Body Composition of Healthy Cats and Cats with Chronic Kidney Disease Fed on a Dry Diet Low in Phosphorus with Maintenance Protein.

The aim was to evaluate the effect of feeding a low-phosphorus and maintenance protein diet in healthy cats and cats with chronic kidney disease (CKD) with IRIS stages 1 (CKD-1) and 2 (CKD-2). Cats were initially fed a senior diet (30 days) followed by the renal diet (60 days). Body composition, body weight (BW), muscle mass score (MMS), and body condition score (BCS) were assessed before (T30) and after renal diet intake (T60). General mixed linear models were used to assess the effects of fixed groups and moments (T30 × T60), as well as their interaction, in addition to the random effects of animals within each group. Unlike healthy cats and cats with CKD-1, cats with CKD-2 had a loss of BW, lower BCS (p < 0.005), and lower MMS (p = 0.0008) after 60 days of consuming the renal diet. The fat mass and lean body mass (LBM), determined by the deuterium isotopes method, did not change in all cats between T0 and T60. In healthy cats and cats with CKD-1, the renal diet resulted in maintenance of BW, BCS and MMS; but cats with CKD-2 presented lower BCS and did not reduce phosphatemia after consumption.

Vitamin D Metabolism and Its Role in Mineral and Bone Disorders in Chronic Kidney Disease in Humans, Dogs and Cats.

Some differences regarding Vitamin D metabolism are described in dogs and cats in comparison with humans, which may be explained by an evolutionary drive among these species. Similarly, vitamin D is one of the most important regulators of mineral metabolism in dogs and cats, as well as in humans. Mineral metabolism is intrinsically related to bone metabolism, thus disturbances in vitamin D have been implicated in the development of chronic kidney disease mineral and bone disorders (CKD-MBD) in people, in addition to dogs and cats. Vitamin D deficiency may be associated with Renal Secondary Hyperparathyroidism (RSHPT), which is the most common mineral disorder in later stages of CKD in dogs and cats. Herein, we review the peculiarities of vitamin D metabolism in these species in comparison with humans, and the role of vitamin D disturbances in the development of CKD-MBD among dogs, cats, and people. Comparative studies may offer some evidence to help further research about vitamin D metabolism and bone disorders in CKD.

The Role of Vitamin D in Small Animal Bone Metabolism.

Dogs and cats have differences in vitamin D metabolism compared to other mammalian species, as they are unable to perform vitamin D cutaneous synthesis through sun exposure. Therefore, they are dependent on the dietary intake of this nutrient. The classic functions of vitamin D are to stimulate intestinal calcium and phosphate absorption, renal calcium and phosphate reabsorption and regulate bone mineral metabolism. Thus, it is an important nutrient for calcium and phosphorus homeostasis. This review highlights the evidence of the direct and indirect actions of vitamin D on bone mineral metabolism, the consequences of nutritional imbalances of this nutrient in small animals, as well as differences in vitamin D metabolism between different size dogs.

Total serum magnesium in cats with chronic kidney disease with nephrolithiasis.

OBJECTIVES: Magnesium has been 'the forgotten ion' for many years. Over the past decade, however, the role of magnesium in essential physiological functions and several illness conditions have been elucidated. Nevertheless, the investigation of magnesium in cats with chronic kidney disease (CKD) and nephrolithiasis is yet to be determined. The purpose of this study was to investigate whether CKD cats with nephrolithiasis have changes in total serum magnesium concentrations, and whether magnesium disorders may be associated with other electrolyte disturbances, as well as with prognosis. We also aimed to evaluate whether total serum magnesium concentration differs between CKD cats with and without nephrolithiasis. METHODS: Total serum magnesium concentrations were assessed in 42 cats with CKD with stage 1-4 nephrolithiasis. The correlation between magnesium and other electrolytes, as well as Kaplan-Meier survival analysis, were performed. We also selected 14 control cats with CKD without nephrolithiasis age-matched with 14 cats with CKD with nephrolithiasis. RESULTS: Hypermagnesemia was observed in 16/42 (38.1%) and hypomagnesemia in 6/42 (14.3%) cats. Serum magnesium abnormalities were observed in cats of all stages, and marked hypermagnesemia was noted in cats with stage 4 CKD with nephrolithiasis (P <0.001). There was a negative correlation between total serum magnesium and ionized calcium (r = -0.64; P <0.01), and a positive correlation between total serum magnesium and serum phosphorus (r = 0.58, P = 0.01). Cats with CKD with nephrolithiasis and hypomagnesemia or hypermagnesemia had higher mortality than those with normal total serum magnesium concentration (P <0.01), regardless of CKD stage. There was no difference in total serum magnesium concentration between CKD cats with and without nephrolithiasis. CONCLUSIONS AND RELEVANCE: Cats with CKD with nephrolithiasis have magnesium abnormalities. Hypomagnesemia and hypermagnesemia were associated with an increase in mortality, and thus total serum magnesium abnormalities may be used as prognostic factors in these cases.

