Management of hyperphosphatemia in patients with renal failure

Ghazali, A; F, Ben Hamida; Bouzernidj, M; N, el Esper; Pf, Westeel; Fournier, A

doi:10.1097/00041552-199307000-00007

Cited by 19 publications

(7 citation statements)

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“…Because the conventional 3 sessions/week hemodialysis remove only 1,950 mg of phosphate per week, the use of phosphate binders is necessary to prevent phosphate accumulation (3). Because of the aluminum toxicity induced by long‐term administration of Al(OH) 3 , alkaline salts of calcium are presently the most commonly used phosphate binders (4,5). Most studies have confirmed the higher efficiency of calcium acetate relative to CaCO 3 in controlling hyperphosphatemia when given at the same dose of elemental calcium (6–8), a comparable control of hyperphosphatemia being obtained even by our group (9,10) with half the dose of elemental calcium given as acetate.…”

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confidence: 99%

Role of Calcium Carbonate Administration Timing in Relation to Food Intake on Its Efficiency in Controlling Hyperphosphatemia in Patients on Maintenance Dialysis

et al. 1998

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A study has claimed that at an equal elemental calcium dose, CaCO3 was not less but equally as efficient in controlling predialysis hyperphosphatemia as calcium acetate, provided both calcium salts were ingested 5 min before meals instead of during meals because the higher acidity of the fasting gastric juice would allow for better dissociation of CaCO3. However, this study did not directly demonstrate that the efficiency of CaCO3 in controlling hyperphosphatemia was actually greater when it was administered before a meal than during a meal. To examine this point, we performed a 3 month randomized crossover trial in 12 reliable and stable patients maintained on chronic hemodialysis. Their plasma concentrations of calcium, protein, phosphate, bicarbonate, urea, and creatinine were measured before the first dialysis of each week and the amount of intact parathyroid hormone (PTH) at the beginning and at the end of each of the 3 months. Comparison of the plasma concentrations measured during the 2 modes of administration showed no significant differences in creatinine, urea, bicarbonate, or intact PTH. The mean (+/-SD) plasma concentration of PO4 was not significantly lower (1.88+/-0.50 vs. 1.74+/-0.41 mM) whereas the corrected level of plasma Ca was significantly lower (2.30+/-0.17 vs. 2.38+/-0.16 mM; p < 0.04) when CaCO3 was given before meals than during meals. In conclusion, the administration of CaCO3 before a meal does not increase its efficiency in controlling hyperphosphatemia because the level of plasma PO4 was actually slightly higher with this timing of administration whereas the comparison of the creatinine and urea levels suggested a stability of phosphate intake and the comparison of the PTH and bicarbonate levels suggested the stability of osteolysis and of the transcellular membrane shift of phosphate. Also, administration of CaCO3 before a meal is associated with significantly lower plasma corrected calcium, suggesting less absorption of calcium, which may be an advantage but only in hypercalcemic patients. There is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before meals rather than during meals.

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confidence: 99%

Role of Calcium Carbonate Administration Timing in Relation to Food Intake on Its Efficiency in Controlling Hyperphosphatemia in Patients on Maintenance Dialysis

et al. 1998

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“…Indeed, in patients suffering from ABD developed under calcium salt therapy, the very low capacity of bone to incorporate and to buffer an extra calcium load would result in hypercalcemia, which occurs in 8 -36% of the measurements in dialysis patients (47,48), and extraosseous calcifications (49). The minimal PTH level was between 5-6% of the maximal PTH level in all patients, including those with high BFR, i.e.…”

Section: Discussionmentioning

confidence: 99%

Bone Mass and Dynamic Parathyroid Function According to Bone Histology in Nondialyzed Uremic Patients after Long-Term Protein and Phosphorus Restriction

