Abstract
Background:
Hyperkalemia has multiple etiologies, and although primary adrenocortical insufficiency is a well-known hormonal cause, hyperkalemia may also result from hyporeninaemic hypoaldosteronism, in which impaired renin secretion reduces aldosterone production and mineralocorticoid activity.

Case Description:
A 15-year-old spayed female Miniature Dachshund presented with persistent hyperkalemia. The dog exhibited systemic hypertension (systolic blood pressure: 192 mmHg) and mild renal insufficiency without evidence of urinary obstruction, hemolysis, cellular lysis, or potassium-sparing drug administration. An ACTH stimulation test revealed normal cortisol concentrations (pre: 4.3 µg/dL; post: 20.7 µg/dL), excluding primary hypoadrenocorticism. The plasma renin activity (PRA) and aldosterone concentration were evaluated. PRA was undetectable (<0.2 ng/mL/h), and aldosterone concentrations were low before (<17 pg/mL) and after (124.6 pg/mL) ACTH stimulation. These findings supported hyporeninaemic hypoaldosteronism with concurrent renal insufficiency and hypertension. Fludrocortisone therapy (0.05–0.1 mg/kg PO SID) successfully reduced plasma potassium to 5.2–5.4 mEq/L. Hydralazine (2 mg/kg PO BID) was administered for blood pressure control. The dog remained clinically stable before dying of aspiration pneumonia on day 94.

Conclusion:
Renal insufficiency, metabolic acidosis, hypertension, suppressed PRA, and low aldosterone levels supported the diagnosis of acquired type IV renal tubular acidosis. Hyperkalemia responded well to mineralocorticoid supplementation. In dogs with renal disease and persistent hyperkalaemia, hyporeninaemic hypoaldosteronism should be considered, and measurement of PRA and aldosterone is recommended when primary adrenal insufficiency is excluded.

Key words: Aldosterone; Hyperkalaemia; Hyporeninaemic hypoaldosteronism; Renin; Type IV renal tubular acidosis.