Aluminium-Induced Anaemia in Haemodialysis Patients

McGonigle, R; Parsons, V.

doi:10.1159/000183328

Cited by 86 publications

(20 citation statements)

References 46 publications

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“…was eliminated unchanged over 24 h [10]. These results indi cate that ranitidine is appreciably removed by hemodialysis, possibly due to low protein binding, as well as the low molecular weight and high water solubility of the drug [7].…”

Section: Discussionmentioning

confidence: 72%

“…The mean renal clearance of ranitidine in subjects with normal kidney function has been reported to be 530 ml/min [3], suggest ing extensive tubular secretion [4], Raniti dine elimination is reduced in patients with kidney failure [5,6]. Due to the high water solubility and low protein binding of raniti dine, ranitidine is expected to be removed from the plasma by both hemodialysis and peritoneal dialysis [7]. The literature on rani tidine kinetics during and after dialysis is limited [7,8].…”

Section: Introductionmentioning

confidence: 99%

“…Due to the high water solubility and low protein binding of raniti dine, ranitidine is expected to be removed from the plasma by both hemodialysis and peritoneal dialysis [7]. The literature on rani tidine kinetics during and after dialysis is limited [7,8]. This paper describes the phar macokinetics and removal of ranitidine by hemodialysis in chronic renal failure patients undergoing maintenance hemodialysis.…”

Section: Introductionmentioning

confidence: 99%

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Pharmacokinetics of Ranitidine after Intravenous Administration in Hemodialysis Patients

et al. 1985

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The pharmacokinetics of ranitidine and its removal by hemodialysis were determined in 9 patients with chronic renal failure requiring hemodialysis. Ranitidine (50 mg) was administered as an intravenous bolus at the beginning of the dialysis procedure, which lasted for 4 h. The elimination half-life, plasma clearance and volume of distribution (VD area) of ranitidine in these patients were 9.0 ± 2.6 h (mean ± SD), 305 ± 152 ml/min and 3.5 ± 1.9 liters/kg, respectively. About 8% of the administered dose was removed during a single dialysis procedure. The elimination of ranitidine is appreciably reduced in these patients. These results suggest that the dose of ranitidine should be adjusted in patients with severe renal failure who are undergoing hemodialysis, and a suitable schedule for dosing such patients is suggested.

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Section: Discussionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pharmacokinetics of Ranitidine after Intravenous Administration in Hemodialysis Patients

et al. 1985

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“…Thus, Al has been recognized as an important toxic factor in vitamin D-resistant low turnover osteodystrophy [1], lethal encephal opathy [2], and microcytic hypochromic anemia unre lated to iron deficiency [3].…”

Section: Introductionmentioning

confidence: 99%

Effect of Lactate on the Absorption and Retention of Aluminum in the Remnant Kidney Rat Model

Ittel

Griessner²,

Sieberth³

1991

Nephron

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In previous investigations we found the gastrointestinal absorption of aluminum (Al) to be enhanced in uremic rats and this phenomenon could not be attributed to either calcitriol deficiency or secondary hyperparathyroidism. The purpose of this study was to examine whether carboxyl ligands such as lactate could affect the absorption of Al in our model and, if so, whether this would impose additional alterations on the Al absorption in uremia. Uremic rats and controls were studied with single oral loads of either Al chloride or Al lactate and, subsequently, urinary Al excretion was measured for 5 days. Compared with Al chloride, administration of Al lactate resulted in significantly higher urinary excretion rates of Al in uremic rats (55.5 ± 22.7 vs. 27.4 ± 7.0 μg; 2.06 ± 0.84 vs. 1.01 ± 0.26 μmol) and in controls (23.6 ± 8.5 vs. 11.9 ± 4.3μg; 0.87 ± 0.31 vs. 0.44 ± 0.16 μmol). However, with either Al load the recovery of Al from urine was substantially higher in uremic animals. In contrast, only in controls was there a more pronounced rise in serum Al concentrations following ingestion of Al lactate, whereas in uremic rats this increase had a similar magnitude following Al chloride and Al lactate, suggesting a larger apparent volume of distribution of the latter. Adjustment of the pH of the Al lactate-containing solution to 7.0 or oral administration of sodium lactate together with Al chloride yielded essentially similar results. These observations indicate that the enhanced intestinal absorption of Al in uremia is further augmented by lactate regardless of the mixture of hydroxolactato complexes employed. By means of a larger apparent volume of distribution Al lactate may accelerate the accumulation of Al in uremia by an increase in both intestinal absorption and tissue distribution.

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“…This effect may be directly mediated through heme-synthetic enzymes that are thought to be inhibited by aluminum, such as ferrochelatase (24) or uroporphyrin decarboxylase (25,26). Studies of levels of delta-levulinic acid dehydrogenase have been inconclusive (27)(28)(29). Alternatively, aluminum may interfere indirectly with the normal metabolism ofiron (30).…”

Section: Introductionmentioning

confidence: 99%

Aluminum inhibits erythropoiesis in vitro.

Mladenovic¹

1988

J. Clin. Invest.

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Anemia has been associated with aluminum intoxication in patients on chronic dialysis and in animals. In studies presented here, in vitro human erythroid culture was used to delineate the effects of aluminum on normal hemnatopoiesis. Aluminum by itself in routine culture, even at very high levels (1,035 ng/ml), did not significantly affect erythroid colony growth. The addition of human transferrin to the culture, however, resulted in a marked dose-dependent inhibition of erythroid, but not myeloid colony growth. At all doses, CFU-E progenitors showed greater inhibition than burst-forming units (BFU-E). Aluminum inhibition was not overcome by increasing the dose of erythkopoietin or adding additional burst-promotihg activity to the culture. Inhibition by aluminum was directly related to the number of binding sites on transferrin in the culture, and was not observed in the presence of fully ironsaturated transferrin.

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Aluminium-Induced Anaemia in Haemodialysis Patients

Cited by 86 publications

References 46 publications

Pharmacokinetics of Ranitidine after Intravenous Administration in Hemodialysis Patients

Pharmacokinetics of Ranitidine after Intravenous Administration in Hemodialysis Patients

Effect of Lactate on the Absorption and Retention of Aluminum in the Remnant Kidney Rat Model

Aluminum inhibits erythropoiesis in vitro.

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