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PubMed2004

Predictors of bone mineral density in patients on hemodialysis.

Renal osteodystrophy is a universal complication of uremia. Renal failure patients are at risk for low bone mineral density (BMD) and fractures. Parathyroid hormone (PTH) plays a pivotal role in the pathophysiology of uremic bone disease. Histomorphometric studies suggest that the maintenance of PTH levels between two and four times the upper limit of normal is associated with the lowest prevalence of two common forms of osteodystrophy: osteitis fibrosa cystica and adynamic bone disease. The purpose of this study was to investigate whether the above recommendation for PTH levels in dialysis patients corresponds to a more optimal BMD with a special emphasis on diabetic versus nondiabetic subjects. Twenty-eight patients with chronic renal failure on hemodialysis underwent measurement of PTH levels, as well as BMD at the lumbar spine, hip, and forearm. They were divided into three groups based on the mean PTH level over the 5 years prior to having BMD measured. Osteoporosis was diagnosed in 55% of men and 87% of women on dialysis. Predictors of BMD were gender, duration on hemodialysis, and diabetes. Our study supports the histomorphometry-based studies suggesting that the maintenance of intact PTH levels two to four times the upper limit of normal may be associated with better skeletal health in uremic patients on hemodialysis, and that the diabetic subgroup is at particular risk for low BMD.

Adult↗

PubMedDate not supplied

Effectiveness of surgical parathyroidectomy for secondary hyperparathyroidism in renal dialysis patients in Qatar.

Pharmacologic interventions designed to control hyperparathyroidism (HPT) in uremic patients have limitations and potentially serious adverse clinical consequences. Hence, one still has to resort to surgical parathyroidectomy (PTX) in a considerable number of dialysis patients. The aim of the present study was to illustrate our experience with 26 renal dialysis patients who underwent surgical PTX. The main indications for PTX included iPTH > 1000 pg/mL associated with severe osteitis fibrosa, debilitating pruritus, marked soft tissue calcification, or hypercalcemia with hyperphosphatemia, which sometimes complicated vitamin D therapy. All patients were resistant to more conservative measures, including control of serum phosphate, attention to oral intake and dialysate calcium levels, and oral/intravenous administration of active vitamin-D-pulse therapy. Ultrasound and technetium 99-sestamibi scan were used to image the thyroid and the parathyroid glands. Total PTX with autotransplantation was performed in 23 patients; subtotal PTX was performed in 3 patients. Histology of frozen sections taken intraoperatively showed nodular changes in 14 and diffuse hyperplasia in 12 cases. During the 2-year follow-up period significant reductions in parathyroid hormone, alkaline phospatase blood levels, skeletal changes, and soft tissue calcifications were observed. Pruritus improved in half the cases. Some improvement in hemoglobin and hematocrit was also noticed. The complication rate after PTX was low. Transient postoperative hypocalcemia requiring intensification of calcium and vitamin D therapy was seen in cases with high preoperative alkaline phosphatase levels. Recurrence was observed in two cases. Hypoparathyroidism was not recorded. We conclude that surgical reduction of parathyroid mass is a safe and effective treatment for symptomatic disease not suppressible by pharmacologic means.

Adolescent↗

PubMed1989

Primary hyperparathyroidism.

Hyperparathyroidism was described initially in the mid 1920s in patients suffering from a rare and severe form of bone disease, osteitis fibrosa cystica. In the 1940s and 1950s renal stone disease was recognized as a far more frequent complication of primary hyperparathyroidism than bone disease, and approximately half of the patients with primary hyperparathyroidism in clinical series published through the 1970s presented with renal stones. The introduction of routine determination of serum calcium concentration in the mid 1970s has had a dramatic impact on the frequency with which primary hyperparathyroidism is diagnosed in the population, particularly in older individuals with predominantly nonspecific symptoms of the disease. Stone complications appear to occur in less than 10 per cent of such patients. Underlying primary hyperparathyroidism is diagnosed in approximately 1 to 5 per cent of the patients with calcium stone disease. The predominant risk factor for stone formation in primary hyperparathyroidism is hypercalciuria, and patients typically present with moderate to marked hypercalciuria but with only mild hypercalcemia, in the range of 11 mg. per dl. or less. Hypercalciuria in these patients is principally the result of 1,25-dihydroxyvitamin D-mediated hyperabsorption of calcium from the intestine. The pattern of hypercalciuria disproportionate to the degree of hypercalcemia that typifies patients with primary hyperparathyroidism and stone disease reaches an extreme degree in patients with so-called subtle or normocalcemic primary hyperparathyroidism, in whom diagnosis by routine techniques may be difficult. Parathyroid exploration remains the treatment of choice in patients with primary hyperparathyroidism and stone complications.

