patients, in contrast to the considerably higher frequency of abnormalities ordinarily found in haemodialysis patients. However, the radial BMC was significantly reduced (mean 13.5%) and identical with the BMC value in haemodialysis patients. We conclude that some regression of renal osteodystrophy may take place after a successful kidney transplantation, but that decreased mineralisation of the appendicular skeleton persists. Whether this latter finding is due to long-term steroid treatment or is an indicator of an irreversible component in renal osteodystrophy cannot be stated.

Adult↗
PubMed1977

Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy.

Patients with severe symptomatic renal osteodystrophy were treated with either 1,25(OH)2D3 or 1 alpha(OH)D3. In 39 instances, there was either reversal of symptoms and/or a marked fall in plasma alkaline phosphatase. Bone biopsies showed improvement of either osteomalacia or osteitis fibrosa, and serum iPTH often fell. In thirteen patients, no improvement occurred. In seven patients, bone biopsy disclosed osteomalacia, and serum iPTH was normal or only slightly elevated. Thus, there was a defect in mineralisation. apparently unrelated to the lack of 1,25(OH)2D3 and in the absence of evidence of phosphate depletion. The other 'treatment failure' group showed osteitis fibrosa on biopsy and iPTH levels were markedly elevated. They are presumed to have marked secondary hyperparathyroidism. These 'treatment failure' groups had higher pre-treatment levels of serum Ca and Mg than in those showing a favourable response; also, hypercalcaemia developed rapidly during 1,25(OH)2D3 treatment. Thus, 1,25(OH)2D3 is efficacious in treating symptomatic osteodystrophy in many uraemic patients, and in other patients, it may help identify bone disease of other, as yet unknown, pathogenesis.

Adolescent↗
PubMed1978

Bone scintigraphy in renal osteodystrophy.

Bone scintigraphy with Tc-99m HEDP was performed in 30 patients on maintenance hemodialysis, and the results of quantitative analysis were compared with those of a normal group. To permit this comparison, elevated background activity due to the absence of renal radiotracer excretion was reduced by hemodialysis to levels found in the normals. Histologic proof of renal osteodystrophy had been obtained in all patients. The incidence of radiographic abnormalities was 46%, whereas abnormal scans were found in 25 patients (83%); skeletal lesions were also more pronounced and detected earlier. However, even when the scans appeared normal, the quantitative analysis showed increased skeletal activity in all patients. The total skeletal activity proved to be a good index of the severity of renal osteodystrophy and appeared dependent on both osteomalacia and hyperparathyroidism. These findings show that bone scintigraphy is a sensitive method to detect skeletal involvement in renal osteodystrophy.

Adolescent↗
PubMed1979

Terminal phalangeal tufts: earliest site of renal osteodystrophy findings in hemodialysis patients.

Direct magnificaiton of the hands of 44 patients on maintenance hemodialysis showed that the earliest unequivocal changes of renal osteodystrophy occur in the tufts. Some workers made a similar observation, but no previous objective study confirmed or refuted the sensitivity of the tufts in the diagnosis of renal osteodystrophy. The macroradiograph is consistently reproducible and serves as an excellent visual record of subtle changes.

Chronic Kidney Disease-Mineral and Bone Disorder↗
PubMed1978

A possible role for propranolol in the treatment of renal osteodystrophy.

The effect of propranolol upon parathyroid hormone (P.T.H) concentrations was investigated in patients undergoing chronic haemodialysis. 9 patients receiving propranolol for the treatment of hypertension or angina pectoris were compared with 25 similar patients not taking the drug. P.T.H. and alkaline phosphatase concentrations were lower in patients receiving propranolol and there was less radiological evidence of renal osteodystrophy in these patients. Prospective studies are needed to determine whether propranolol may be helpful as an adjunct to other therapy in reversing or preventing renal osteodystrophy.

Adolescent↗
PubMed1979

25-hydroxycholecalciferol in the treatment of renal osteodystrophy in haemodialysed patients.

The effects of 25-OHD3 on renal osteodystrophy have been studied in 6 patients on maintenance haemodialysis. Administration of 25-OHD3, 50 microgram/day, did not improve biochemical data and intestinal absorption of calcium. With a dose of 100 microgram/day in all patients an increase in blood calcium levels eventually reaching hypercalcemic values was observed. In two cases a fall in alkaline phosphatase toward normal values was noted. In the same cases the treatment-induced hyperphosphatemia, uncontrolled by AI(OH)3 supplementation and similarly high iPTH levels were observed. In two cases repeated bone biopsy following 8 months treatment and not show substantial improvement of bone lesions. In one case addition of 1,25-(OH)2D3 to the treatment with 25-OHD3 led to a more rapid improvement in biochemical parameters and iPTH serum levels. Doses of 25-OHD3 capable to correct blood calcium levels and intestinal absorption of calcium, may have minimal benefit on the osteitis fibrosa component of the bone lesion.

