Effect of dietary phosphoric acid supplementation on acid-base balance and mineral and bone metabolism in adult cats

Martin J. Fettman From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Jodi M. Coble From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Dwayne W. Hamar From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Robert W. Norrdin From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Howard B. Seim From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Richard D. Kealy From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Quinton R. Rogers From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Karen McCrea From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Kelly Moffat From the Departments of Pathology (Fettman, Coble, Hamar, Norrdin, McCrea, Moffat) and Clinical Sciences (Fettman, Seim), College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, Pet Nutrition and Care Research, Ralston Purina Co, St Louis, MO 63164 (Kealy), and the Department of Physiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616 (Rogers).

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Summary

Experimental evidence indicates that maintenance of urinary pH ≤ 6.4 is the single most effective means of preventing feline struvite crystalluria or urolithiasis of noninfectious causes. This may be accomplished by dietary acidification, but must be moderated to avoid potential adverse effects of excessive acidification, including bone demineralization, negative calcium balance, potassium depletion, and renal disease. Effects of chronic dietary phosphoric acid supplementation on acid-base balance and on mineral and bone metabolism were investigated in adult, domestic cats. One group of 6 cats was fed a basal, naturally acidifying diet without added acidifiers, and another group of 6 cats was fed 1.7% dietary phosphoric acid. Changes observed during 12 months of study included development of noncompensated metabolic acidosis, increased urinary calcium excretion, and lower but positive calcium balance in cats of both groups. Urinary pH decreased in cats of both groups, but was significantly (P < 0.05) and consistently maintained ≤ 6.4 in cats given dietary phosphoric acid. Urinary phosphorus excretion increased in cats of both groups, but was significantly (P < 0.05) greater in phosphoric acid-supplemented cats, leading to lower overall phosphorus balance as well. Potassium balance decreased in cats of both groups, but was only transiently negative in the phosphoric acid-supplemented cats midway through the study, and normalized at positive values thereafter. Plasma taurine concentration was not affected by dietary acidification, and remained well within the acceptable reference range for taurine metabolism. Double labeling of bone in vivo with fluorescent markers was followed by bone biopsy and histomorphometric measurement of several static and dynamic variables of bone formation. Overall indices of bone formation decreased in cats of both groups with age and confinement, but were not affected by dietary phosphoric acid supplementation. Dietary supplementation with phosphoric acid used as the principal inorganic P source to achieve moderate and stable degree of urinary acidification, did not appear over the course of 1 year, to have induced adverse effects on mineral, bone, or taurine balance in these adult domestic cats.

Summary

Experimental evidence indicates that maintenance of urinary pH ≤ 6.4 is the single most effective means of preventing feline struvite crystalluria or urolithiasis of noninfectious causes. This may be accomplished by dietary acidification, but must be moderated to avoid potential adverse effects of excessive acidification, including bone demineralization, negative calcium balance, potassium depletion, and renal disease. Effects of chronic dietary phosphoric acid supplementation on acid-base balance and on mineral and bone metabolism were investigated in adult, domestic cats. One group of 6 cats was fed a basal, naturally acidifying diet without added acidifiers, and another group of 6 cats was fed 1.7% dietary phosphoric acid. Changes observed during 12 months of study included development of noncompensated metabolic acidosis, increased urinary calcium excretion, and lower but positive calcium balance in cats of both groups. Urinary pH decreased in cats of both groups, but was significantly (P < 0.05) and consistently maintained ≤ 6.4 in cats given dietary phosphoric acid. Urinary phosphorus excretion increased in cats of both groups, but was significantly (P < 0.05) greater in phosphoric acid-supplemented cats, leading to lower overall phosphorus balance as well. Potassium balance decreased in cats of both groups, but was only transiently negative in the phosphoric acid-supplemented cats midway through the study, and normalized at positive values thereafter. Plasma taurine concentration was not affected by dietary acidification, and remained well within the acceptable reference range for taurine metabolism. Double labeling of bone in vivo with fluorescent markers was followed by bone biopsy and histomorphometric measurement of several static and dynamic variables of bone formation. Overall indices of bone formation decreased in cats of both groups with age and confinement, but were not affected by dietary phosphoric acid supplementation. Dietary supplementation with phosphoric acid used as the principal inorganic P source to achieve moderate and stable degree of urinary acidification, did not appear over the course of 1 year, to have induced adverse effects on mineral, bone, or taurine balance in these adult domestic cats.

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