title: Adynamic bone disease in patients with uremia.
abstract: Adynamic (or aplastic) bone disease is a bone histologic pattern characterized by decreased bone formation rate, low cellularity, and normal or decreased osteoid thickness. It was first described in symptomatic patients undergoing dialysis who were overloaded with aluminum because of contaminated dialysate or chronic ingestion of aluminic phosphate binders; the evidence of the overload was extensive coloration (more than 25%) with aurin tricarboxylic acid, whereas the Perls stain coloration for iron was negative. We have, however, reported these histologic changes in asymptomatic patients with uremia who were never exposed to aluminum, in two patients before end-stage renal failure and in six patients undergoing dialysis. The main step in the prevention of adynamic bone disease is the absolute exclusion of aluminum exposition even by so-called "safe doses" of aluminum phosphate binders because in the long term they are never actually safe. Because idiopathic adynamic bone disease may nevertheless occur, parathyroid hormone suppressive treatment by oral calcium taken with meals as phosphate binders (+/- 1 alpha-hydroxyvitamin D3 derivatives) should be carefully monitored by measurements of plasma concentrations of not only calcium and phosphate but also of intact parathyroid hormone levels. In order to have normal bone formation rate levels, patient intact parathyroid hormone levels should be between one and three times the upper limit of the normal level. Although adynamic bone disease may not be a true bone disease when not due to aluminum, it is a risk factor for increased incidence of hypercalcemia and hyperphosphatemia and therefore for metastatic calcifications. Therefore, when hypercalcemia occurs with hyperphosphatemia and normal intact parathyroid hormone in patients treated with 1 alpha-hydroxyvitamin D3, it is proposed that the latter drug should be discontinued first, whereas oral calcium is increased to correct hyperphosphatemia, and calcium concentration is decreased in the dialysate to prevent hypercalcemia, even though plasma parathyroid hormone may increase up to three times the upper limit of the normal level. In patients previously exposed to aluminum, a deferoxamine test should be performed and a deferoxamine treatment started if the test is positive.
authors.affiliation: Department of Nephrology, Hôpital Sud, Amiens, France.
authors.forename: A
authors.initials: A
authors.lastname: Fournier
authors.forename: P H
authors.initials: PH
authors.lastname: Yverneau
authors.forename: P
authors.initials: P
authors.lastname: Hué
authors.forename: S
authors.initials: S
authors.lastname: Said
authors.forename: N
authors.initials: N
authors.lastname: Hamdini
authors.forename: H M
authors.initials: HM
authors.lastname: Eldin
authors.forename: S
authors.initials: S
authors.lastname: Mohageb
authors.forename: R
authors.initials: R
authors.lastname: Oprisiu
authors.forename: A
authors.initials: A
authors.lastname: Marie
authors.forename: M E
authors.initials: ME
authors.lastname: Solal
mesh_terms: D000535:Aluminum / Q000378:metabolism; D000818:Animals; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000097:blood / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy; D003937:Diagnosis, Differential; D006801:Humans; D012307:Risk Factors; D014511:Uremia / Q000150:complications*
chemical_list: D000535:Aluminum