Presentation Description / Session Abstract: Phosphate overload as a result of dietary phosphate intake exceeding renal excretion on a daily basis is a feature of early stage CKD. Whilst plasma phosphate concentration does not increase until later stages (IRIS CKD stage 3 for example), phosphate accumulation is occurring in some cats long before plasma phosphate increases. This is important as accumulation of phosphate may lead to soft tissue mineralisation (kidneys and vasculature in particular). Vascular calcification, in particular, is a significant risk factor for cardiovascular problems in human patients. Magnesium is recognised as an important element protecting against vascular calcification, a phenomenon that is poorly understood but one which leads to significant morbidity and mortality of CKD human patients. However, restriction of dietary intake of phosphate in cats with CKD is not appropriate or necessary for all cats with early stage CKD and may increase the risk of hypercalcaemia occurring in some. Understanding the role of FGF23 and alpha-klotho in the regulation of phosphate and calcium at an early stage may become important to tailoring the management and monitoring of CKD feline patients to ensure their diet is optimal for their stage of CKD and their individual physiology.
Bone and mineral disturbances are common, even prior to the onset of azotemia, in the feline CKD patient
Not all feline CKD patients in the early stages need phosphate restriction and understanding the hormonal adaptations to phosphate overload may help define those needing treatment and avoid the problem of diet induced hypercalcaemia
Serum magnesium is important to measure in cats with CKD as it impacts on the severity of bone mineral disturbances