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Renal osteodystrophy in dialysis patients: diagnosis and treatment.
Artif Organs. 1998 Jul; 22(7):530-57.AO

Abstract

This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion: osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1alpha hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1alpha(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 microg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children.

Authors+Show Affiliations

Nephrology Department, Amiens University Hospital, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

9684690

Citation

Fournier, A, et al. "Renal Osteodystrophy in Dialysis Patients: Diagnosis and Treatment." Artificial Organs, vol. 22, no. 7, 1998, pp. 530-57.
Fournier A, Oprisiu R, Hottelart C, et al. Renal osteodystrophy in dialysis patients: diagnosis and treatment. Artif Organs. 1998;22(7):530-57.
Fournier, A., Oprisiu, R., Hottelart, C., Yverneau, P. H., Ghazali, A., Atik, A., Hedri, H., Said, S., Sechet, A., Rasolombololona, M., Abighanem, O., Sarraj, A., El Esper, N., Moriniere, P., Boudailliez, B., Westeel, P. F., Achard, J. M., & Pruna, A. (1998). Renal osteodystrophy in dialysis patients: diagnosis and treatment. Artificial Organs, 22(7), 530-57.
Fournier A, et al. Renal Osteodystrophy in Dialysis Patients: Diagnosis and Treatment. Artif Organs. 1998;22(7):530-57. PubMed PMID: 9684690.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal osteodystrophy in dialysis patients: diagnosis and treatment. AU - Fournier,A, AU - Oprisiu,R, AU - Hottelart,C, AU - Yverneau,P H, AU - Ghazali,A, AU - Atik,A, AU - Hedri,H, AU - Said,S, AU - Sechet,A, AU - Rasolombololona,M, AU - Abighanem,O, AU - Sarraj,A, AU - El Esper,N, AU - Moriniere,P, AU - Boudailliez,B, AU - Westeel,P F, AU - Achard,J M, AU - Pruna,A, PY - 1998/7/31/pubmed PY - 1998/7/31/medline PY - 1998/7/31/entrez SP - 530 EP - 57 JF - Artificial organs JO - Artif Organs VL - 22 IS - 7 N2 - This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion: osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1alpha hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1alpha(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 microg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children. SN - 0160-564X UR - https://www.unboundmedicine.com/medline/citation/9684690/Renal_osteodystrophy_in_dialysis_patients:_diagnosis_and_treatment_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0160-564X&date=1998&volume=22&issue=7&spage=530 DB - PRIME DP - Unbound Medicine ER -