The aim of this study was to evaluate the role of aldosterone as an initiating and/or perpetuating factor in hypertension associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Thirteen dogs with PDH and 11 healthy control dogs were used. In all dogs, arterial blood pressure and plasma sodium, potassium, basal aldosterone, post-ACTH aldosterone, basal cortisol and post-ACTH cortisol concentrations were measured. The tests were repeated 10 days and three months after the beginning of o,p'-DDD treatment in PDH dogs. In untreated PDH dogs, plasma aldosterone was significantly decreased, whereas cortisol, sodium and arterial blood pressure were significantly increased compared to healthy dogs. Hypertension remained in most treated PDH dogs despite normalisation of cortisol and persistently low aldosterone levels. These results did not demonstrate that aldosterone is involved in the development and perpetuation of hypertension in PDH. However, glucocorticoids seemed to play a major role as an initiating and perpetuating factor in PDH in dogs.

One hundred and four dogs with clinical signs of urinary tract infection were selected by 15 practitioners in a multicentric, controlled and randomised study. The clinical diagnosis was confirmed by urinalysis and imaging. Each dog received either marbofloxacin (2 mg/kg orally once daily or 4 mg/kg by subcutaneous injection every four days) or amoxicillin-clavulanic acid tablets (12.5 mg/kg twice daily) for 10 or 28 days, depending on the clinical diagnosis. Rectal temperature, general condition, appetite, urinary signs, defecation disorders and pain on abdominal palpation were monitored at each visit, the timetable depending on diagnosis: three urinalyses and at least three examinations per case were performed. Side effects were also thoroughly sought at each examination. Marbofloxacin and amoxicillin-clavulanic acid both yielded good bacteriological cure rates (96.2 per cent versus 85.0 per cent, respectively) and clinical cure rates (83.3 per cent versus 69.7 per cent). Fewer relapses were observed in those dogs that received marbofloxacin. Few mild side effects were recorded with both products.

Simultaneous measurement of both urea and creatinine is of limited diagnostic value over the analysis of a single variable. Creatinine is the preferred analyte as it is affected by fewer extrarenal factors of variation.

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BackgroundChronic kidney disease (CKD) is an important cause of morbidity and mortality in dogs.ObjectiveTo evaluate the efficacy in prolonging survival and safety of benazepril administration to dogs with CKD.AnimalsForty‐nine client‐owned dogs with CKD.MethodsDogs were randomized to benazepril (0.25 to <0.5 mg/kg) or placebo once daily for up to 2 years in a prospective, multicenter, blinded clinical trial. The primary endpoint variable was the renal survival time, defined as the time from inclusion in the study to the treatment failure endpoint of death or euthanasia or need for administration of parenteral fluids related to renal failure.ResultsNo benefit of benazepril versus placebo was detected for renal survival time in all dogs; median (95% confidence interval (CI)) survival times were 305 (53–575) days in the benazepril group and 287 (152‐not available) in the placebo group (P = .53). Renal survival times were not significantly longer with benazepril compared to placebo for subgroups: hazard ratios (95% CI) were 0.50 (0.21–1.22) with P = .12 for initial urine protein‐to‐creatinine ratio (UPC) >0.5, and 0.38 (0.12–1.19) with P = .080 for initial UPC >0.5 plus plasma creatinine ≤440 μmol/L. Proteinuria, assessed from the UPC, was significantly (P = .0032) lower after treatment with benazepril compared to placebo. There were no significant differences between groups for clinical signs or frequencies of adverse events.Conclusions and Clinical RelevanceBenazepril significantly reduced proteinuria in dogs with CKD. Insufficient numbers of dogs were recruited to allow conclusions on survival time.