A review of phosphorus homeostasis and the impact of different types and amounts of dietary phosphate on metabolism and renal health in cats.

Dottie Laflamme,David Polzin,Gail Czarnecki‐Maulden,Scott Brown,Richard Butterwick,Robert Backus,Andrea Fascetti,Jonathan Elliott

doi:10.1111/jvim.15961

Abstract

Elevated concentrations of serum phosphate are linked with progression and increased case fatality rate in animals and humans with chronic kidney disease. Elevated concentrations of serum phosphate can be a risk factor for development of renal and cardiovascular diseases or osteoporosis in previously healthy people. In rodents, an excess intake of dietary phosphorus combined with an inverse dietary calcium : phosphorus ratio (<1 : 1) contributes to renal calcification. Renal injury also has occured in cats fed experimental diets supplemented with highly soluble phosphate salts, especially in diets with inverse calcium : phosphorus ratios. However, not all phosphorus sources contribute similarly to this effect. This review, which focuses on cats, summarizes the published evidence regarding phosphorus metabolism and homeostasis, including the relative impact of different dietary phosphorus sources, and their impact on the kidneys. No data currently shows that commercial cat foods induce renal injury. However, some diets contain high amounts of phosphorus relative to recommendations and some have inverse Ca : P ratios and so could increase the risk for development of kidney disease. While limiting the use of highly soluble phosphates appears to be important, there are insufficient data to support a specific upper limit for phosphate intake. This review also proposes areas where additional research is needed in order to strengthen conclusions and recommendations regarding dietary phosphorus for cats.

Highlights

Elevated concentrations of blood phosphate or maladaptive activation of hormonal systems involved in regulating phosphate could have direct toxic effects on the kidneys and cardiovascular system.[5,6]
Evidence in humans suggests that elevated serum phosphate concentration (sPi) can be a risk factor for development of renal disease, cardiovascular disease, or osteoporosis, and is associated with increased mortality.[13,14,15,16]
This review summarizes the published evidence regarding P metabolism and homeostasis, including how these factors affect the kidneys

Summary

| INTRODUCTION

Active absorption of P is up- or down-regulated depending on the animal's needs and various regulating factors, while paracellular diffusion is more dependent on the total amount consumed.[21,22,23] Parathyroid hormone (PTH), 1-25-dihydroxy vitamin D3 (1,25D3), fibroblast growth factor 23 (FGF23), thyroid hormone, glucocorticoids, estrogens and metabolic acidosis are just some of the endogenous metabolic factors that can modify intestinal P uptake either directly or indirectly.[2,23,24,25] In addition, P absorption in most species is dependent on the intestinal pH, P needs of the animal, source of P, and interactions with other dietary factors such as dietary Ca, magnesium (Mg), and phytates.[2,21,24,25,26,27,28,29,30,31] Metabolic acidosis upregulates sodium-dependent P uptake in the intestines of mice while simultaneously increasing urinary excretion of phosphate (Pi).[2] Dietary Ca and Ca : P ratio exert an influence over P availability, with intestinal absorption of P inversely affected by dietary Ca and Ca : P ratio, increasing when Ca : P is low This has been demonstrated in dogs and cats, as well as other animals.[21,32] Likewise, dietary Mg affects intestinal uptake of both Ca and P in both rats and cats, with higher Mg decreasing uptake of Ca and P.26,31,33,34.

Calcium phosphate

Sodium polymetaphosphate

Findings

NRb NRb