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Pathologic studies of the osteoporosis of Von Gierke's disease (glycogenosis 1a).

Pathologic and point count-morphometric studies of ribs, vertebrae, and iliac crests of 7 patients with Von Gierke's glycogenesis type Ia aged 5 months to 30 years were performed. The bone lesion is a pure osteoporosis (reduction in mass of bone matrix) with no evidences of significant physeal cartilage abnormality or of osteitis fibrosa or osteomalacia (reduced mineralization of bone matrix). The osteoporosis was already marked in the youngest patient studied (5 months). The discrepancy between normal and glycogen storage disease (GSD) bones increased progressively with age for ribs and was less severe for vertebrae. Available biochemical data give no indication of primary disturbance of calcium or phosphate metabolism, of parathyroid activity, or of vitamin D metabolism. Clinical data suggest that the osteoporosis of Von Gierke's disease is due to hypoglycemia or a metabolic sequela thereof, such as insulinopenia, but pathologic study of patients treated by newer techniques of maintaining euglycemia in GSD is needed.

Adult↗

Pulmonary alveolar septal calcinosis causing progressive respiratory failure in acute lymphoblastic leukemia in childhood.

A syndrome of pulmonary alveolar septal calcinosis, pneumothorax, and pneumomediastinum, leading to rapidly progressive acute respiratory insufficiency and death was observed in 2 children with acute lymphoblastic leukemia (ALL). Primary clinical and radiological considerations in these patients were pulmonary edema and infection, and the diagnosis of pulmonary alveolar septal calcification was established only at autopsy. One patient, a 15-year-old girl, was found also to have parathyroid hyperplasia typical of familial hyperparathyroidism. The other, a 16-month-old girl, showed osteitis fibrosa of the bones and parathyroid hyperplasia of secondary type, suggesting that the pulmonary calcinosis resulted from hypercalcemia caused by a parathormone or prostaglandin-secreting tumor. The cause of pneumothorax and pneumomediastinum may have been rupture of calcified alveolar septa induced by high PEEP during ventilation of these patients. Other possible mechanisms contributing to hypercalcemia and pulmonary calcinosis in children with acute leukemia include bone resorption due to marrow infiltration, immobilization syndrome, renal failure, and administration of calcium, phosphate, or bicarbonate. This complication of acute leukemia in childhood is rare (2 patients in 430 autopsied over the period 1961-1982 at Childrens Hospital of Los Angeles). How often the process can be reversed if diagnosed before severe respiratory insufficiency is present is not known.

Adolescent↗

Ossifying fibroma.

Our experience includes seven cases of ossifying fibroma. The condition also appears in the literature under diagnostic names such as congenital fibrous dysplasia, congenital osteitis fibrosa, congenital fibrous defect of the tibia, and osteofibrous dysplasia of the tibia and fibula. The lesions develop in childhood and are located in the diaphysis of the tibia, or fibula. Of seven patients, we performed wide excision with free vascularized fibular graft in five cases, wide resection of the distal one-third of the fibula in one case, and curettage and bone graft in one case. Two of the patients who had wide excision with free vascularized fibular graft had recurrence. One case of recurrence occurred where incomplete wide excision with free-vascularized fibular graft was performed because the lesion was too close to the distal epiphysis of the tibia. One of the patients who had curettage and bone graft also had recurrence. It was concluded that children who have an ossifying fibroma requiring surgery can safely be treated with wide excision with or without free-vascularized fibular graft.

Adolescent↗

Soluble IL-6 receptor levels in patients on chronic hemodialysis.