Urinary Fractional Excretion of Phosphorus in Dogs with Spontaneous Chronic Kidney Disease.

The increase of urinary fractional excretion of phosphorus (uFEP) may indicate phosphorus retention before the onset of hyperphosphatemia in the early stages of chronic kidney disease (CKD). The hypothesis of this study is whether uFEP may increase during the early stage of CKD as a compensatory mechanism to prevent hyperphosphatemia as well as whether hyperphosphatemia in the late stages is associated with increase or decrease in uFEP in dogs with naturally occurring CKD; therefore, the aim of this study was to determine the uFEP in CKD dogs with different stages. Forty-nine CKD dogs were included, and they were divided into stage 1 (serum creatinine < 1.4 mg/dL), stage 2 (serum creatinine 1.5 to 2.0 mg/dL), stage 3 (serum creatinine 2.1 to 5.0 mg/dL) and stage 4 (serum creatinine > 5.0 mg/dL), according to the IRIS staging criteria. The stage 3 was subdivided into stage 3-A (serum creatinine 2.1 to 3.5 mg/dL) and stage 3-B (serum creatinine 3.6 to 5.0 mg/dL). The control group comprised 10 dogs, and uFEP ≤ 40% was considered as normal. A progressive increase in uFEP along the progression of CKD was found. However, similar results of uFEP levels were observed in late CKD, since there were no differences between stages 3 (A, B) and 4. Interestingly, some CKD dogs with stage 4 showed normal or reduced uFEP, besides hyperphosphatemia; conversely, some dogs in early CKD had increased uFEP values and normophosphatemia. Our findings suggest that uFEP may act as a compensatory mechanism to avoid the onset of hyperphosphatemia in early CKD, but not in later stages. uFEP assessment may be considered as an additional tool for the diagnostic and monitoring of phosphate disorders in dogs with CKD, since it may help to identify disturbances of phosphorus balance. More studies are needed to elucidate the role of uFEP in phosphorus homeostasis in dogs with CKD.

Urinary Tamm-Horsfall protein, albumin, vitamin D-binding protein, and retinol-binding protein as early biomarkers of chronic kidney disease in dogs.

Proteinuria is a marker and mediator of chronic kidney disease (CKD). In clinical practice, the urinary protein-to-creatinine ratio (UP/C) is of limited usefulness, because it indicates only the magnitude of proteinuria and not the origin of the loss (glomerular or tubular). The complete assessment of proteinuria includes quantitative and qualitative evaluations, both of which are required in order to optimize the therapy. In addition to measuring the UP/C, we performed SDS-PAGE and western blotting to determine the expression of albumin, vitamin D-binding protein (VDBP), retinol-binding protein (RBP), and Tamm-Horsfall protein (THP) in urine samples of 49 dogs: healthy (control) dogs (n = 9); and dogs with CKD (n = 40), stratified by stage. In the dogs with stage 3 or 4 CKD, there was a predominance of tubular proteins. Neither VDBP nor RBP was observed in the urine of the control dogs. Among the dogs with stage 1 or 2 CKD, VDBP and RBP were detected in those without proteinuria or with borderline proteinuria. The expression of urinary albumin was significantly higher in the stage 4 group than in any other group (P ≤ 0.01). In the stage 4 group, urinary THP was either undetectable or lower than in the control group (P ≤ 0.01). In conclusion, urinary VDBP and RBP might act as early markers of kidney injury, and a decrease in urinary THP could be an indicator of CKD progression.