Adult↗

PubMed1982

Meningeal osteomas and chronic renal failure.

Osteomas, although usually found in the frontal and ethmoid sinuses or the mandible, may be located on the inner table of the skull. We report the incidence, distribution, histologic features, and clinical correlates of intracranial osteomas arising in the dura mater and the falx cerebri in 200 consecutive adult autopsies. Ten patients (5 per cent of autopsies) were found to have meningeal osteomas. The tumors were usually located at the dural-falx junction at the superior longitudinal sinus. Histologically, they resembled osteomas arising from other sites, but undecalcified sections generally demonstrated histologic features of active bone remodeling--namely, the presence of abundant osteoid and numerous osteoclasts, and, in some instances, osteitis fibrosa. The age and sex distributions were similar among autopsied patients with meningeal osteomas (mean age, 66 years; 60 per cent female) and those without (mean age, 64 years; 58 per cent female). Although the incidence of uremia in the general autopsy population was only 13 per cent, 60 per cent of patients with osteomas died with concomitant renal failure. The authors consider these cases of meningeal ossifications and reports of meningeal calcifications to represent osteomas arising from the dura mater and the falx cerebri. Thus, intracranial osteomas may be more common than was previously recognized. In some instances, the abnormal biochemical state accompanying chronic renal failure may stimulate new bone formation in the osteogenic tissue of the dura mater.

Aged↗

PubMed1985

S-100 protein immunostaining in the differential diagnosis of chondroblastoma.

In an effort to investigate the utility of immunostaining for S-100 protein in the differential diagnosis of chondroblastoma, the expression of S-100 protein in nine chondroblastomas was compared with that in six giant cell tumors, six aneurysmal bone cysts, four giant cell reparative granulomas, six cases of fibrous dysplasia, two cases of osteitis fibrosa cystica, two nonossifying fibromas, and one clear cell chondrosarcoma. Five enchondromas, three typical chondrosarcomas, and one mesenchymal chondrosarcoma were also included as control tumors. The proliferating stromal cells in seven of the nine chondroblastomas stained for S-100 protein, as did the lacunar chondrocytes in all of the enchondromas and chondrosarcomas and rare stromal cells in the clear cell chondrosarcoma. In contrast, none of the other tumefactive bone lesions included in this study demonstrated S-100 protein immunoreactivity. These results suggest that immunohistochemical assessment of S-100 protein may be a method for diagnostically separating chondroblastoma from pathologic entities that could be histologically confused with it in the presence of limited biopsy material. However, clear cell chondrosarcoma would appear to represent an exception to this general statement.

Adolescent↗

PubMed1999

Control of hypercalcaemia of parathyroid carcinoma by immunisation.

BACKGROUND: Patients with parathyroid tumours can develop extreme hypercalcaemia and osteitis fibrosa cystica. Clinical features result from the action of parathyroid hormone (PTH) on bone receptors. Because this hormone is produced in microgram quantities, inhibition of its metabolic effects with potent PTH antibodies should be possible. We tested whether an immunisation with synthetic human and bovine PTH peptides could stimulate autoantibodies against PTH. METHODS: A patient with metastatic parathyroid carcinoma in the lungs and pleura developed severe bone disease and extreme hypercalcaemia that proved resistant to conventional therapy. She was immunised with 200 microg human and bovine PTH peptides and 50 microg human PTH. Booster doses were also given at 4 weeks and 11 weeks. The patient was then seen every week. FINDINGS: Antibodies against PTH were produced within 4 weeks of initial immunisation and titres increased with repeated doses of immunogens. Total serum calcium concentrations, which had ranged from 3.5 mmol/L to 4.2 mmol/L over the previous 18 months, fell to between 2.5 mmol/L and 3.0 mmol/L over 6 months of therapy. This fall was accompanied by striking clinical improvement. INTERPRETATION: We believe this is the first use of immunotherapy to control remote, non-metastatic complications of malignant disease. B-cell tolerance to human PTH was broken by immunisation with PTH peptides in adjuvant. This therapeutic approach could be used to control excess hormone production in several types of endocrine tumour and may have applications in other diseases.