Osteitis fibrosa, a part of the spectrum of renal osteodystrophy, is characterized by high bone turnover as a result of high circulating levels of parathyroid hormone (PTH). It is well accepted that the bone resorptive effects of PTH occur, at least in part, by inducing osteoblasts to secrete cytokines that stimulate both differentiation and activation of osteoclasts. One such cytokine, interleukin 6 (IL-6), exerts its actions via the IL-6 receptor (IL-6R), which has alpha and beta subunits. The alpha subunit binds IL-6 and exists in both membrane bound and soluble forms which can interact with the signal transducing components of the receptor or beta subunits and result in the same biological effect. Abnormalities in the IL-6 system have the potential to affect bone turnover and to modulate the effects of PTH. In this regard, we examined the levels of circulating soluble IL-6 receptor (sIL-6R) and plasma intact PTH in 27 patients on hemodialysis, of whom 15 were on therapy with vitamin D compounds and 12 were vitamin D naive. The results were compared to values obtained from 9 healthy controls. Blood samples were obtained pre-dialysis and sIL-6R levels were determined using a commercially available enzyme immunoassay, which measures biologically active sIL-6R. In patients on chronic hemodialysis, plasma levels of sIL-6R were 123.4 +/- 11.01 ng/ml. In healthy controls, the levels were 99.61 +/- 11.52 ng/ml, values not significantly different from those found in dialysis patients. PTH values ranged from 7-1,709 pg/ml in patients on hemodialysis; however, there was no correlation between intact PTH levels and the levels of sIL-6R. Similarly, vitamin D therapy did not influence the levels of sIL-6R. These data indicate that using an assay which is specific for biologically active sIL-6R, the levels of this receptor in patients on hemodialysis are similar to those found in normal individuals and neither the levels of PTH nor vitamin D therapy alter this aspect of IL-6 action.

Adult↗

A case of secondary hyperparathyroidism whose high turnover bone improved after the direct injection of acetic acid into the parathyroid glands.

A 48-year-old male was admitted to our hospital because of increasing knee pain and thigh muscle weakness. He had been undergoing hemodialysis for 15 years. His serum intact PTH value was 1,600 pg/ml with elevated ALP (387 IU/l) and osteocalcin (400 ng/ml). Ultrasound (US) examination disclosed 2 enlarged parathyroid glands. Because of poor cardiac function, an US-guided acetic acid injection into the enlarged parathyroids (percutaneous acetic acid injection therapy; PAIT) was performed. Soon after the PAIT, his arthralgia disappeared. Serum PTH fell to 220 pg/ml with the regression of bone marker 1 year following the PAIT. The size of his parathyroid glands dramatically regressed and 1 of the enlarged glands finally disappeared. Repeated bone biopsies following double tetracycline labeling showed a significant improvement from osteitis fibrosa to the mild lesion. This is the first known case report of severe secondary hyperparathyroidism whose PTH and high turnover bone was successfully managed by the direct injection of acetic acid into the parathyroid glands. As long as we pay attention to avoiding recurrent nerve palsy induced by acetic acid, US-guided PAIT may be an alternative to percutaneous ethanol injection therapy (PEIT) or surgical parathyroidectomy (PTx).

Acetic Acid↗

New worldwide trends in presentation of renal osteodystrophy and its relationship to parathyroid hormone levels.

AIMS: Abnormal mineral metabolism in chronic renal disease is associated with bone disease and extraskeletal calcifications. High turnover, hyperparathyroid bone disease, the most common form of renal osteodystrophy, has been the target for aggressive therapy. More recently, an increasing occurrence of low turnover bone disease has been reported. The present study was undertaken to evaluate the current prevalence of different forms of bone disease in a large population on chronic hemodialysis and its relationship to parathyroid hormone (PTH) levels. METHODS: Ninety-six chronic hemodialysis patients underwent double tetracycline-labeled bone biopsy. Serum PTH levels were obtained in 52 patients at the time of biopsy. Bone formation rate (BFR/BS) was plotted vs. PTH levels in all patients and in subgroups with PTH ranges between 0-150, 150-500 and 500 - 1,200 pg/ml. RESULTS: The histomorphometric data showed that 40% of all patients were affected by osteitis fibrosa cystica (OFC). In the remaining 60%, various forms of low-turnover bone disease were observed. There was no correlation between PTH and BFR/BS in all patients (r = 0.28) and in subgroups whose PTH levels ranged between 150 - 500 and 500 - 1,200 pg/ml (r = 0.027, r = 0.21), respectively. A close correlation between PTH and BFR/BS (r = 0.84, p < 0.05) was found only in the subgroup with a PTH level ranging low-turnover bone disease. The predictive between 0 - 150 pg/ml. CONCLUSIONS: The histomorphometric findings present a wide spectrum of renal osteodystrophy with a shift towardsvalue of PTH is limited as high-turnover osteodystrophy may present with low PTH levels and that with low turnover may occur with high PTH levels. In the latter parathyroidectomy should be avoided. We share the view that bone biopsy remains the "gold standard" diagnostic tool for renal osteodystrophy.

