The most commonly used intestinal phosphate-binding agents in dogs and cats contain aluminum as hydroxide, oxide, or carbonate salts.¹ Aluminum-containing binding agents generally appear to be well-tolerated and safe in dogs and cats; as such, they probably represent first-choice drugs for phosphate binding. Alternative drugs include calcium carbonate, calcium acetate, sevelamer hydrochloride (Renagel —Geltex), or lanthanum carbonate (Fosrenol—Shire). Experience with these drugs in dogs and cats is limited, but hypercalcemia may be a problem with the calcium-based products, particularly when they are administered with calcitriol. An intestinal phosphate binder composed of a mixture of calcium carbonate and chitosan is marketed for use in dogs and cats (Epakitin—Vétoquinol).

Moderate evidence (grade 2) supports a phosphorus-restricted diet in dogs with chronic kidney disease⁶; however, the evidence in cats with chronic kidney disease is less sound (grade 4).⁴ While strong evidence supports feeding a renal diet to both dogs and cats with chronic kidney disease, the specific effect of phosphorus intake on clinical outcome has only been documented in dogs with induced chronic kidney disease in which dietary phosphorus restriction was shown to slow the progression of chronic kidney disease and improve survival.⁶

Once therapeutic targets have been attained, re-evaluate dogs and cats in stages 2 through 4 every three to four months to ensure continued compliance and therapeutic success at maintaining the target.

Hypokalemia. The goal of therapy for hypokalemia is to bring the serum potassium concentration above 4 mEq/L. Hypokalemia is primarily of concern in cats with chronic kidney disease or in patients with renal tubular disorders such as Fanconi's syndrome. Hypokalemia in cats with chronic kidney disease is presumed to result from inadequate potassium intake and enhanced urinary losses; however, recent findings suggest that increased urinary losses may also result, in part, from enhanced activation of the renin-angiotensin system in response to low sodium intake.⁷ The clinical effects of hypokalemia may include varying degrees of skeletal, smooth, and cardiac muscle weakness and impaired kidney function.

Enhancing food intake and administering potassium orally or parenterally may correct hypokalemia. Potassium gluconate and potassium citrate are the preferred salts for oral administration; potassium chloride is used parenterally. Descriptive studies and pathophysiologic justification (evidence grade 4) support potassium supplementation to stabilize or improve renal function in cats with chronic kidney disease. A randomized controlled clinical trial examining the effect of oral potassium supplementation on total body potassium concentrations and kidney function failed to yield conclusive findings.⁸

Once therapeutic targets have been attained, re-evaluate dogs and cats in stages 2 through 4 every three to four months to ensure continued compliance and therapeutic success at maintaining the target.

Hyperkalemia. Hyperkalemia has primarily been of concern in chronic kidney disease stage 4 when the kidneys are no longer able to excrete the daily potassium load. However, it may also occur in patients with less advanced chronic kidney disease in association with therapeutic blockade of the renin-angiotensin system and with hyporeninemic hypoaldosteronism. The primary clinical consequence of hyperkalemia is cardiotoxicosis. Treatment usually involves reducing potassium intake; however, hyperkalemia resulting from therapeutic blockade of the renin-angiotensin system may require lowering the drug dosage should a clinically important risk of cardiotoxicosis develop.

#5 Correct metabolic acidosis. Intervention to correct metabolic acidosis is indicated in dogs and cats with chronic kidney disease stages 1 through 4 when the blood bicarbonate concentration drops below the therapeutic target range of 18 to 24 meq/L (19 to 25 meq/L for total carbon dioxide concentration; evidence grade 4). Metabolic acidosis in chronic kidney disease results primarily from impaired renal ammoniagenesis, although impaired acid excretion and bicarbonate reabsorption may contribute as well. Metabolic acidosis also occurs in patients with renal tubular acidosis (RTA) either due to impaired bicarbonate reabsorption (proximal RTA) or impaired urine acidification (distal RTA). The clinical effects of metabolic acidosis may include progressive renal injury and increased protein catabolism with loss of lean tissue.¹ Treatment involves administering an alkalinizing salt, usually sodium bicarbonate or potassium citrate, in an amount sufficient to increase the blood bicarbonate concentration into the normal range.