Animals↗

PubMed1990

Pharmacokinetics of calcitriol in continuous ambulatory and cycling peritoneal dialysis patients.

Oral calcitriol is commonly used for the treatment of secondary hyperparathyroidism in patients undergoing long-term dialysis, but it has been suggested that intravenous (IV) or intraperitoneal (IP) administration enhances the therapeutic efficacy of the sterol. To examine potential mechanisms for this difference, the bioavailability of calcitriol was evaluated after single oral (PO), IV, and IP doses of 60 ng/kg in each of six adolescent patients with osteitis fibrosa undergoing continuous ambulatory peritoneal dialysis (CAPD) or continuous cycling peritoneal dialysis (CCPD). Serum calcitriol levels were 3.6 +/- 4.3, 8.2 +/- 7.5, and 2.5 +/- 3.0 pg/mL, respectively, before IV, PO, and IP doses of the sterol; these values increased to similar levels at 24 hours: 55.6 +/- 14.6 pg/mL after PO, 56.4 +/- 17.6 pg/mL after IV, and 53.8 +/- 20.1 pg/mL after IP. Serum calcitriol levels were higher 1, 3, and 6 hours after IV injections than after PO or IP doses; values thereafter did not differ among groups. The bioavailability of calcitriol, determined from the 24-hour area under the curve (AUC0-24) for the increase in serum calcitriol concentration above baseline values was 50% to 60% greater after IV, 2,340 +/- 523 pg.mL-1.h-1, than after PO, 1,442 +/- 467 pg.mL-1.h-1, or IP, 1,562 +/- 477 pg.mL-1.h1, dosages, P less than 0.05. These differences were due to higher values for AUC during the first 6 hours after calcitriol administration. Although IP calcitriol did not increase sterol bioavailability, radioisotope tracer studies indicated that 35% to 40% of the hormone adheres to plastic components of the peritoneal dialysate delivery system.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1986

Renal osteodystrophy in asymptomatic hemodialysis patients: evidence of a sex-dependent distribution and predictive value of serum aluminum measurements.

Bone histologies and serum concentrations of calcium, phosphate, alkaline phosphatase, iPTH, 25 OHD, 1,25(OH)2D3, and aluminum were obtained from 113 chronically hemodialyzed patients free of symptoms and signs of renal osteodystrophy. All patients had a pathologic bone histology; in 69.0%, a mixed form with predominant osteitis fibrosa and concomitant osteoidosis. In 30.1%, we found pure hyperosteoidosis, nearly half of these cases showing osseous aluminum deposits. Hyperosteoidosis was much more frequent in women (35.7%) than in men (20.9%), although the prescribed intake of aluminum-containing phosphate binders was the same. It is possible that female hemodialysis patients were more prone to aluminum accumulation or that they had a better compliance in taking the aluminum hydroxide. Serum parameters alone were not very helpful in predicting the underlying bone disease. Mean iPTH concentrations tended to be lower in the patients with hyperosteoidosis than in those with the mixed lesion, but there was wide variation. Serum aluminum was only predictive for aluminum deposits in the bone when concentrations exceeded 100 micrograms/L.

Adult↗

PubMed1989

Deferoxamine test and bone disease in dialysis patients with mild aluminum accumulation.

Aluminum bone disease is a frequent complication of dialysis patients. The deferoxamine (DFO) test has been advocated as a noninvasive procedure for the diagnosis of AI bone lesion. However most of these studies have been performed in symptomatic patients with significant AI bone disease. Whether this test may provide similar data at an earlier stage of AI toxicity is not known. The present study evaluates prospectively 28 patients with mild AI load. Patients studied ranged in age from 21 to 65 years; duration of dialysis was 5.6 +/- 3.2 years; deferoxamine, 40 mg/kg body weight, was infused at the end of dialysis. Serum AI was measured before DFO administration and before the next dialysis treatment. Bone biopsies were performed in all patients. Cortical bone AI was determined biochemically; trabecular and cortical bone AI were also determined histochemically. Mean basal serum AI (43.2 +/- 30.8 micrograms/L) and cortical bone AI (25.7 +/- 35.2 micrograms/g) were moderately increased. Basal serum AI correlated (r = 0.77) with the increment in serum AI after DFO infusion. After DFO, stainable trabecular and cortical bone AI correlated in a similar manner with both basal serum AI and increment in serum AI. Only biochemically determined cortical bone AI was not significantly related to basal serum AI. Nineteen of the 28 patients had evidence of osteitis fibrosa on bone biopsy. Stained AI surfaces but not trabecular AI were different in patients with low and patients with high bone formation rates. The bone findings, assessed as bone formation rates and resorption surfaces, did not correlate with biochemically or histochemically determined bone AI.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗

PubMed1996

Spontaneous tendon ruptures in patients on chronic dialysis.

