# Addisonian Crisis Mimicking Acute Kidney Injury in Dogs: A Retrospective Study of 34 Dogs Diagnosed with Acute Kidney Injury in Romania

## TL;DR

This study shows that Addison’s disease in dogs can look like acute kidney injury, and early diagnosis is crucial to avoid serious complications.

## Contribution

The study highlights the importance of considering Addison’s disease in dogs with AKI and electrolyte imbalances to prevent misdiagnosis.

## Key findings

- Three out of 34 dogs diagnosed with AKI had primary hypoadrenocorticism.
- Electrolyte and renal parameters normalized after hormone replacement therapy.
- Early endocrine evaluation is essential to differentiate Addison’s disease from true AKI.

## Abstract

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.