Adolescent↗
PubMed1977

[Treatment of renal osteodystrophy: physiopathology and secondary effects].

The prophylaxis and treatment of renal osteodystrophy are based on pathophysiological principles. Development of secondary hyperparathyroidism should be averted by early prevention of hyperphosphatemia through diet and phosphate ligants, and by normalization of the calcium balance through calcium supplements and vitamin D or its analogues. This treatment requires close clinical and laboratory control in order to avoid several hazards (hypercalcemia, hypophosphatemia, and refractory constipation). In cases with severe secondary hyperparathyroidism, subtotal parathyroidectomy is sometimes required. Nevertheless, in one such case this operation resulted in sudden hypoparathyroidism two years postoperatively.

Aluminum Hydroxide↗
PubMed1978

Increased growth after long-term oral 1alpha,25-vitamin D3 in childhood renal osteodystrophy.

We evaluated oral 1,25-vitamin D3 for as long as 26 months in six prepubescent children with renal osteodystrophy previously treated with vitamin D2. Therapy was given at 14 to 41 ng per kilogram per day to correct hypocalcemia and reverse bone disease. Serum levels of 1,25-vitamin D3 were initially reduced at 15 +/- 5 pg per milliliter (mean +/- S.E.M.) and after treatment rose to 54 +/- 13. Serum calcium rose from 7.5 +/- 1.6 mg per deciliter (mean +/- S.D.) to 9.8 +/- 0.6 after one month (P less than 0.02). Alkaline phosphatase activity fell from 536 +/- 298 to 208 +/- 91 IU per liter after 12 months (P less than 0.05). Serum immunoreactive parathyroid levels fell from 900 +/- 562 microliter eq per milliliter 411 +/- 377. Healing of rickets and subperiosteal erosions was found. Remineralization of bone was demonstrated by the photon absorption technic. In four patients growth velocity, evaluated for 12 months before and after therapy, increased from 2.6 +/- 0.8 to 8.0 +/- 3.2 cm per year. Growth velocity per year increased from less than third percentile in each to the 10th to 97th percentile after therapy. Height increment ranged from 27 to 113 per cent of that expected for change in chronologic age and 40 to 114 per cent expected for change in bone age after therapy. This trial demonstrates that oral 1,25-vitamin D3 can reverse renal bone disease and increase growth in uremic children.

Administration, Oral↗
PubMed1977

Osteocyte ultrastructure in renal osteodystrophy.

The ultrastructure of the osteocyte has been studied in 80 needle biopsies from the iliac crest of uremic subjects with renal osteodystrophy. Different types of osteocytes were present in the osseous trabeculae. Those recognizable in completely uncalcified osteoid tissue looked like normal osteocytes, even though the matrix was not mineralized. Those present in hypomineralized areas showed enlarged and irregular lacunae when examined under the light microscope; under the electron microscope these osteolytic-like changes were not evident and were found to have been produced by defective calcification of the perilacunar matrix. Osteocytes placed in matrix whose mineralization was normal were often surrounded by a border of crystals protruding side-to-side from the bone matrix into the lacunar space. Other osteocytes were placed in unusually wide lacunae. They showed evidence of osteolytic activity, chiefly consisting of irregularity of the lacunar wall, presence of flocculent, granular and filamentous material in the pericellular space, and calcification of mitochondria. Degenerating and degenerate osteocytes were also recognizable.

Adolescent↗
PubMed1979

[Renal osteodystrophy in two children : a comparison of the effects of 1 alpha-hydroxycholecalciferol (author's transl)].

Two children suffering from renal osteodystrophy were treated by 1 alpha hydroxycholecalciferol (1 alpha OHD3) 1 microgr. each day, for 18 months. In both the level alkaline phosphatase decreased at the same time as endogenous immunoreactive CT increased, iPTH did not change steadily, whereas plasma creatinine rise. As plasma calcium concentration did not increase, it is suggested that the increase in endogenous CT concentration is a part of the favourable response to the treatment by 1 alpha OHD3.

Alkaline Phosphatase↗
PubMed1976

[Collagen metabolism and mineralization of uremic bone--aspects of the molecular pathology of renal osteodystrophy].

Importance sequelae of uremia are hormonal changes in calcium homeostasis combined with chronic calcium imbalance causing structural alteration and functional insufficiency of bone. Morphological findings of the so called renal osteodystrophy are osteomalacia, osteitis fibrosa and osteoporosis. Osteitis fibrosa and abnormal skeletal metabolism (changes of collagen turnover, insufficient maturation of stable bone crystals) impair the mechanical qualities of bone. Probably the uremia per se influences the collagen metabolism; additional factors such as secondary hyperparathyroidism and deficiency of vitamin D3 are discussed.

Animals↗