Adolescent↗

Mild asymptomatic primary hyperparathyroidism is not a risk factor for vertebral fractures.

STUDY OBJECTIVE: To determine the prevalence of vertebral fractures in patients with mild asymptomatic primary hyperparathyroidism and to ascertain whether this prevalence is increased in comparison with the rate in a retrospective control group previously studied at the same institution or with current estimates of the risk for vertebral fractures in subjects of similar age. DESIGN: Prospectively collected data were retrospectively analyzed and compared with data from a historical control group at the same institution and with published data. SETTING: The outpatient department of a bone and mineral metabolism clinic. PATIENTS: A consecutive series of patients with mild asymptomatic primary hyperparathyroidism diagnosed between 1 January 1976 and 31 December 1985. Criteria for inclusion in the study were the absence of symptoms due to hyperparathyroidism, no current kidney stone disease, no radiographic evidence of osteitis fibrosa, a serum calcium level of less than 3.00 mmol/L, a serum creatinine level of less than 133 mumol/L, and a forearm bone density value not more than 2.5 standard deviations below the age-, sex-, and race-adjusted normal value. INTERVENTIONS: A conservative nonintervention study. MEASUREMENTS AND MAIN RESULTS: The prevalence of vertebral fractures in 174 patients (mean age, 62 years) with mild asymptomatic primary hyperparathyroidism was 1.7%; in a subset of white women, the prevalence was 2.8%. These rates were not higher than those expected, by comparison with the rate in a retrospective control group or with the risk for vertebral fractures in subjects of similar age, and may even be lower. CONCLUSIONS: The risk for vertebral fractures is not increased in patients with mild asymptomatic primary hyperparathyroidism and is not a reason to recommend surgical intervention in asymptomatic patients. The increased rates of vertebral fractures that occurred in other series are probably due to the use of inappropriate controls and the influence of referral or selection bias, the inclusion of patients with severer disease, and the effect of geographic differences in vitamin D nutrition on the expression of disease. Possible differences between lateral spine and lateral chest radiographs for determining vertebral body shape need further study.

Aged↗

Recombinant human erythropoietin in anemic patients with end-stage renal disease. Results of a phase III multicenter clinical trial.

STUDY OBJECTIVE: To determine the effectiveness and safety of recombinant human erythropoietin (rHuEpo). PATIENTS: Hemodialysis patients (333) with uncomplicated anemia (hematocrit less than 0.30). All received rHuEpo intravenously, three times per week at 300 or 150 U/kg body weight, which was then reduced to 75 U/kg and adjusted to maintain the hematocrit at 0.35 +/- 0.03 (SD). RESULTS: The baseline hematocrit (0.223 +/- 0.002) increased to 0.35, more than 0.06 over baseline within 12 weeks in 97.4% of patients. Erythrocyte transfusions (1030 within the 6 months before rHuEpo therapy) were eliminated in all patients within 2 months of therapy. Sixty-eight patients with iron overload had a 39% reduction in serum ferritin levels after 6 months of therapy. The median maintenance dose of rHuEpo was 75 U/kg, three times per week (range, 12.5 to 525 U/kg). Nonresponders had complicating causes for anemia, myelofibrosis, osteitis fibrosa, osteomyelitis, and acute or chronic blood loss. Adverse effects included myalgias, 5%; iron deficiency, 43%; increased blood pressure, 35%; and seizures, 5.4%. The creatinine, potassium, and phosphate levels increased slightly but significantly. The platelet count increased slightly but there was no increase in clotting of vascular accesses. CONCLUSIONS: The anemia of hemodialysis patients is corrected by rHuEpo resulting in the elimination of transfusions, reduction in iron overload, and improved quality of life. Iron stores and blood pressure must be monitored and treated to maintain the effectiveness of rHuEpo and to minimize the threat of hypertensive encephalopathy.

