Treatment of Uremic Hyperphosphatemia -Is There Still a Need for Aluminum Salts?

Schaefer, K.; Herrath, D. von; Erley, Christiane M.

doi:10.1159/000167578

Cited by 19 publications

(11 citation statements)

References 8 publications

(13 reference statements)

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“…Because of the toxic effects of aluminum [ 18] calcium salts have nowadays widely replaced aluminum hydrox ide as phosphate binders in patients with chronic renal failure. In addition to phosphate binding, calcium salts are useful in increasing the concentration of ionized cal cium of extracellular fluid, which is known to be the most important regulator of PTH secretion.…”

Section: Discussionmentioning

confidence: 99%

Acute Effects of Calcium Carbonate and Citrate on Secondary Hyperparathyroidism in Chronic Renal Failure

Saha

Pietilä²,

Mustonen³

et al. 1991

Am J Nephrol

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Two grams of elemental calcium as carbonate or citrate were given after an overnight fast to 14 patients with advanced renal failure (serum creatinine 759 ± 365 µmol/l, mean ± SD). The suppressibility of their hyperparathyroidism was confirmed with a calcium infusion test. Both calcium citrate and carbonate increased significantly plasma ionized calcium (6.8 and 4.5%, respectively) and total calcium (9.3 and 6.0%), p < 0.001. In the majority of the patients, calcium citrate but not carbonate increased plasma calcium sufficiently to induce the suppression of hyperparathyroidism. The decrease of plasma intact parathyroid hormone was 35.9 ± 24.8% (mean ± SD); p < 0.001) after calcium citrate and 9.2 ± 18.9% (mean ± SD; NS) after calcium carbonate.

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Section: Discussionmentioning

confidence: 99%

Acute Effects of Calcium Carbonate and Citrate on Secondary Hyperparathyroidism in Chronic Renal Failure

Saha

Pietilä²,

Mustonen³

et al. 1991

Am J Nephrol

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“…Plasma ionized calcium was significantly lower with calcium ketoglutarate than with calcium carbonate. Both drugs caused a reduction in plasma P i ,and there was no difference in plasma P i or PTH levels [87,88]. Some 29% of patients taking calcium ketoglutarate withdrew from the study due to gastrointestinal discomfort.…”

Section: Currently Available P I Bindersmentioning

confidence: 93%

“…It is also a potent inhibitor of hydroxyapatite crystal formation, the initial stage in calciumphosphate precipitation [107]. 3-Phosphocitric acid, another inhibitor of calcium-phosphate precipitation, has been shown to prevent renal calcifications and progression of renal failure in 5/6th nephrectomized rats fed a high-phosphorus diet [12,87,108]. The potential in vivo effect of PFA in preventing calcium-phosphate precipitation has not been investigated.…”

Section: The Need For Phosphate Inhibitorsmentioning

confidence: 99%

Phosphate binders for control of phosphate retention in chronic renal failure

Loghman‐Adham

1999

Pediatric Nephrology

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In patients with chronic renal insufficiency, phosphate retention is a major factor in the development of secondary hyperparathyroidism, renal osteodystrophy, and soft tissue calcification, and may contribute to progression of renal failure. Prevention of phosphate retention with dietary and pharmacological means, along with the administration of calcitriol, may prevent or reverse secondary hyperparathyroidism. With more-advanced renal failure, phosphate binders become necessary to maintain phosphate balance and to prevent hyperphosphatemia. Because of toxicity, aluminum-containing phosphate binders are no longer used. Currently, calcium-containing phosphate binders, such as calcium carbonate and calcium acetate, are the most widely prescribed. Although calcium salts eliminate the problems associated with aluminum toxicity, they often result in transient hypercalcemia, requiring discontinuation of calcitriol and the use of low-calcium dialysate. Several new non- aluminum- and non-calcium-containing phosphate binders are currently at various stages of development, and may provide an alternative to the currently used binders. It is unlikely, however, that the newer compounds will completely replace calcium salts, since mild hypercalcemia may be necessary in chronic renal failure patients to suppress parathyroid hormone production. Other areas of investigation must include the development of drugs to inhibit soft tissue and renal calcifications, and to enhance urinary phosphate excretion.

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“…In addition to being alu minum-free, it has the potential advantage of causing less hypercalcemia than other cal cium-containing phosphate binders. No other clinical studies of calcium alginate have been published, although another group re ported it to be less effective than the initial studies suggested [4], Therefore, we compared the efficacy of calcium alginate to that of aluminum hydroxide in patients on hospital hemodialysis.…”

mentioning

confidence: 99%