Ștefania RoșCa

Serum phenobarbital (PB) monitoring is recommended after treatment initiation and periodically thereafter, but real-world data on monitoring practice are scarce, particularly where imepitoin is not marketed and PB is a controlled substance. All in-house PB determinations performed on a point-of-care analyser reporting PB with a hepatic panel at a Romanian university referral hospital between January 2022 and August 2026 were retrieved and linked to the hospital register. A total of 143 canine runs from 66 dogs were obtained; 10 (7.0%) were suppressed by severe lipaemia. At the first valid determination, 47 of 65 dogs with a valid result (72.3%; 95% CI 60.4–81.7) were within the 15–35 µg/mL target range and 16 (24.6%; 95% CI 15.8–36.3) were below it. The median dose, given as fractionated human 100 mg tablets, was 5.62 mg/kg/day and was not associated with concentration; dogs under 10 kg received almost twice the weight-based dose of larger dogs without reaching higher concentrations. Alkaline phosphatase was increased in 36% of runs and was not associated with concentration in mixed-effects models. At least one determination was obtained in 79% of dogs in continued care and 88% of dogs with six or more prescriptions, but only 40% (95% CI 27–56%) of newly treated dogs were determined within 90 days and none of the 17 dogs seen only once or twice after initiation was determined. Monitoring therefore follows continuity of care; scheduling the first determination at initiation and coupling sampling with prescription renewal are proposed measures whose effectiveness requires prospective evaluation.

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.