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18 – THE THIN, INAPPETENT CAT  337


           Dietary management of chronic renal failure.   ● The mechanisms of these effects are unclear, but
            ● Treatment of cats with chronic renal failure by  may be hemodynamically mediated by causing
              dietary modification has been proven to significantly  renal vasodilation especially of the efferent arteri-
              increase survival. Generally, commercially available  ole, and reducing glomerular capillary pressure.
              “renal diets” are recommended. These diets have  ● Preliminary studies of ACE inhibitor use in natu-
              restricted protein, calcium, sodium, phosphorus and  rally occurring chronic renal failure in cats have
              acid-load, and added potassium.                shown significantly increased survival times for the
                                                             subgroup of renal-failure cats with urine protein/cre-
           Dietary protein restriction is frequently advocated.
                                                             atinine ratios > 1.
            ● In moderate to severe chronic renal failure, con-
                                                          ● By reducing glomerular pressure, ACE inhibition
              trolled restriction of non-essential protein will
                                                             would be expected to cause a decrease in glomeru-
              reduce the accumulation of nitrogenous waste prod-
                                                             lar filtration rate and so may increase azotemia.
              ucts that are believed to contribute to the uremic
                                                             A rise in creatinine of > 50% warrants withdrawal
              syndrome.
                                                             of the drug.
            ● More controversially, the use of a restricted protein
              diet in early CRF may slow the rate of progression  Treatment of renal secondary hyperparathyroidism
              to end-stage renal failure by preventing maladaptive  should be instituted in a staged manner.
              changes in surviving nephrons. However, evidence
                                                          The cornerstone of therapy is dietary phosphate
              for a beneficial effect of protein restriction on renal
                                                          restriction.
              function in cats with early renal failure is not avail-
                                                          ● After initiation of phosphate restriction, plasma
              able.
                                                             phosphate levels usually stabilize at a lower level by
            ● Poor appetite and the decreased palatability of
                                                             2–8 weeks, however PTH concentrations may con-
              restricted protein diets make mal-nutrition a seri-
                                                             tinue to decline without additional intervention.
              ous problem in renal-failure patients. Monitor
                                                          ● Proteinaceous foods are the main source of phos-
              carefully for weight loss and decreasing muscle
                                                             phate in the diet, so phosphate restriction is gener-
              mass.
                                                             ally combined with protein restriction.
            ● Dietary protein intake should be tailored to the
                                                          ● The aim of dietary phosphate restriction is to
              metabolic needs of the individual cat. Usually a diet
                                                             reduce plasma phosphorus to the lower limit of
              containing at least 21% of gross energy as protein is
                                                             the reference range, the point at which the most
              required (usual maintenance diets contain 35–55%
                                                             effective control of PTH secretion is usually
              gross energy as protein). The goal is to maintain a
                                                             attained.
              BUN of ≤ 29 mmol/L (80 mg/dl). In general, the
              more severe the renal dysfunction, the greater the  If after 4 weeks dietary management alone is not
              protein restriction required, but protein should not  achieving this, or if PTH concentrations are not
              be decreased below 19–20% of gross energy   decreasing, then intestinal phosphate-binding agents
              (metabolizable energy).                     should be introduced to further restrict phosphate
                                                          intake.
           A number of other dietary components have been stud-
                                                          ● Intestinal phosphate-binding agents form non-
           ied for their effect to modify the rate of progression
                                                             absorbable salts of phosphate, binding phosphate in
           including calorie intake and fatty acid composition.
                                                             both the diet and intestinal secretions. To achieve
           Dietary phosphate restriction is discussed under the sec-
                                                             efficient phosphate binding, the medication should
           tion on renal secondary hyperparathyroidism.
                                                             be given, ideally mixed through the food or imme-
           Angiotensin-converting enzyme (ACE) inhibitors    diately before feeding.
           may have a renoprotective effect, which is inde-  ● Aluminum hydroxide should be dosed at 30–100
           pendent of any effect on systemic blood pressure.  mg/kg/day PO in divided doses with each meal,
           ACE inhibitor therapy may also be useful in       titrated to effect based on plasma phosphate concen-
           reducing the degree of proteinuria in cats with   trations. Dose can be increased to 200–300 mg/kg if
           chronic renal failure. benazepril 0.25–0.5 mg/kg  necessary to control phosphate. If the cat refuses to eat
           PO q 24 h.                                        it with food, a compounding pharmacy can formulate
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