Primary hypoadrenocorticism (Addison’s disease) is an uncommon but potentially life-threatening endocrine disorder in dogs. Affected animals may present with clinicopathological features mimicking acute kidney injury (AKI). The challenge in diagnosing hypoadrenocorticism arises from its highly heterogeneous and non-specific clinical presentation, including acute kidney injury (AKI). This retrospective observational study aimed to evaluate dogs presenting with AKI and to identify cases in which primary hypoadrenocorticism was the underlying etiology. Thirty-four dogs diagnosed with acute kidney injury were evaluated at the Clinical Hospital for Companion Animals of the “Ion Ionescu de la Brad” University of Life Sciences, Iași, Romania, among which three (8.8%) were endocrinologically confirmed to have primary hypoadrenocorticism. The evaluation protocol included a complete clinical examination, hematological, biochemical, and hormonal investigations, urinalysis, abdominal ultrasonography, and an ACTH stimulation test. These dogs exhibited hyponatremia, hyperkalemia, a reduced sodium-to-potassium ratio, and azotemia at admission, closely resembling intrinsic AKI. Following fluid therapy and hormone replacement, rapid normalization of electrolyte and renal parameters was observed. These findings support hypovolemia and electrolyte imbalance as the primary mechanisms underlying reversible prerenal azotemia in these cases. If not diagnosed early, this condition has a significant risk of progressing to acute tubular necrosis. The findings highlight the need for careful differentiation between primary AKI and renal dysfunction secondary to Addison’s disease, as well as the importance of promptly initiating hormone replacement therapy. In conclusion, hypoadrenocorticism should be considered in dogs presenting with AKI and electrolyte imbalance. Early endocrine evaluation and prompt initiation of targeted therapy are essential to avoiding misdiagnosis and optimizing clinical outcomes.

Mesenteric abscesses are an uncommon cause of septic peritonitis in dogs, and serial quantitative monitoring of bacterial load in peritoneal exudate has rarely been reported. This case report describes the diagnostic work-up and treatment response of a 14-month-old, 33 kg intact male Cane Corso with a mesenteric abscess complicated by septic peritonitis, two weeks after treatment for babesiosis. The dog presented with a 72 h history of anorexia, vomiting, and abdominal pain. Abdominal radiography revealed decreased peritoneal serosal contrast and findings suggestive of foreign material ingestion. Serial ultrasonography identified a mesenteric abscess with peritoneal effusion. Exploratory laparotomy confirmed the diagnosis; the abscess was excised, and the abdominal lavage was performed. Histopathology confirmed a mesenteric abscess with marked neutrophilic infiltration. Bacterial culture isolated Escherichia coli and Enterococcus faecium, with antimicrobial therapy guided by susceptibility testing. Serial quantitative bacterial counts of the peritoneal exudate on three postoperative occasions showed a progressive decline, paralleling clinical and hematological improvement. The dog fully recovered, with complete clinical and laboratory normalization confirmed at the 60-day reassessment. This case suggests that a multimodal diagnostic approach may assist in guiding management and confirming treatment response in canine mesenteric abscess with septic peritonitis, although the role of serial quantitative monitoring requires further evaluation.