Acute kidney injury (AKI), an abrupt loss of renal function, is a commonly encountered emergency in small animal practice. This article, the first of two on AKI, reviews the pathophysiology and diagnosis of the condition in dogs and cats. The second article, to be published in the June issue of In Practice, will cover the treatment, recovery and prognosis associated with AKI.
An 11-month-old Border collie presented collapsed and continued to deteriorate rapidly despite supportive treatment. The dog had a history of failure to thrive and recurring respiratory infection. Laboratory abnormalities included neutrophilic leucocytosis, Heinz body anaemia, hyperammonaemia, hyperbilirubinaemia, proteinuria and hypocobalaminaemia. Post-mortem examination revealed multi-focal necrosis within the heart, kidneys, pancreas, liver, meninges and cerebral cortex. Fungal hyphae in lesions were identified as Scedosporium prolificans following culture. Subsequent genotyping confirmed that the dog carried the CUBN:c.8392delC mutation in a homozygous state, verifying hereditary cobalamin deficiency (a.k.a. Imerslund-Gräsbeck syndrome). Cobalamin deficiency may have been a predisposing factor for the development of systemic fungal infection in this dog.
A two-year-old female neutered Tibetan terrier was referred following a one-month history of lethargy, inappetence and pancytopenia, which had been poorly responsive to immunosuppressive and fluoroquinolone treatment. The dog was diagnosed with pure red cell aplasia and was found to be positive for Ehrlichia canis by both antibody titre measurement and polymerase chain reaction. The dog lived in London and had not travelled outside the UK. The dog was treated with doxycycline, prednisolone and ciclosporin, but died as a result of gastrointestinal tract haemorrhage. To the authors' knowledge, this represents the first reported case of Ehrlichia canis in a dog in the UK with no previous travel history.
Acute kidney injury (AKI) is a commonly encountered emergency in small animal practice. Dogs and cats with AKI are mostly presented in the maintenance phase of the disease, by which point renal function has been severely compromised and clinical signs are apparent. The first article in this two-part series, which was published in the May issue of In Practice discussed the pathogenesis and diagnosis of AKI. This article considers both specific therapy and general supportive treatment in dogs and cats.
The use of human serum albumin (HSA) is described in dogs receiving critical care. However, despite the high degree of homology, anaphylactic and delayed hypersensitivity reactions are reported. Delayed type III hypersensitivity reactions can lead to glomerulonephritis and acute kidney injury (AKI). Undiluted 20% HSA was administered to a 4.8 yr old intact male Labrador Retriever with severe hypoalbuminemia, following surgical management of septic peritonitis of gastrointestinal origin. Nineteen days after HSA administration, the dog developed peracute high magnitude renal proteinuria and AKI. Rapid immunosuppression, using a combination of prednisolone and mycophenolate mofetil, resulted in full resolution of AKI, hypoalbuminemia, and proteinuria. Addition of mycophenolate mofetil may have resulted in the first documented case of full renal recovery from hypersensitivity-induced AKI caused by HSA administration.
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