Renal Disease in Dogs: TUMS?

Kidney Failure in Dogs

How to Improve the Survival of Dogs With Kidney Failure

Hyperphosphataemia in patients with chronic kidney disease, particularly those on dialysis, can be ameliorated by oral phosphate binders in conjunction with dietary phosphate restriction.

Although phosphate binders reduce serum phosphate in these patients, it remains uncertain whether they improve clinical outcomes.

Calcium-based binders are frequently used, but their popularity is waning due to emerging evidence of accelerated vascular calcification.

The use of aluminium-based binders has been limited by a perceived risk of aluminium accumulation.

The non-calcium-based phosphate binders – sevelamer hydrochloride, lanthanum carbonate and sucroferric oxyhydroxide – have become available and subsidised by the Pharmaceutical Benefits Scheme for patients on dialysis.

The pill burden and adverse effects (particularly gastrointestinal intolerance) associated with the expensive, non-calcium – non-aluminum phosphate binders (sevelamer ) often contribute to poor medication adherence.

Calcium carbonate is the most common form of phosphate binder prescribed, particularly in non-dialysis chronic kidney disease. It is typically given to patients with advanced chronic kidney disease, including those receiving dialysis. As with all phosphate binders, calcium-based binders are most effective when taken with meals (which also limits calcium absorption).10 They should be prescribed in conjunction with moderate dietary phosphate restriction, ideally supervised by an accredited practising dietitian. Phosphate-rich foods with a high phosphate to protein ratio (processed foods, fast foods and cola drinks) are best avoided, while foods with a high biologic value (e.g. meats and eggs) should be retained to maintain nutritional status.11,12

Calcium-containing phosphate binders
Calcium binders have historically been an appealing first choice, because they also address the hypocalcaemia that is often seen with hyperphosphataemia in patients with chronic kidney disease. However, hypercalcaemia and accelerated vascular calcification are the main concerns with calcium-containing phosphate binders, particularly when they are combined with vitamin D therapy.5,15-18 The Kidney Disease Outcomes Quality Initiative Guidelines suggest that doses should not exceed 1500 mg/day of elemental calcium,19 based on evidence that this produces a positive calcium balance (excess body stores of calcium leading to soft-tissue and vessel calcification) in chronic kidney disease.20 However, there is little evidence of patient outcomes to support this recommendation. Another common adverse effect of these drugs is gastrointestinal upset, particularly constipation. The other main advantage of calcium-based binders is that they are inexpensive.

Calcium-based binders were associated with significantly lower serum phosphate (mean difference 0.07 mmol/L) when compared with sevelamer. However, sevelamer was associated with a lower risk of hypercalcaemia (risk ratio 0.45, 95% CI* 0.35–0.59) and a higher risk of adverse gastrointestinal events (risk ratio 1.58, 95% CI 1.11–1.25). There was no difference in all-cause mortality between calcium-based binders and sevelamer.51

Phosphate binders therefore effectively reduce serum phosphate in patients with chronic kidney disease, but it is uncertain whether they improve clinical outcomes. There may be a mortality difference between calcium-based and non-calcium-based binders, but it is not clear if this reflects a harmful effect of calcium-based binders, a beneficial effect of non-calcium-based binders or both.


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