Adynamic Bone Disease in Uremia: May It Be Idiopathic? Is It an Actual Disease?

Fournier, A; Morinière, P.; Solal, M. E. Cohen; Boudailliez, B; Achard, Jean Michel; Mariè, A.; Sébert, J. L.

doi:10.1159/000186369

Cited by 51 publications

(32 citation statements)

References 32 publications

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“…In agreement with the data of Fournier et al [3], we can say with confidence that aluminium is not the cause of IAB. None of the patients had any aluminium staining in their biopsies at the time that the diagnosis was made.…”

Section: Discussionsupporting

confidence: 92%

“…Iron has also been proposed as a possible aetiological agent in adynamic bone, along with diabetes, hypothy roidism, corticosteroid therapy, fluoride, hypophosphataemia, acidosis, deficiency of insulin-like growth factors, and older age [3]. None of the patients in this report had positive iron staining at the time IAB was diagnosed, and none of them has diabetes or clinical evidence of hypothy roidism (no T4 levels were measured).…”

Section: Discussionmentioning

confidence: 70%

“…Further examination of these adynamic biopsies revealed that roughly one third had <5% surface-stainable aluminium, leading to the conclusion that this lesion is characterized by relatively 'suppressed' lev els of PTH rather than aluminium accumulation. In a review of potential aetiological factors which could have a depressive effect on bone formation, Fournier et al [3] concluded that non-aluminium-related adynamic bone can at present be considered to be idiopathic, although other aetiological factors such as hypoparathy roidism, hypothyroidism, diabetes, and older age may be involved. This review goes on to report biochemical and radiological follow-up of 5 patients with histologically demonstrated adynamic bone, but 2 of these had been transplanted, and unfortunately only 1 of the 5 underwent repeat bone biopsy.…”

Section: Introductionmentioning

confidence: 99%

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Histological, Radiological, and Biochemical Features of the Adynamic Bone Lesion in Continuous Ambulatory Peritoneal Dialysis Patients

et al. 1994

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Adynamic bone is being found with increasing frequency in dialysis patients. Little is known about its aetiology, and even less about its natural history. We found 10 cases of asymptomatic adynamic bone among a group of 32 continuous ambulatory peritoneal dialysis patients, most of whom had never been exposed to aluminium-containing phosphate binders. Compared to the remaining 22 patients, they had an older mean age (54 ± 11.4 vs. 42 ± 11.8 years; p < 0.05), probably a longer pre-dialysis duration of renal failure (10.9 vs. 7.1 years), higher mean ionized calcium (1.30 ± 0.04 vs. 1.15 ± 0.02 mmol/l; p < 0.01), and lower mean intact parathyroid hormone (31.5 vs. 200.3 pg/ml; p < 0.001). The bone density was not different between the two groups, but 9 of the 10 adynamic patients had significant vascular calcification seen on plain radiology as compared with only 7 of 20 in the comparison group (p < 0.05). Follow-up of the adynamic patients showed a close association with serum intact parathyroid hormone and ionized calcium levels. With one exception, adynamic bone did not appear to be associated with lower bone density than other types of osteodystrophy, but a longer-term study is required to determine the complete natural history of this lesion.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

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Histological, Radiological, and Biochemical Features of the Adynamic Bone Lesion in Continuous Ambulatory Peritoneal Dialysis Patients

et al. 1994

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“…Fournier et al have reviewed the possible cases of adynamic bone diseases and proposed hypophosphatemia as a potential etiologic factor, which could have an inhibitory effect on bone formation by decreasing PTH secretion (8).…”

Section: Introductionmentioning

confidence: 99%

Iron Lactate-Induced Osteomalacia in Association with Osteoblast Dynamics

et al. 2003

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Osteomalacia was induced in rats fed a diet containing 50,000 ppm (5%) iron lactate for 13 weeks. The histopathology and histomorphometrical dynamics of osteoblasts under this condition were examined. Bone histomorphometry of the proximal tibial metaphysis revealed that the osteoblast surface, osteoid volume, osteoid surface and labeled surface ratio, which are the parameters of bone formation had increased. The blood chemistry revealed the greatest elevation in the osteocalcin level; however, the parathyroid hormone (PTH) secretion and inorganic phosphorus level were very low. From the serum biochemical, histopathological and histomorphometrical findings, the bone lesion in iron lactate-overloaded rats was considered to be similar to low turnover osteomalacia showing decreased trabeculae in secondary spongiosa and increased lamellar osteoid. Furthermore, an ironpositive reaction was detected at the interface between osteoid and mineralized bone. In the bone lesions induced by chronic iron overload, osteoblast recruitment exceeded that of mineralization or, alternatively, the iron within osteoblasts along the trabecular bone suppressed the remodeling and led to an increase in osteoid thickness.Keywords. Iron lactate; osteomalacia; parathyroid hormone; hypophoshatemia; osteoclast; osteoblast. INTRODUCTIONOsteomalacia is bone change characterized by decreased calcium deposition of the bone trabecular and nonmineralized osteoid accumulating on the bone surface in layers of excessive thickness. Osteomalacia is known to be induced by many factors, that is, vitamin D deficiency, malabsorption, disturbance of di-hydroxylation of vitamin D 3 , excessive inactivation of vitamin D metabolites, phosphate deficiency (especially iron and aluminum) and in situ inhibition of mineralization (25). In diseased animals (conditions), serum levels of calcium, phosphorus, or active vitamin D are decreased, and osteoblasts cannot produce sufficient alkaline phosphatase (18). Osteomalacia in patients on long-term hemodialysis have been associated with aluminum accumulation in bone (10). Aaron et al elucidated the etiology of aluminum-induced osteomalacia showing that aluminum reduced the rate of direct hydroxyapatite formation and transformation of amorphous calcium phosphate to hydroxyapatite, and the crystal growth rate of hydroxyapatite seed (23). Iron might effect growth of hydroxyapatite as an additional means of causing osteomalacia.Low serum phosphate and parathyroid hormone (PTH) levels are also observed in older maintenance hemodialysis patients with decreased protein intake who present a higher incidence of adynamic bone disease, have lower PTH levels, and require lower doses of phosphate binders to achieve adequate control of phosphorus levels (13). Fournier et al have reviewed the possible cases of adynamic bone diseases and