Adolescent↗

Osteomalacia after parathyroidectomy in patients with uremia.

Five patients on maintenance dialysis had symptoms of osteomalacia, proven by biopsy, after parathyroidectomy. In all five patients clinical and radiographic manifestations of secondary hyperparathyroidism were present before surgery, and in two patients preoperative biopsy of bone confirmed the existence of osteitis fibrosa. Like previously described patients with osteomalacia all five had multiple fractures and normal or high serum calcium concentrations that rose to abnormally high values on treatment with vitamin D or dihydrotachysterol. Quantitative histomorphometry of biopsy after parathyroidectomy showed no residual parathyroid hormone effect and nearly complete cessation of mineralization. Four patients had forearm autografts of parathyroid tissue that appeared to be functioning at very low rates according to paired venous sampling, and all five patients had relatively low circulating concentrations of parathyroid hormone. This and earlier experiences reported by others suggest that secondary hyperparathyroidism may have an important facilitative role in the mineralization of bone in uremic patients.

Adult↗

Clinical profile of 128 subjects operated for primary hyperparathyroidism.

From 1960 to 1990, one hundred twenty eight (128) subjects with primary hyperparathyroidism were operated in the University Hospital. The medical records were reviewed. Serum and urine chemistries were done by conventional methods, serum PTH was done by RIA's (N-, C-, and midregion) and intact by IRMA and 1,25 dihydroxycholecalciferol by a non equilibrium receptor assay from calf thymus and preceded by double Sep-Pak chromatography. The distal third of the radius (nondominant arm) was used to evaluate radial bone density (RBD), using single photon absorptiometry (Norland) and the lumbar bone density (LBD) was measured by dual energy X Ray absorptiometry (DEXA). The RBD was done in 41 females and 15 males and the LBD in 12 females and 4 males. The series comprised 95 females, age range from 15 to 79 years, and 33 males, age range from 14 to 69 years. Prominent clinical features included nephrolithiasis in 72 subjects (56%), osteitis fibrosa cystica in 2, isolated familial hyperparathyroidism in 4 subjects in one family, 7 subjects with MEN-1 in 3 families, and 4 subjects with MEN-2 in one family. Only 7 subjects were asymptomatic. Serum calcium was elevated in all, serum alkaline phosphatase was elevated in 24% and urinary hydroxiproline was increased in 48%. Serum phosphorus was low in 92%. PTH assay was either elevated or inappropriately normal for the serum calcium in all patients tested. Serum 1,25 D was elevated in 57%. The PTH level was positively correlated with the serum calcium (r = 0.70), but had no significant correlation with the serum phosphorus and the 1,25 D. The RBD expressed as the standard deviation from that of the mean for age and sex matched controls was > or = 2 SD below the mean in 39% of females and in 40% of males. In contrast to the RBD none of the subjects tested had a LBD > or = 2 SD below the age and sex adjusted mean. 103 subjects had adenomas, 20 primary hyperplasia, 2 carcinomas and in 3 surgical exploration was unsuccessful. As to the outcome of Surgery, 117 (93%) were cured. Thus, in this series, successful surgery for primary hyperparathyroidism is the rule. Primary hyperparathroidism is rarely asymptomatic and appendicular bone disease and nephrolithiasis are commonly seen.

Adenoma↗

Serum proteins as indicators of poor dietary intake in patients with chronic renal failure.

A study of serum proteins in patients on regular hemodialysis has shown that many have low serum transferrin levels but near normal serum albumin and normal or raised pre-albumin levels. Hemoglobin values were related to transferrin levels. Low transferrin levels also occurred in patients with advanced osteitis fibrosa. Deficient protein intake seems the likely explanation. Measurement of pre-albumin does not reflect low protein intake in chronic renal failure; reasons for this discussed.