Large tendon rupture is a rare catastrophic occurrence in dialysis patients. Pathogenesis of this has been variably thought to be due to malnutrition, insufficient dialysis, amyloidosis, chronic acidosis, or hyperparathyroidism. We investigated contributory causes and timing of this complication in 44 dialysis patients (42 hemodialysis and two peritoneal dialysis patients). Five cases were our own; the other 39 were reported in the literature during the last two decades. Data were compared with a hospital database of 916 patients. The patients who experienced tendon ruptures had been on dialysis longer (mean duration, 7.6 years v 4.0 years; P = 0.001), were younger (mean age, 39.7 years v 48.4 years; P = 0.0001), had much higher parathyroid hormone levels (1,802 pg/mL v 202 pg/mL; P = 0.0001), had a higher phosphate level (6.8 mg/dL v 5.9 mg/dL; P = 0.001), had a slightly higher calcium level (9.2 mg/dL v 8.8 mg/dL; P = 0.038), and had a higher alkaline phosphatase level (649 IU/L v 109 IU/L; P = 0.0001) than control patients. Patients with tendon ruptures had no evidence of malnutrition (albumin 3.7 g/dL v 3.8 g/dL; P = 0.237) and had the same acidosis (bicarbonate 22.2 mEq/L v 22.0 mEq/L; P = 0.180). The time on dialysis to rupture was inversely related to the patient's age (r = 0.47, P = 0.004). Most patients had evidence of years of poorly controlled hyperparathyroidism with high and increasing levels of parathyroid hormone and alkaline phosphatase. Previous steroid use was also much more common in patients with tendon ruptures, as was radiographic evidence of osteitis fibrosa. The disease led to long hospitalization and prolonged morbidity, with mobility limitations in several patients. Spontaneous large tendon rupture in patients is secondary to hyperparathyroidism; is more common in young patients, particularly if exposed to corticosteroids; leads to long-lasting morbidity; and should be preventable by better supervision and treatment of hyperparathyroidism.

Adult↗

PubMed2000

Pathophysiology and diagnosis of primary hyperparathyroidism--strategy for asymptomatic primary hyperparathyroidism.

Primary hyperparathyroidism (PHPT), the most common cause of hypercalcemia due to excessive secretion of PTH, is usually associated with hypophosphatemia and elevated serum chloride. Although PHPT was often complicated by renal stone disease and osteitis fibrosa in the past, routine screening of serum calcium (Ca) and development of sophisticated assay of parathyroid hormone have contributed to earlier detection of asymptomatic PHPT (APHPT). The proportion of APHPT patients, who have a mild elevation of serum Ca levels, usually within 1.0 mg/dL above the upper limit of normal, rose from 10-20% to approximately 45% of all PHPT patients in 1990-1995 in our clinic. Although it has been reported that the prevalence of PHPT is about 0.1% of the American population, the prevalence of PHPT appears to be far less in the Japanese population. Determination of a strategy for the increasing number of APHPT patients, is a pressing need but has yet to be accomplished. Treatment with bone antiresorptive drugs has met with some success, although the long-term efficacy of this treatment is not clear. The therapeutic effects of Ca-sensing receptor agonists appear promising.

Hormone Antagonists↗

PubMed1997

Renal osteodystrophy.

Renal osteodystrophy is a general complication of chronic renal failure and end-stage renal disease. The nature of renal osteodystrophy has changed since osteomalacia due to aluminum intoxication has become less prevalent. Osteomalacia has been replaced by the adynamic bone disorder. Suppression of osteitis fibrosa, calcitrol and control of secondary hyperparathyroidism has been shown to produce the adynamic bone disorder. Thus, many other factors besides secondary hyperparathyroidism and calcitrol deficiency contribute to the pathogenesis of renal osteodystrophy. Some of these factors, according to our current state of knowledge, are discussed in this chapter along with the presentation and treatment of renal osteodystrophy.

