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Evaluating sucralfate as a phosphate binder

Quimby J, Lappin M. Evaluating Sucralfate as a Phosphate Binder in Normal Cats and Cats with Chronic Kidney Disease. J Am Anim Hosp Assoc. 2016 Jan-Feb;52(1):8-12. 

Chronic kidney disease (CKD) is commonly discussed on this blog, as it is a major concern in our aging felines. CKD in cats is a chronic process whereby cats lose the ability to concentrate their urine, build up toxins in their bloodstream that would normally be filtered by the kidneys, and lose the ability to regulate many important electrolytes.  There are a multitude of processes that influence the progression of CKD, including diet, hydration, proteinuria, blood pressure, and a host of other factors.  It is well established that blood phosphorus concentrations play a major role in kidney disease.

As kidney disease develops and progresses, cats develop “renal secondary hyperparathyroidism”, a hormonal imbalance that promotes increased levels of phosphorus in the blood. This in turn promotes fibrosis and mineralization of the kidneys, accelerating the progression of renal disease. High blood phosphorus levels may also lead to negative physiologic effects on other organs.

In the early stages of CKD, phosphorus levels may be regulated by simply limiting intake (ie by the use of low protein, low mineral diets). However, as CKD progresses, oral phosphate binders are often needed. These compounds bind phosphorus in the diet, preventing its absorption and decreasing its levels in the bloodstream.  Many products are available on the market to bind phosphorus; these include chitosan or calcium carbonate based products, metals such as aluminum hydroxide or lanthanum, and specific drugs such as sevelamer . Aluminum hydroxide is a commonly used option as it may have greater efficacy than chitosan, less risk of hypercalcemia than calcium carbonate, and is more readily available than lanthanum.  However, AlOH is a generally a fine white powder that may be difficult to dose in cats not eating canned diets.

Sucralfate is a readily available solution of AlOH with sucrose-sulfate. It is commonly used in human and veterinary medicine for the treatment of ulcers, gastro-esophageal reflux disease, and other GI diseases. In human medicine sucralfate is also used as an effective phosphate binder. The use of sucralfate as a phosphate binder is an attractive option in feline medicine, as it is readily available, inexpensive, and available as a liquid which may be attractive for administration.

The purpose of this study was to determine the efficacy of orally administrated sucralfate as a phosphate binder in healthy cats, normophosphatemic cats with CKD, and cats with CKD with elevated blood phosphorus.

Several groups of cats were administered sucralfate in his study. 6 clinically healthy, normophosphatemic cats were given 500mg every 8 hours for two weeks. Blood and urine samples were collected and phosphorus (and other biochemical) values determined.  Urinary phosphorus excretion was also calculated. Samples were also collected for one week prior to sucralfate administration for comparison.

Five normophosphatemic  cats with CKD received the same therapy as above, and the same samples were collected. Fecal samples were also collected to evaluate stool phosphorus content.  Five other normophosphatemic CKD cats were enrolled and kept on normal therapy for comparison. No cats were receiving any other phosphate binder.

No difference was found in urinary,  or blood phosphorus levels in healthy cats on sucralfate therapy when compared with control cats. This suggests that in healthy cats sucralfate is not an effective phosphorus binder. Further to this, vomiting occurred in 14.7% of cats after administration. 15% vomiting rates may be a significant barrier to quality of life and owner compliance.

In cats with CKD, findings were more concerning. There was still no significant change in blood and urine phosphorus balance, suggesting an absence of efficacy. Of the 5 cats administered sucralfate, 3 experienced clinical decompensation including anorexia, constipation, and azotemia. One cat required IV fluid therapy. All cats improved when sucralfate was discontinued.  No control cats experienced any decompensation.

The study was terminated prematurely due to concerns for the health of animals involved. This was a very surprising development, as sucralfate as a commonly used therapy in veterinary medicine that is generally regarded as very safe. However, it appears that in cats, at the doses required for theoretical phosphate reduction there are significant and intolerable side effects.

The findings of this paper suggest that sucralfate is not an appropriate intestinal phosphate binder in cats. There was no evidence of reduction of phosphorus at the dose used, and significant side effects were found including vomiting and decompensation of renal disease. While disappointing, this is valuable information for all cats with renal disease. Based on this study’s recommendation, pure aluminum hydroxide (or alternatives such as chitosan, lanthanum, or sevelamer) should be used to bind phosphorus in cats with chronic renal disease, and sucralfate should not be considered a viable option. (MRK)

See also:
Kidder AC, Chew D. Treatment options for hyperphosphatemia in feline CKD: what’s out there? J Feline Med Surg. 2009 Nov;11(11):913-24.