The Control of Hyperphosphatemia in Chronic Kidney Disease: Which Phosphate Binder?

2009 ◽  
Vol 32 (2) ◽  
pp. 95-100 ◽  
Author(s):  
Markus Ketteler
2016 ◽  
Vol 52 (1) ◽  
pp. 8-12 ◽  
Author(s):  
Jessica Quimby ◽  
Michael Lappin

Control of hyperphosphatemia is an important part of the management of chronic kidney disease (CKD). The purpose of this study was to determine the efficacy of sucralfate as a phosphate binder in normal cats and normophosphatemic CKD cats. A 500 mg sucralfate slurry was administered orally q 8 hr for 2 wk, and serum phosphorus, urine fractional excretion of phosphorus, and fecal phosphorus concentrations were measured. In normal cats treated with sucralfate, significant changes in serum phosphorus concentration or urinary excretion of phosphorus were not detected, and vomiting occurred after 14.7% of administrations. Of the five normophosphatemic cats with CKD treated with sucralfate, three experienced clinical decompensation, including vomiting, anorexia, constipation, and increased azotemia. Administration of sucralfate did not result in significant changes in fecal phosphorus concentration in these cats. The effects of sucralfate administration on serum phosphorus concentration and urinary excretion of phosphorus in CKD cats was difficult to determine because of dehydration and worsening azotemia associated with decompensation. Due to side effects and the apparent lack of efficacy of the medication, the study was discontinued. This study was unable to confirm efficacy of this sucralfate formulation as a phosphate binder, and side effects were problematic during the study.


2014 ◽  
Author(s):  
Sankar D. Navaneethan ◽  
Ankit Sakhuja ◽  
Susana Arrigain ◽  
John Sharp ◽  
Jesse D. Schold ◽  
...  

Toxins ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 522 ◽  
Author(s):  
Marc Vervloet

Phosphate toxicity is a well-established phenomenon, especially in chronic kidney disease (CKD), where hyperphosphatemia is a frequent occurrence when CKD is advanced. Many therapeutic efforts are targeted at phosphate, and comprise dietary intervention, modifying dialysis schemes, treating uncontrolled hyperparathyroidism and importantly, phosphate binder therapy. Despite all these interventions, hyperphosphatemia persists in many, and its pathological influence is ongoing. In nephrological care, a somewhat neglected aspect of treatment—when attempts fail to lower exposure to a toxin like phosphate—is to explore the possibility of “anti-dotes”. Indeed, quite a long list of factors modify, or are mediators of phosphate toxicity. Addressing these, especially when phosphate itself cannot be sufficiently controlled, may provide additional protection. In this narrative overview, several factors are discussed that may qualify as either such a modifier or mediator, that can be influenced by other means than simply lowering phosphate exposure. A wider scope when targeting phosphate-induced comorbidity in CKD, in particular cardiovascular disease, may alleviate the burden of disease that is the consequence of this potentially toxic mineral in CKD.


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