Albumins↗

Assessment of renal osteodystrophy following renal transplantation.

Serial histological studies in patients after successful renal transplantation indicate that with restoration of adequate renal function osteomalacia invariably improves with symptomatic relief in bone pain. Histological changes of osteitis fibrosa resolve more slowly and radiological changes may persist longer, occasionally in the absence of confirmatory histological evidence of secondary hyperparathyroidism. For accurate and sensitive follow-up a combination of biochemistry, histology and radiology is desirable.

Alkaline Phosphatase↗

[Renal osteodystrophy (2): its treatment in renal insufficiency before dialysis].

1. In the patient with renal insufficiency before dialysis, the phosphocalcic disorders appear insidiously. They are dominated by hyperparathyroidism which will be diagnosed on the initially yearly determination of plasma intact PTH as soon as creatinine clearance decreases below 60 ml/min, eventhough there is still no modification in plasma concentrations of calcium and phosphate. Its diagnosis should lead to initiate the therapeutic measures in order to prevent the irreversible thining of the corticals by endosteal resorption and later the occurrence of histological and radiological osteitis fibrosa favoring fractures. 2. Hyperparathyroidism prevention relies on two main measures: prevention of phosphate retention and hypocalcemia is implemented by progressive phosphate and protein restriction (from 1 g/kg/day when Ccr < 60 ml/min to 0.6 g/kg/day when Ccr < 20 ml/min) and administration of CaCO3 (1.5 g at lunch and dinner to better complex the phosphate) as soon as PTH is above normal; optimal vitamin D repeletion will be implemented by systematic supplementation of native vitamin D or 25OH vitamin D3 in order to bring P25OHD between 30-60 ng/ml (75-150 nmol/l) or more generally around the upper limit of the epidemiologic range of the laboratory; these measures should aim at maintaining plasma intact PTH in its optimal range variable with the degree of renal insufficiency: 0.5-1; 1-2.5 and 2-3 folds the upper limit of normal for creatinine clearance respectively at 60-30; 30-10 and < 10 ml/min. 3. Because of their hyperphosphatemic and hypercalcemic effect, 1 alpha-hydroxylated vitamin D derivatives will be regularly efficient and safe only when non-calcemic non-aluminic phosphate binder will be available and proven to be without side-effects. 4. Instrumental (surgical or by alcohol injection) parathyroidectomy should be considered when plasma intact PTH is > 5 to 7 times the upper limit of normal in the presence of hypercalcemia (> 2.60 mmol/l) and/or hyperphosphatemia (> 1.70 nmol/l) in spite of the above measures, the decision being reinforced by coexistence of bone radiologic abnormalities and metastatic calcifications. 5. Adynamic bone diseases are rare before hemodialysis in the absence of aluminum exposition by the drinking water or the aluminum-phosphate binders. In absence of aluminum it will be prevented by maintaining PTH in its optimal range. 6. Osteomalacia before hemodialysis is mainly due, in the absence of aluminum exposition, to vitamin D deficiency, hypocalcemia and acidosis. It is readily cured by physiological doses of native vitamin D or 25OH vitamin D3 bringing plasma 25 OHD above 16 ng/ml, in association with alkaline salts of calcium and if necessary of sodium bicarbonate.

Chronic Kidney Disease-Mineral and Bone Disorder↗

Bone histomorphometry is still the golden standard for diagnosing renal osteodystrophy.