Bone and Bones↗

PubMed1995

The role of metabolic acidosis in the pathogenesis of renal osteodystrophy.

Renal osteodystrophy is thought to be the result of abnormalities in the serum levels of parathyroid hormone, vitamin D, calcium, and phosphorus, and excess exposure to certain substances such as aluminum and iron. However, a significant amount of data suggest that the metabolic acidosis that develops in the course of chronic renal failure may also play a contributory role. Metabolic acidosis may effect changes in bone by directly inducing dissolution of bone, stimulating osteoclast-mediated bone resorption, inhibiting osteoblast-mediated bone formation, and altering the serum concentrations or the biological actions of parathyroid hormone and vitamin D. As a consequence, in some patients with normal renal function, osteoporosis and osteomalacia have been reported that are linked in part to metabolic acidosis. Also, in patients with chronic renal failure before and after initiation of dialysis, the severity of the metabolic acidosis appears to have a bearing on the presence and degree of hyperparathyroidism, osteitis fibrosa, and osteomalacia. Taken as a whole, these data suggest that correction of the metabolic acidosis of chronic renal failure may have a beneficial effect on the bone disease observed in these patients. This article reviews (1) the data indicating the mechanisms by which metabolic acidosis causes alterations in bone; (2) the types of bone lesions observed in animals and humans with metabolic acidosis in the presence of normal and abnormal renal function; (3) the impact of correction of the acidosis on the bone lesions; and (4) specific recommendations for treatment in patients with chronic renal failure both before and after initiation of maintenance dialysis.

Acid-Base Equilibrium↗

PubMed2005

Synchronous parathyroid and papillary thyroid carcinoma.

Concomitant thyroid disease is not unusual among patients with primary hyperparathyroidism. However, the simultaneous occurrence of parathyroid and thyroid carcinoma is extremely rare. We report a 38-year-old man with primary hyperparathyroidism who presented with osteitis fibrosa cystica complicated with pathologic femoral neck fracture. Preoperative investigation for exclusion of multiple endocrine neoplasia did not find evidence of medullary thyroid carcinoma or pheochromocytoma, but imaging studies revealed the presence of nodules in the right lobe and a parathyroid lesion over the left inferior pole of the thyroid gland. Total thyroidectomy, left parathyroidectomy, and bipolar hemiarthroplasty of the left hip were then performed simultaneously. The resected specimens were pathologically identified as papillary thyroid carcinoma and parathyroid carcinoma, respectively. After the operation, 131I ablation therapy was administered at a dose of 120 mCi. Additional doses of 30 mCi were given yearly as serum thyroglobulin level became elevated. Serum calcium level remained normal during yearly follow-up. Although parathyroid carcinoma is an uncommon cause of parathyroid hormone-dependent hypercalcemia, it should nonetheless be given due consideration because its surgical approach differs from that of parathyroid adenoma. As the coexistence of parathyroid and non-medullary thyroid carcinoma has previously been reported, the possibility of both malignancies must also be considered in the setting of primary hyperparathyroidism with thyroid nodules. If confirmed with preoperative parathyroid scintigraphic and other laboratory studies, an optimal outcome may be achieved with complete resection of both tumors at the time of initial operation, followed by adjunctive therapy.

Adult↗

PubMed1976

Effects of 25-hydroxycholecalciferol on bone lesions of children with terminal renal failure.

Quantitative histology was performed on serial iliac crest biopsies obtained from 14 children with terminal renal failure. A long-term study on the comparative effects of vitamin D2 and 25-hydroxycholecalciferol [25-(OH)D3], in five patients with severe lesions of osteomalacia and/or osteitis fibrosa, demonstrated the efficiency of 25 to 200 mug/day of 25-(OH)D3 and the lack of therapeutic action of 345 to 685 mug/day of vitamin D2. In nine subjects with normal roentgenograms or minimal skeletal alterations, the first biopsy taken at the beginning of intermittent hemodialysis showed evidence of defective mineralization and/or lesions of resorption. Four of these children were treated with 25-(OH)D3 (25 to 50 mug/day) and calcium supplementation orally (0.5 to 1.5 g/day); five children received calcium orally (0.5 to 0.75 g/day) alone. Aggravation of bone lesions during intermittent hemodialysis was observed in patients treated with calcium supplements alone. In subjects who were given 25-(OH)D3, mineralization improved and marrow fibrosis disappeared. However, as the two groups of patients were different in composition and in the manner in which they were treated, it is difficult to state whether the beneficial effects observed were solely attributable to 25-(OH)D3 administration. 25-(OH)D3 therapy induced severe intoxication in two patients. A rise in plasma calcium concentration to 11.0 to 11.5 mg/100 ml was observed in two other patients. It is concluded that: a) pharmacologic doses of 25-(OH)D3 are highly effective in healing bone lesions of children with terminal renal failure; b) such treatment requires strict clinical surveillance as 25-(OH)D3 intoxication may occur even in anephric patients.

