Veterinary Medicine - December 2007 - (Page 790)

Chronic kidney disease O P E E R - R E V I E W E D TABLE 2 CORRECT DEFICITS AND EXCESSES IN FLUIDS, ACID-BASE BALANCE, AND ELECTROLYTES Maintain serum phosphorus concentrations below target levels. Excessive phosphorus intake and inappropriately high serum phosphorus concentrations appear to promote progressive kidney injury. 4,6 Intervention is indicated in dogs and cats with chronic kidney disease stages 2 through 4 when the phosphorus concentrations rise above stage-specific therapeutic target concentrations. The targets proposed for serum phosphorus concentrations reflect a consensus of expert opinion (evidence grade 4). Ideally, the serum phosphorus concentration should be below 4.5 mg/dl in stage 2 chronic kidney disease, below 5 mg/dl in stage 3, and below 6 mg/dl in stage 4. When the serum phosphorus concentration exceeds these target concentrations, initiate dietary phosphorus restriction by feeding a renal diet. In most dogs and cats with chronic kidney disease stages 2 and 3, dietary phosphorus restriction alone will maintain the concentration below the target concentration. However, in some patients with stage 3 chronic kidney disease and in most patients with stage 4 disease, adding an intestinal phosphate-binding agent will be necessary. If calcium-based phosphate binding agents are used, it is particularly important to monitor serum calcium concentrations. In patients with elevated serum calcium concentration or reduced serum albumin concentrations, it is desirable to measure ionized calcium concentrations. The most commonly used intestinal phosphate-binding agents in dogs and cats contain aluminum as hydroxide, oxide, or carbonate salts.1 Aluminumcontaining 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 A Summary of Chronic Kidney Disease Substage Based on the Urine Protein/Creatinine Ratio* Urine Protein/Creatinine Ratio** Dogs Cats 0.5 0.4 Substage of Disease These animals do not have proteinuria. These animals have borderline proteinuria. These animals have proteinuria. #3 *Adapted from www.iris-kidney.com and the ACVIM proteinuria consensus statement at www.acvim.org. **Measured in patients without evidence of urinary tract inflammation or hemorrhage or dysproteinemias. Confirm persistence by collecting three urine samples at two-week intervals. 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 disease 6; 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. Maintain serum potassium concentrations within the target range. Intervention to manage serum potassium concentrations is indicated in dogs and cats when the concentrations fall outside the target range of 3.5 to 5.5 mEq/L, regardless of the chronic kidney disease stage. 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 #4 790 December 2007 VETERINARY MEDICINE http://www.iris-kidney.com http://www.acvim.org

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Veterinary Medicine - December 2007 Contents Letters Editors' Guest Thanking Our Valued Reviewers The Veterinary Medicine Interview: Dr. Joseph Harari Clinical Exposures Idea Exchange Answers to Three Commonly Asked Questions About Lyme Disease Practical Ideas for Managing Common Internal Medicine Problems A Tip for Interpreting Leptospira Species Titers Investigating Proteinuric Kidney Disease Counseling New Puppy Owners: Normal Play vs. Aggressive Tendencies 11 Guidelines for Conservatively Treating Chronic Kidney Disease CE Form Product Preview Advertiser Index Marketplace/Classifieds Mind Over Miller Merial Insert

Veterinary Medicine - December 2007

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