Objectives The aim of this case-control study was to identify early-life risk factors associated with the occurrence of owner-reported mobility changes in 6-year-old cats by examining prospective data from a longitudinal cohort study of pet cats, the Bristol Cats study. Methods Data on potential risk factors were obtained from seven sequential questionnaires completed between the ages of 2–4 months and 5 years. Mobility-related questions from the study questionnaire distributed at the age of 6 years were used to calculate each cat’s mobility score. Cats with mobility scores of ⩾2 and 0 were allocated to the case and control groups, respectively, and the cat’s status was the outcome variable. Results Of the 799 cats included for analysis, 238 (29.8%) had owner-reported mobility changes. Binomial logistic regression using backwards elimination identified four risk factors for owner-reported mobility changes at 6 years of age: entire neuter status at 6 months of age (odds ratio [OR] 1.97; 95% confidence interval [CI] 1.26–3.07), sustained trauma before 6 years of age (OR 1.85; 95% CI 1.30–2.60), outdoor access at 6 years of age (OR 1.67; 95% CI 0.96–2.90) and overweight/obese status at 6 years of age (OR 1.62; 95% CI 1.13–2.33). Conclusions and relevance Risk factor analysis demonstrated that obesity, outdoor access and a history of trauma may predispose cats to developing owner-reported mobility changes associated with degenerative joint disease, whereas neutering before 6 months of age appears to decrease that risk.

Chronic kidney disease (CKD) is defined as a chronic sustained reduction in renal function and/or structural change. CKD therefore, by this definition, includes patients with tubulointerstitial nephritis, considered the typical finding in CKD, and also patients with primary glomerular disease. The distinction between these is important as they may differ in aetiology and approach to management. In patients with CKD, proteinuria can develop as a result of tubular or glomerular injury. In addition, proteinuria may cause renal injury and contribute to the progression of CKD. This article will review the pathophysiology of proteinuria in CKD, its diagnostic workup and management.

Objectives The aim of this blinded, nested case-control study was to compare cats with and without early owner-reported mobility changes using subjective and objective outcome measures (owner-completed questionnaires, orthopaedic examination). Methods A total of 57 cats with and without early owner-reported signs of impaired mobility were allocated to the case (n = 30) and control (n = 27) groups, respectively. Participating owners completed one inclusion and two pre-visit questionnaires (Feline Musculoskeletal Pain Index, VetMetrica). Cats were then visited in their own homes, where they underwent an orthopaedic examination, an assessment of their body condition score and temperament, and the placement of an accelerometer on their collar for 2 weeks. Results There was no significant difference between groups for age category, breed, sex, temperament and body condition score. Case cats scored significantly lower for the Feline Musculoskeletal Pain Index ( P = 0.003) and the VetMetrica domain of Comfort ( P = 0.002), but not Vitality ( P = 0.009) or Emotional Wellbeing ( P = 0.018). Total pain ( P <0.0001), crepitus ( P = 0.002) and thickening ( P = 0.003) scores were higher in case cats, as was the presence of bilateral disease ( P = 0.005, odds ratio 14) and the number of bilaterally affected joints ( P = 0.001). Conclusions and relevance Both the Feline Musculoskeletal Pain Index and orthopaedic examination were able to differentiate cats with early owner-reported signs of impaired mobility from healthy cats. VetMetrica Comfort domain scores indicated a compromised quality of life for cats with early owner-reported signs of impaired mobility compared with healthy cats. Being able to recognise signs of mobility impairment earlier would allow interventions aimed at slowing disease progression, thereby improving feline health and welfare.

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Calcitonin, released by C-cells of the thyroid gland in response to increased serum ionised calcium concentration (iCa), protects against hypercalcaemia by inhibition of osteoclasts, but does not have an important physiologic role in all species. In cats, experimentally-induced hypercalcaemia elicits a calcitonin response in some but not all animals, possibly causing non-responders to be more susceptible to hypercalcaemia. Ionised hypercalcaemia is increasingly recognised in cats, some of which have chronic kidney disease (CKD). The aim of this study was to explore the calcitonin response to ionised hypercalcaemia in cats with CKD. Twenty-eight cats diagnosed with CKD (including 13 cats developing hypercalcaemia within 8 months) were selected for this retrospective observational cohort study. iCa >1.40 mmol/L was classified as hypercalcaemia. Calcitonin was measured by