Dogs with protein-losing enteropathy (PLE) are suggested to be at increased risk of developing thromboembolic events. However, with some exceptions, there are very few reports of thromboembolism in such dogs. This multicentre retrospective observational study describes a case series of thromboembolism (TE) in eight dogs with PLE secondary to non-neoplastic, chronic small intestinal disease. Seven dogs had poorly controlled PLE when the thromboembolic event occurred. Pulmonary thromboembolism (PTE) occurred in six dogs, while one dog developed splenic vein thrombosis and another had concurrent splenic vein and aortic TE. Six dogs died, all with PTE. Antithrombin activity was decreased in one of two dogs in which it was measured. Serum cobalamin and folate concentrations were measured in three dogs and cobalamin was subnormal in all three. Serum magnesium, measured in two dogs, was low in both. Dogs with uncontrolled chronic small intestinal disease and PLE are at risk for developing serious life-threatening TE, mostly PTE.

XANTHINE urolithiasis is uncommon in dogs, with case series giving a prevalence of between 0.07 and 0.46 per cent (Houston and Moore 2009, Osborne and others 2009, Low and others 2010). The most common cause of canine xanthinuria is iatrogenic when allopurinol is administered, inhibiting xanthine dehydrogenase (XDH) (Bartges and Kirk 2008). In human beings, primary xanthinuria may be caused by enzyme deficiency or a cofactor abnormality. XDH deficiency may be isolated (type I), due to a missense mutation in the encoding gene for XDH, or in association with aldehyde oxidase deficiency, due to a missense mutation of the MCSU gene. Both are inherited in an autosomal recessive manner (Levartovsky and others 2000, Ichida and others 2001). Human beings with these defects may be asymptomatic with incidental hypouricaemia (Holmes and others 1974). Clinical signs, when they occur, are related to muscle deposition of xanthine causing myopathy, or renal dysfunction due to renal deposition (Nyhan 2005). A final cause of primary xanthinuria is an abnormality of the molybdenum cofactor required by xanthine oxidase, aldehyde oxidase and sulphite oxidase. Sulphite oxidase deficiency results in dramatic clinical signs of neonatal seizures and ophthalmic abnormalities (Wadman and others 1983). Xanthine uroliths appear uncommon in cats, with a prevalence of 0.1 per cent reported in uroliths submitted to the Minnesota Urolith Center, USA (Osborne and others 2004). There are case reports of xanthinuria in two domestic shorthair cats and one Himalayan cat (White and others 1997, Tsuchida and others 2007, Schweighauser and others 2009). Single nucleotide polymorphism analysis of the XDH gene in a xanthinuric Himalayan cat suggested that it had two distinct alleles, making type I xanthinuria unlikely (Tsuchida and others 2007). Primary xanthinuria appears to be rare in dogs, with cases reported in eight dachshunds, two related Cavalier King Charles spaniels (CKCS) in the Netherlands, one CKCS each in Germany and Sweden, and one King Charles spaniel in the UK in which xanthine uroliths were identified postmortem (

Dogs with primary hepatopathies have increased concentrations of whole blood manganese although these concentrations are not as high as those in dogs with congenital portosystemic shunts. The role of altered manganese homeostasis in canine hepatic encephalopathy is worthy of further study.

Asymptomatic xanthinuria was not detected in this UK Cavalier King Charles spaniel population. This data may be used as a reference for urinary purine metabolite concentrations in the dog.