Adolescent↗

PubMed1978

Skeletal X-ray findings and bone histology in patients on hemodialysis.

X-ray films of the hand skeleton (mammography technique), serum chemistry, and quantitative bone histology (micromorphometry of undecalcified sections, iliac crest spongiosa) were compared in 25 patients on maintenance hemodialysis. The X-ray findings correlated better with serum PTH levels than with bone histology. Of all radiological signs of renal osteodystrophy, pronounced subperiosteal resorption (radial aspect, second finger, middle phalanx) and periosteal new bone formation (middle phalanx) correlated best with histological indicators of osteitis fibrosa. These signs were never seen in control patients. Acroosteolysis (endphalanx) and intracortical or endosteal resorption (middle phalanx) were less specific (i.e., seen even in the absence of metabolic bone disease) and correlated less with bone histology. Osteosclerosis in iliac cancellous bone was paralleled by abnormal texture of spongy bone in the proximal metaphysis of the middle phalanx (second finger).

Adult↗

PubMed1980

Hemodialysis encephalopathy with osteomalacic fractures and muscle weakness.

The hemodialysis unit at Columbia, South Carolina, opened in April, 1974. By June of 1977, 7 patients had died from dialysis encephalopathy, and 16 of the 51 surviving patients showed speech disorders, fits, and myoclonic jerks. Pathologic fractures were seen in 22 patients. Bone histomorphometry showed severe osteomalacia with minimal, if any, osteitis fibrosa, and serum alkaline phosphatase activity was normal. The mean serum aluminum concentration in 33 random patients was elevated at 83.5 microgram/liter (control group, 13.9 microgram/liter, P less than 0.001). The mean bone aluminum concentration in 4 patients who died from this syndrome was 307 ppm of bone ash (normal, less than 10 ppm). Dialysis fluid aluminum was high at 140 microgram/liter. Purification of the dialysis fluid with a water softener, reverse osmosis and a deionizer and abandoning extra-strength Basaljel resulted in a notable clinical and EEG improvement. None of 81 new patients who started hemodialysis between July of 1977 and July of 1979 after the change in treatment have developed any such symptoms. A syndrome of hemodialysis encephalopathy accompanied by pathologic osteomalacic fractures is described. Recovery is possible. The syndrome was eradicated after purification of the dialysis fluid.

Aged↗

PubMed1981

Aluminum localization in bone from hemodialyzed patients: relationship to matrix mineralization.

It has been suggested that in uremic bone, aluminum interferes with normal mineralization. Aluminum content and aluminum localization were studied in iliac crest biopsies of two groups of patients on regular hemodialysis; one group had histologic osteomalacia, and little or no bone resorption (group 1); the other, osteitis fibrosa and no mineralization defect (group 2). Group 1 patients had significantly higher plasma aluminum concentrations than those of group 2. No difference was found in bone aluminum content, which was above normal in both groups. In the bone samples of the osteomalacic subjects, aluminum was mainly localized at the limit between osteoid and calcified tissue, the site where the bone mineral is normally first deposited. Osteomalacia could not be related to hypocalcemia or to phosphate depletion. Active vitamin D derivatives (25-hydroxycholecalciferol and 1alpha-hydroxycholecalciferol) failed to prevent or to improve the bone disease. In the bone samples of group 2 subjects, aluminum could not be localized by the methods used, except in the two cases with greatly elevated bone aluminum, where it was mainly localized on cement lines. In group 2 subjects, immunoreactive parathyroid hormone plasma concentration, osteoclast surface, and marrow fibrosis were significantly higher than they were in group 1 subjects. It is concluded that in bone from uremic patients on regular dialysis, aluminum can induce a particular form of osteomalacia, resistant to the vitamin D active derivatives. The bone disease is only observed in the absence of severe secondary hyperparathyroidism. This suggests that parathyroid hormone may be involved in the development of the aluminum-induced mineralization defect.

Adult↗