Lafage-Proust¹,

Combe²,

Barthe

et al. 1999

The Journal of Clinical Endocrinology &Amp; Metabolism

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One year of a very low protein diet (VLPD) can reverse secondary hyperparathyroidism in uremic patients. We studied bone histology, bone mineral density (BMD), and dynamic parathyroid function (calcium/PTH curves) in 16 nondialyzed patients with advanced renal failure who had been receiving a VLPD for a mean of 5 yr (mean protein intake, 0.34 +/- 0.12 mg/kg x day; mean phosphorus intake, 8.2 +/- 2.1 mg/kg x day) and daily supplementation with essential amino acids and their ketoanalogs (1000 IU vitamin D2 and 1-2 g calcium carbonate). Three patients exhibited a high bone formation rate (BFR), 7 patients had normal bone remodeling, and 6 patients had a low BFR, including 2 with osteomalacia and 4 with adynamic bone disease without aluminum overload. A longer diet duration and lower caloric intake were associated with low BFR. More than half of the patients exhibited moderate or severe osteoporosis at the appendicular skeleton. The t score of femur BMD explained 65% of the BFR variance. Patients with a low BFR had a dynamic parathyroid function similar to that of patients with a normal BFR, except they had a lower capacity to buffer a calcium load, whereas patients with a high BFR had a higher basal PTH/maximum PTH and a steeper calcium/PTH curve slope; the calcium set-point was identical in the three groups.

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“…Hyperphosphataemia, defined as a serum phosphate concentration greater than 1.7 mmol L − 1 , occurs in 64 % of haemodialysis patients (Ansell & Feest 1997), and may lead to secondary hyperparathyroidism and renal osteodystrophy (Ghazali et al 1993 ;Knochel & Agarwal 1996). The treatment of hyperphosphataemia involves administration of compounds to complex with or bind phosphate in the gastrointestinal tract, thus preventing its absorption.…”

Section: Introductionmentioning

confidence: 99%

“…This accumulation of aluminium may cause dialysis encephalopathy, microcytic anaemia and osteomalacia (Alfrey et al 1976 ;Parkinson et al 1979 ;Short et al 1980). The current binders of choice are therefore calcium salts, which have been used with only varying degrees of success (Ghazali et al 1993 ;Pflanz et al 1994). Other metal-based compounds have been put forward as viable alternatives, including magnesium, lanthanum and zirconyl salts (O'Donovan et al 1986 ;Oe et al 1987 ;Graff & Burnell 1995a, b ;Dewberry et al 1997), although safety associated with long-term ingestion may be an issue.…”

Section: Introductionmentioning

confidence: 99%

The evaluation of novel mixed metal hydroxy-carbonates as phosphate binders: an in-vivo study in the rat

Rankin

Thewles

Lote

et al. 2001

Journal of Pharmacy and Pharmacology

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A number of novel phosphate binders based on mixed metal hydroxide structures incorporating Fe and Ca, or Fe and Mg (classified as CT, Crosfield test compounds), were compared with the established phosphate binders Mg(OH)2, Al(OH)3, CaCO3 and a commercial hydrotalcite (Al- and Mg-based) using a rat model. The changes in urine and soluble faecal phosphate were used to evaluate efficacy of phosphate binding. The binders were mixed into a standard rat maintenance food at a concentration of 1% (w/w). Four rats were used for each binder study group and fed over 7 days. Urine and faeces were collected (in a metabolic cage) over the last 24-h study period and the phosphate content measured. The urinary phosphate was significantly reduced (P < 0.001) with CTFeCa (72+/-44 microm), CTFeMg (13+/-4 microm), CT100 (26+/-11 microm), and Mg(OH)2 (65+/-53 microm), compared with control (766+/-188 microm), Al(OH)3 (1,256+/-279 microm), and CaCO3 (857+/-25 microm). The soluble phosphate content of the faeces was significantly reduced (P < 0.05) by up to 60 % with CTFeCa, CTFeMg and Mg(OH)2, and up to 40% with CT100 and Al(OH)3, compared with 30% in controls and 10% with CaCO3. The new mixed metal hydroxy-carbonate compounds based on FeCa or FeMg are effective phosphate binders in-vivo and warrant further testing in patients.

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Management of hyperphosphatemia in patients with renal failure

Cited by 19 publications

References 0 publications

Role of Calcium Carbonate Administration Timing in Relation to Food Intake on Its Efficiency in Controlling Hyperphosphatemia in Patients on Maintenance Dialysis

Role of Calcium Carbonate Administration Timing in Relation to Food Intake on Its Efficiency in Controlling Hyperphosphatemia in Patients on Maintenance Dialysis

Bone Mass and Dynamic Parathyroid Function According to Bone Histology in Nondialyzed Uremic Patients after Long-Term Protein and Phosphorus Restriction

The evaluation of novel mixed metal hydroxy-carbonates as phosphate binders: an in-vivo study in the rat

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