AIM: The clinical picture of renal osteodystrophy (RO) is very uncharacteristic. The diagnosis is made by means of biochemical indicators, intact parathormone (iPTH) concentration, bone X-rays, bone densitometry and particularly bone histomorphometry. The aim of our study was to establish whether a combination of non-invasive methods can bring us closer to the diagnosis as to avoid bone biopsy. PATIENTS AND METHODS: We chose 30 patients treated by chronic hemodialysis. Only 4 of them had no symptoms of RO. Biochemical parameters (Ca, P) and iPTH concentrations were determined. bone X-rays were taken (the parathyroid series), bone mineral density was measured by quantitative digital radiography (QDR), and bone biopsy specimens were taken for bone histomorphometry. The data were analyzed by the Statistica by StatSoft and SPSS computer programs. RESULTS: With respect to bone histomorphometry, 10 patients had osteitis fibrosa (OF), 15 had mixed osteodystrophy (MO), 5 adynamic bone disease (ABD). There was a good correlation of iPTH and alkaline phosphatase (AP) concentrations with histomorphometric parameters. There was also a correlation between radiological changes and histomorphometric parameters. After the analysis of discrimination using the SPSS computer program, taking only iPTH into consideration, 36.6% of patients were correctly classified according to their diagnosis. Considering iPTH and densitometry, 46.6% were classified correctly. Considering iPTH and radiological changes, 60% of patients were classified correctly. CONCLUSION: To diagnose 73.3% of patients correctly, it was necessary to consider the above mentioned non-invasive parameters, as well as AP, P, concentrations and the patient age. Histomorphometry remains the "golden standard" for diagnosing RO.

Adult↗

[Selected parameters of bone metabolism in hemodialyzed and peritoneally dialyzed patients].

Renal osteodystrophy is a metabolic bone disease occurring in patients with end-stage renal failure. The aim of the study was to compare serum concentrations of some bone markers in hemodialysed (HD) patients and in patients undergoing continuous ambulatory peritoneal dialysis (CADO). We studied two groups of patients with end-stage renal failure: 52 hemodialysed individuals aged 24-74 years and 19 peritoneally dialysed patients aged 20-70 years. Serum calcium and phosphate concentration, cholesterol, triglycerides, total protein, albumin, alkaline phosphatase, urea before and after HD, urea in CADO patients were determined by standard laboratory methods. Serum PTH, osteocalcin, 1,25(OH)2D3 and insulin-like growth factor (IGF-1) concentrations were measured by commercially available radioimmunoassay. Serum tumor necrosis factor (TNF-alpha) and interleukin-1 (IL-1) concentrations were measured by ELISA. There were no differences between serum concentrations of the studied bone markers in hemodialysed patients and CAPD patients. All dialysed patients presented high concentrations of serum PTH, osteocalcin, alkaline phosphatase activity, lower serum IGF-1 concentration and normal serum calcitriol concentration. High serum PTH and osteocalcin concentrations may indicate intensification of bone synthesis, what is typical for osteitis fibrosa.

Adult↗

Renal ostodystrophy during the developing stage of maintenance dialysis in Transylvania. Early development of periarticular calcifications and beta 2 microglobulin amyloidosis in spite of a relatively good prevention of secondary hyperparathyroidism.

