No abstract
These findings indicate that Sr accumulation in chronic renal failure rats resulted in the development of osteomalacic lesions, in contrast to the Al group where adynamic bone disease was induced in the present set-up. Further studies are required to define the mechanism by which way Sr causes osteomalacia in chronic renal failure rats.
Our findings indicate that the role of Sr in the development of bone lesions in renal failure is complex and that, depending on the dose, the element may act via multiple pathways.
Low bone turnover in patients with renal failure. Renal failure can be encountered, a summary of which is presented inevitably leads to metabolic bone disease. Low turnover disin Fig. 1. In most cases, the definite diagnosis of the type ease or adynamic bone disease (ABD) is characterized by a of ROD still must rely on the histomorphometric analysis low number of osteoblasts with normal or reduced numbers of a bone biopsy [1, 2]. If the biopsy is performed after of osteoclasts. Mineralization proceeds at a normal rate, redouble tetracycline labeling, the bone formation rate sulting in normal or decreased osteoid thickness. Recently, it became clear that the relative contribution of the various types (BFR) can be calculated by multiplying the mineral opof renal osteodystrophy (ROD) to the spectrum of the histoposition rate by the extent of the labeled surfaces [3]. logic picture in renal failure patients underwent profound Low bone turnover leads to two distinct types of ROD: changes during the last 25 years. At the moment, the exact adynamic bone disease and osteomalacia. physiopathological mechanisms behind ABD are not yet elucidated, and thus the reason(s) for its increasing prevalence remains poorly understood. A number of epidemiological and ADYNAMIC BONE DISEASE experimental data suggest a multifactorial pathophysiologic process, in which hypoparathyroidism and suppression of the The first type of low turnover disease, adynamic bone osteoblast are the main actors. Compared to adynamic bone disease (ABD), is characterized by a low number of disease, osteomalacia has now become a much rarer disease osteoblasts, the osteoclast number usually being normal (around 4%), at least in Western countries. On the other hand, or reduced. Mineralization proceeds at a normal rate, recent studies indicate that this particular bone disease entity might still regularly occur in less developed countries. Osteoresulting in normal or decreased osteoid thickness [3]. malacia originates from a direct effect on the mineralization Recently, it became clear that the relative contribution process. With this type of renal bone disease, the effects of of the various types of ROD to the spectrum of the secondary hyperparathyroidism on bone are overridden by ahistologic picture in renal failure patients underwent pronumber of metabolic abnormalities that finally result in a defective bone mineralization, as occurs, for instance, when the found changes over the last 25 years. A summary of the lag time between osteoid deposition and its mineralization is literature data on biopsy proven prevalence rates of the increased. The relationship between exogenous and endogedifferent types of ROD reported over the years is prenous vitamin D deficiency (mainly calcitriol) and the histologic sented in Table 1 [4][5][6][7][8][9][10][11][12][13][14][15][16].finding of osteomalacia in uremic patients is well known. Re-Before 1989, ABD was either not encountered or had cent data showed distinctly lowered 25-(OH) vitamin D 3 levels in the presence of unaf...
Background: Little is known about trace metal alterations in the bones of dialysis patients or whether particular types of renal osteodystrophy are associated with either increased or decreased skeletal concentrations of trace elements. Because these patients are at risk for alterations of trace elements as well as for morbidity from skeletal disorders, we measured trace elements in bone of patients with end-stage renal disease. Methods: We analyzed bone biopsies of 100 end-stage renal failure patients enrolled in a hemodialysis program. The trace metal contents of bone biopsies with histological features of either osteomalacia, adynamic bone disease, mixed lesion, normal histology, or hyperparathyroidism were compared with each other and with the trace metal contents of bone of subjects with normal renal function. Trace metals were measured by atomic absorption spectrometry. Results: The concentrations of aluminum, chromium, and cadmium were increased in bone of end-stage renal failure patients. Comparing the trace metal/calcium ratio, significantly higher values were found for the bone chromium/calcium, aluminum/calcium, zinc/calcium, magnesium/calcium, and strontium/calcium ratios. Among types of renal osteodystrophy, increased bone aluminum, lead, and strontium concentrations and strontium/calcium and aluminum/calcium ratios were found in dialysis patients with osteomalacia vs the other types of renal osteodystrophy considered as one group. Moreover, the concentrations of several trace elements in bone were significantly correlated with each other. Bone aluminum was correlated with the time on dialysis, whereas bone iron, aluminum, magnesium, and strontium tended to be associated with patient age. Bone trace metal concentrations did not depend on vitamin D intake nor on the patients’ gender. Conclusions: The concentration of several trace elements in bone of end-stage renal failure patients is disturbed, and some of the trace metals under study might share pathways of absorption, distribution, and accumulation. The clinical significance of the increased/decreased concentrations of several trace elements other than aluminum in bone of dialysis patients deserves further investigation.
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