Calcium Carbonate and Magnesium Hydroxide in the Prevention of Renal Osteodystrophy or the Demise of Aluminum Toxicity in Uremia

Morinière, P; Fournier, A; Pf, Westeel; Idrissi, Abdeslem El; Renaud, H; Hocine, C.; Belbrik, S.; Mariè, A.; Leflon, P.; Jl, Sebert

doi:10.1159/000415728

Cited by 4 publications

(2 citation statements)

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“…Randomized controlled trials in dial ysis patients with oral calcitriol have shown that it was an effective treatment for the prevention of radiological [12] and histological [13] hyperparathyroidism but not a safe one because of the increased need of Al(OH), [12,13] and the induction of aluminic osteomalacia [13]. Therefore, accord ing to our 10-year-long experience, we think that this pre ventive treatment should rely essentially on the use of oral calcium (either CaCO, or Ca acetate) given primarily as phosphate binder with the meals rich in phosphate, eventu ally in association, when necessary and only in dialysis patients, with Mg(OH)2 while the dialysate calcium is 1.62 mmol to maintain a neutral intradialytic balance and the dialysate Mg 0.2 mmol in order to prevent the hypermagne semia [14]. This approach has been proved quite effective and safe [15] in the prevention of severe biological hyperpar athyroidism diagnosed on the elevation of the alkaline phosphatase since the addition of oral la-OH-D, was ne cessary in only 1 of 6 patients [14].…”

Section: Introductionmentioning

confidence: 99%

Prevention of Hyperparathyroidism in Patients on Maintenance Dialysis by Intravenous 1-Alpha-Hydroxyvitamin D3 in Association with Mg(OH)2 as Sole Phosphate Binder

Mornière

Maurouard²,

Boudailliez³

et al. 1992

Nephron

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The purpose of this study is to evaluate the place of intravenous 1α-hydroxyvitamin D₃ (1α-OH-D₃) in the prevention of radiologically obvious hyperparathyroidism (HPT) in patients on maintenance dialysis while excluding aluminium phosphate binder and using a dialysate calcium concentration of 1.62 mmol which keeps the intradialytic calcium balance neutral. Therefore, 47 patients without subperiosteal resorption and previously treated by oral CaCO₃ and if necessary Mg(OH)₂ as phosphate binder while their dialysate calcium had a Ca level of 1.62 and a Mg level of 0.2 mmol/l were randomized into a control group of 24 who were maintained on the same treatment and an experimental group of 23. This group discontinued CaCO₃ and received intravenous 1α-OH-D₃ after each dialysis at increasing doses up to 4 μg and increased Mg(OH)₂ as their sole phosphate binder. When plasma Ca increased above 2.7 mmol/l, the dose of 1α-OH-D₃ was decreased. When plasma P0₄ increased above 2 mmol/l, the dose of Mg(OH)₂ was increased to the highest dose not inducing diarrhea, hypermagnesemia ( < 2 mmol/l) or hyperkalemia ( < 6 mmol/l). In case of persistent hyperphosphatemia, the dose of 1α-OH-D₃ was decreased. Since mean plasma alcaline phosphatase was normal, HPT was monitored on the plasma concentration of 1-84 PTH for which a previous histological study showed that frank osteitis fíbrosa was present only when they were above 70 pg/ml, i.e. (about twice the upper limit of the normal value). Before the study, plasma PTH was below this limit in 16 patients of the CaCO₃ group and in 14 patients of the 1α-OH-D₃ group. After 6 months, they remained below this limit in all patients except 2 of each group. Plasma PTH was initially above 70 pg/ml in 8 of the CaCO₃ and did not change significantly throughout the study, 2 patients having at 6 months a PTH level below 70 pg/ml. In contrast with intravenous 1α-OH-D₃, all the 9 patients with initial frank HPT decreased their PTH levels after 2 months, the levels being below 70 pg/ml in 6 cases. However, because of hypercalcemia and/or of hyperphosphatemia in spite of a highest tolerable dose of Mg(OH)₂, 1α-OH-D₃ doses had to be decreased down to 0.4 μg per dialysis at the 6th month so that at 6 months 6 of 9 patients had their PTH levels above 70 pg/ml, a number comparable to that of patients treated with CaCO₃ (6 of 8). Conclusion: (l) CaCO₃ and intravenous 1α-OH-D₃ are comparably capable of preventing HPT in two thirds of the dialyzed patients; (2) only intravenous 1α-OH-D₃ is able to correct an established frank HPT but this correction is only transient when Mg(OH)₂ is the sole phosphate binder. As a matter of fact, the highest tolerable doses of Mg(OH)₂ cannot prevent the hyperphosphatemia worsening induced by intravenous 1α-OH-D₃, which ...

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Section: Introductionmentioning

confidence: 99%

Prevention of Hyperparathyroidism in Patients on Maintenance Dialysis by Intravenous 1-Alpha-Hydroxyvitamin D3 in Association with Mg(OH)2 as Sole Phosphate Binder

Mornière

Maurouard²,

Boudailliez³

et al. 1992

Nephron

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“…The long-term efficiency and safety of high doses of CaC03 was recently ascertained on the basis of our 5 years' experience with 50 patients on chronic hemodial ysis [15] half of them having their plasma phosphate controlled only by C aC03 and the other half by a combi nation of CaCC>3 and Mg(OH)> while their dialysate magnesium was decreased to prevent hypermagnesemia. Small doses of la-OH vitamin D 3 was necessary in only 9 of them in order to prevent an increase of alkaline phosphatase, and surgical parathyroidectomy for failure of this preventive measure was necessary in only 2 cases.…”

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confidence: 99%

The Approach to the Treatment of Secondary Hyperparathyroidism in Early Renal Failure

Fournier¹,

Morinière²,

Renaud³

1988

Am J Nephrol

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Renal Osteodystrophy

Llach¹

Replacement of Renal Function by Dialysis

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Calcium Carbonate and Magnesium Hydroxide in the Prevention of Renal Osteodystrophy or the Demise of Aluminum Toxicity in Uremia

Cited by 4 publications

References 0 publications

Prevention of Hyperparathyroidism in Patients on Maintenance Dialysis by Intravenous 1-Alpha-Hydroxyvitamin D<sub>3</sub> in Association with Mg(OH)<sub>2</sub> as Sole Phosphate Binder

Prevention of Hyperparathyroidism in Patients on Maintenance Dialysis by Intravenous 1-Alpha-Hydroxyvitamin D<sub>3</sub> in Association with Mg(OH)<sub>2</sub> as Sole Phosphate Binder

The Approach to the Treatment of Secondary Hyperparathyroidism in Early Renal Failure

Renal Osteodystrophy

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