BACKGROUND: Dialysis facilities have been introduced only recently in Transylvania with many limitations, in particular a standard high calcium dialysate, Al(OH)3 as phosphate binder and pharmacological doses of native vitamin D2, but neither CaCO3 nor 1 alpha hydroxylated vitamin D. Rheumatological complaints and metastatic calcifications were frequent, leading to suspect either overt hyperparathyroidism, adynamic bone disease or beta 2 microglobulin amyloidosis. AIMS OF THE STUDY: Evaluate the prevalence of radiological osteitis fibrosa, amyloid osteoarthropathy and periarticular calcification and their link with PTH secretion, phophocalcic disorders, acidosis, bone turn over, aluminum and beta 2 microglobulin accumulation in the dialysis population of Sibiu (Transylvania). METHODS: The clinical and radiological rheumatological data of the 49 uremic patients dialyzed in Sibiu since 1990 were reviewed as well as the monthly routine monitoring of their plasma phosphocalcic parameters. Furthermore in July 1994, 36 of them had an X rays of the hands for evaluation of subperiosteal resorption of the phalanges, periarticular calcifications and carpal cysts as well as a determination of plasma concentrations of intact PTH (normal range: 10-55; optimal range: 100-200 pg/ml), osteocalcin, bone alkaline phosphatase, aluminum and 25 OH vitamin D. RESULTS: The prevalence of subperiostal resorption of the phalanges was 8% and that of severe biological hyperparathyroidism (PTH > 400 pg/ml) 22%, whereas that of a relative hypoparathyroidism (PTH < 100 pg/ml) was 31%. Mean plasma concentrations of calcium was 2.07 +/- 0.15; of phosphate 2.50 +/- 0.35; of bicarbonate 15 +/- 2.0 mmol/l, of 25 OHD 30 +/- 20 ng/ml, of aluminum 1.1 +/- 0.5 mumol/l. Plasma PTH concentrations were negatively correlated to dialysis duration, and to plasma concentrations of aluminum, calcium and 25 OH vitamin D but not to those of phosphate and bicarbonate. Multivariate analysis showed however that only duration of dialysis and plasma aluminum concentration were independently and negatively correlated to plasma PTH concentrations. The prevalence of periarticular calcifications (26%) and of carpal cysts suggestive of beta 2 microglobulin amyloidosis (10%) were relatively high considering the young age of the population (42 years) and the short duration of dialysis (2.6 years). Patients with calcifications comparatively to those without calcifications were older, had longer duration on dialysis, higher prevalence of carpal cysts and higher plasma beta 2 microglobulin concentrations, lower plasma PTH (98 versus 313 pg/ml) and higher plasma aluminum concentration (1.3 versus 0.8 mumol/l). Patients with carpal cysts comparatively to those without cyst were older, had a longer duration on dialysis and a higher prevalence of periarticular calcifications. CONCLUSIONS: a) In spite of no use of 1 alpha hydroxylated vitamin D derivatives, and poor control of hyperphosphatemia and acidosis, hyperparathyroidism declined with duration of dialysis due to the use of a high dialysate calcium concentration, Al(OH)3 as sole phosphate binder and high supplement of native vitamin D. b) Considering the relative young age and short duration on dialysis, the prevalence of periarticular calcifications and carpal cysts were high. c) Calcifications were possibly favored by relative hypoparathyroidism and moderate aluminum overload. d) The association of periarticular calcifications and subchondrial cysts suggest a causal relationship.

Adult↗

The pathophysiology and management of renal bone disease in dialysis patients.

As renal function declines, changes in mineral metabolism occur including phosphate retention, calcitriol deficiency, and the development of secondary hyperparathyroidism. Renal bone disease related to disordered mineral metabolism may result in increased patient morbidity and mortality. Uncontrolled parathyroid hormone (PTH) secretion will result in osteitis fibrosa, a high turnover bone disease. The use of calcium and aluminum-based phosphate binders and vitamin D sterols may contribute to the development of low turnover bone diseases such as osteomalacia and aplastic bone disease. Prevention and control of renal bone disease is an important goal for the interdisciplinary health care team. This paper discusses disordered mineral metabolism and its relationship to renal bone disease. Case studies illustrate the development and treatment of renal bone disease related to secondary hyperparathyroidism and aluminum intoxication.

Aged↗

[Renal osteodystrophy (I)].

Renal bone disease represents one of the major complications of end-stage renal disease, accounting for the numerous and various changes at bone level, determined by abnormal calcium and phosphorus homeostasis and by changes in calcitriol and PTH synthesis. PTH represents as well a major uraemic toxin, exerting profound systemic effects, particularly at the cardiovascular level. PTH synthesis is mainly controlled by changes in calcium-phosphorus balance and calcitriol production by the kidneys. Several others factors are important in the development of secondary hyperparathyroidism: acidosis, autonomisation of PTH secretion and peripheral (target-organ) resistance to PTH actions. Although bone biopsy represents the definitive diagnostic test to differentiate between osteitis fibrosa, low-turnover bone disease and bone involvement unrelated to disturbed calcium metabolism (i.e. beta 2-microglobulin-related amyloidosis), plasma intact PTH generally exhibits a reasonably good relation with bone histology parameters. Moreover serum bone-specific alkaline phosphatase isoenzyme, serum pyridinoline and the novel serum markers for bone turnover are highly specific and correlate with bone histomorphometry parameters, so that, preventive and therapeutic strategies should be re-evaluated based solely on biochemical parameters.

Alkaline Phosphatase↗