Abstract
High dietary phosphorus (P), particularly soluble salts, may contribute to chronic kidney disease development in cats. The aim of the present study was to assess the safety of P supplied at 1 g/1000 kcal (4184kJ) from a highly soluble P salt in P-rich dry format feline diets. Seventy-five healthy adult cats (n 25/group) were fed either a low P control (1·4 g/1000 kcal [4184kJ]; Ca:P ratio 0·97) or one of two test diets with 4 g/1000 kcal (4184 kJ); Ca:P 1·04 or 5 g/1000 kcal (4184kJ); Ca:P 1·27, both incorporating 1 g/1000 kcal (4184 kJ) sodium tripolyphosphate (STPP) - for a period of 30 weeks in a randomised parallel-group study. Health markers in blood and urine, glomerular filtration rate, renal ultrasound and bone density were assessed at baseline and at regular time points. At the end of the test period, responses following transition to a commercial diet (total P - 2·34 g/1000 kcal [4184kJ], Ca:P 1·3) for a 4-week washout period were also assessed. No adverse effects on general, kidney or bone (skeletal) function and health were observed. P and Ca balance, some serum biochemistry parameters and regulatory hormones were increased in cats fed test diets from week 2 onwards (P ≤ 0·05). Data from the washout period suggest that increased serum creatinine and urea values observed in the two test diet groups were influenced by dietary differences during the test period, and not indicative of changes in renal function. The present data suggest no observed adverse effect level for feline diets containing 1 g P/1000 kcal (4184 kJ) from STPP and total P level of up to 5 g/1000 kcal (4184 kJ) when fed for 30 weeks.
Highlights
Chronic kidney disease has long been established as the most prevalent metabolic disease and the leading cause of death in domestic cats over the age of 12 years[1,2]
Biochemical markers of kidney health remained within physiological reference ranges in most of these cats, three out of Abbreviations: BAP, bone-specific alkaline phosphatase; BMC, bone mineral content; BMD, bone mineral density; dualenergy X-ray absorptiometry (DXA), dual-energy X-ray absorptiometry; FGF-23, fibroblast growth factor 23; GFR, glomerular filtration rate; ionised Ca (iCa), ionised calcium; MAP, magnesium ammonium phosphate; mean corpuscular Hb (MCH), mean corpuscular haemoglobin; MCV, mean corpuscular volume; P, phosphorus; PTH, parathyroid hormone; RSS, relative super saturation; SDHP, sodium dihydrogen phosphate; SDMA, symmetric dimethylarginine; STPP, sodium tripolyphosphate
Urinary excretion of P was higher in cats fed the moderate test diet than the high test diet (P = 0·033, Fig. 1(a)), whilst P faecal excretion was higher in cats fed the high test diet than the moderate test diet (P < 0·001, Fig. 1(c))
Summary
Chronic kidney disease has long been established as the most prevalent metabolic disease and the leading cause of death in domestic cats over the age of 12 years[1,2]. In a recent feeding study[2], reduced feed intake and vomiting were observed within 4 weeks in adult cats fed high dietary levels of sodium dihydrogen phosphate (NaH2PO4; SDHP) providing 3·6 g/1000 kcal (4184 kJ) P (total P 4·8 g/1000 kcal [4184kJ]; Ca:P ratio 0·6) This led to structural and functional changes in the kidneys as indicated by reduced glomerular filtration rate (GFR) and proteinuria, compatible with early stage chronic kidney disease[2]. This may have been due to the high post-prandial serum phosphate levels induced by the test diet[7]. Recent studies in healthy adult cats investigating post-prandial responses following single meal exposure indicate that soluble P salts, but not organic P sources, induce rapid, dose-dependent increases in serum phosphate and parathyroid hormone (PTH), a key regulator of mineral homoeostasis[7]
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