Alternative phosphate binders for aluminium hydroxide

1990 ◽  
pp. 325-343
Author(s):  
Albert Fournier ◽  
Philippe Moriniere ◽  
Bernard Boudailliez ◽  
J. D. Lalau ◽  
Henri Renaud ◽  
...  
Keyword(s):  
Aluminium Hydroxide ◽  
Phosphate Binders

Highly sensitive NADH detection by utilising an aluminium hydroxide/iron hydroxide/MWCNTs nanocomposite film-modified electrode

2020 ◽  
Vol 15 (14) ◽  
pp. 997-1002
Author(s):  
Yu Wang ◽  
Lingling Yin ◽  
Xia Li ◽  
Ran Shang ◽  
Xiangli Yang ◽  
...  
Keyword(s):  
Modified Electrode ◽  
Aluminium Hydroxide ◽  
Nanocomposite Film ◽  
Iron Hydroxide ◽  
Highly Sensitive

“In vitro” Neutralization with Oxalate Ion of the Anticoagulant Effect of Heparin

1961 ◽  
Vol 05 (02) ◽  
pp. 314-318 ◽  
Author(s):  
W. O Cruz ◽  
L Meis ◽  
C. P Dietrich
Keyword(s):  
Calcium Oxalate ◽  
Aluminium Hydroxide ◽  
Barium Sulfate ◽  
Anticoagulant Effect ◽  
Normal Plasma ◽  
Oxalate Ion

SummaryHeparinized blood or plasma coagulates if, after addition of oxalate, recalcification follows. Of the decalcifying agents only oxalate ion has been suitable for demonstrating this phenomenon. Oxalate seem to accomplish two different roles connected with this effect: a fundamental one, i. e., to sensitize a heparinlipoprotein complex to the action of an anti-heparin factor found in normal plasma or serum and a secondary one, related to its capacity to adsorb this antiheparin factor. The latter is removable by centrifugation. This anti-heparin oxalate factor, which is able to counteract the action of heparin after previous addition of oxalate, was found in sequestrened, Dowex 50 resin plasma or in serum, but is not active in citrated plasma. This factor was removed from plasma by adsorption with barium sulfate, aluminium hydroxide or calcium oxalate and was eluted from these adsorbants after incubation with saline.

Phosphate binders in patients with chronic kidney disease: Between the new and the old.

2019 ◽  
pp. 2-3
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Estimated Glomerular Filtration Rate ◽  
Chronic Kidney Disease Stage ◽  
Disease Stage ◽  
Phosphate Binders ◽  
Advanced Chronic Kidney Disease ◽  
Phosphate Retention ◽  
Stage 4 ◽  
Dietary Phosphate

Impaired phosphate excretion by the kidney leads to Hyperphosphatemia. It is an independent predictor of cardiovascular disease and mortality in patients with advanced chronic kidney disease (stage 4 and 5) particularly in case of dialysis. Phosphate retention develops early in chronic kidney disease (CKD) due to the reduction in the filtered phosphate load. Overt hyperphosphatemia develops when the estimated glomerular filtration rate (eGFR) falls below 25 to 40 mL/min/1.73 m2. Hyperphosphatemia is typically managed with oral phosphate binders in conjunction with dietary phosphate restriction. These drugs aim to decrease serum phosphate by binding ingested phosphorus in the gastrointestinal tract and its transformation to non-absorbable complexes [1].

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