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“…Calcium homeostasis was showed size progression before but not after total PTX when annually controlled by ultrasonography. In group maintained by oral substitution with calcium (group I, expected as a consequence of the beneficial effect of (1) the development of a low bone turnover can be induced by uremia itself [18], and (2) aluminium overload total PTX on the progression of atherosclerotic lesions.We suggest reconsideration of total PTX without auto-has been recognized as an important cause of osteomalacia [19] and adynamic bone disease [20,21]. Thus, it is transplantation in dialysis patients with severe sHPT who are not eligible for renal transplantation.…”

mentioning

confidence: 99%

Long-Term Results of Total Parathyroidectomy without Autotransplantation in Patients with and without Renal Failure

Hampl¹,

Steinmüller²,

Fröhling³

et al. 1999

Mineral Electrolyte Metab

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The optimal surgical procedure for severe renal secondary hyperparathyroidism (sHPT) is still a point of controversy. Total parathyroidectomy (PTX) without auto-transplantation was abandoned for fear of an adynamic bone condition; however, in the case of autotransplantation recurrent sHPT is frequent and promotes atherosclerosis. We studied 11 hemodialysis patients (age 59±12 years) on dialysis for 18 (12–30) years in whom total PTX was performed due to severe sHPT (group I; intact PTH: 1,240±230 pg/ml), and 5 patients (age 55±10 years) without renal insufficiency who inadvertently received total PTX during thyroid surgery (group II). After total PTX (group I, 26±18 [9–59] months; group II, 252±188 [22^480] months) both groups showed no measurable intact PTH levels. Calcium homeostasis was maintained by oral substitution with calcium (group I, calcium dialysate of 2.0 mmol/l), vitamin D and calcitriol (serum parameters in groups I and II: calcium 2.4 and 2.2 mmol/l; phosphate 1.8 and 1.1 mmol/l; 25(OH)-vitamin D₃ 21 and 34 ng/ml; 1,25(OH)₂-vitamin D₃ 32 and 41 pg/ml, respectively). In group I, after total PTX there was a rapid and sustained improvement in bone pain with markedly enhanced physical activity and endurance. High turnover osteopathy markedly improved as indicated by declining levels of native osteocalcin (90±17 vs. 26±18 ng/ml), bone alkaline phosphatase (74±12 vs. 12±6 ng/ml), and carboxyterminal cross-linked telopeptide of type-I collagen (65±16 vs. 40±21 ng/ml) but increasing levels of carboxyterminal propeptide of type-I procollagen (120±36 vs. 148±41 ng/ml). Recalcification of bone was excellent as demonstrated by X-ray and confirmed by bone histology. Itching extravascular calcific deposits and calcifications of blood vessel and cardiac valves immediately stopped after total PTX. Moreover, 6 sHPT patients suffered from severe atherosclerotic lesions such as thoracic aortic aneurysm (n = 3) or abdominal aortic aneurysm (n = 3) which showed size progression before but not after total PTX when annually controlled by ultrasonography. In group II, even long after total PTX, there was no clinical, radiological, histological or biochemical evidence for low turnover osteopathy. In conclusion, our data indicate that substitution with vitamin D₃ metabolites and calcium can prevent deleterious bone effects of hypoparathyroidism in hemodialysis patients and in patients with normal kidney function and may compensate for the missing PTH action. Over this, a better survival rate is expected as a consequence of the beneficial effect of total PTX on the progression of atherosclerotic lesions. We suggest reconsideration of total PTX without autotransplantation in dialysis patients with severe sHPT who are not eligible for renal transplantation.

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Adynamic Bone Disease in Uremia: May It Be Idiopathic? Is It an Actual Disease?

Cited by 51 publications

References 32 publications

Histological, Radiological, and Biochemical Features of the Adynamic Bone Lesion in Continuous Ambulatory Peritoneal Dialysis Patients

Histological, Radiological, and Biochemical Features of the Adynamic Bone Lesion in Continuous Ambulatory Peritoneal Dialysis Patients

Iron Lactate-Induced Osteomalacia in Association with Osteoblast Dynamics

Long-Term Results of Total Parathyroidectomy without Autotransplantation in Patients with and without Renal Failure

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