Effect of trilostane treatment on proteinuria secondary to spontaneous hypercortisolism in dogs.

Trilostane reduces proteinuria in ~48% of hypercortisolemic dogs, with improvement evident by 3 months.

This retrospective longitudinal cohort study evaluated the effect of trilostane on proteinuria in 160 dogs diagnosed with spontaneous hypercortisolism (HC), of which 89% had pituitary-dependent and 10% had adrenal-dependent HC. At diagnosis, 64% of included dogs were proteinuric. Urine protein-to-creatinine ratio (UPC), disease clinical score (DCS), blood pressure (BP), and daily trilostane dosage (TD) were monitored at 30, 90, 180, and 365 days post-treatment initiation. A statistically significant reduction in UPC over time was demonstrated (P = .0005), with meaningful decreases evident at 90, 180, and 365 days compared to baseline. Responders were defined as dogs achieving ≥50% UPC reduction or a final UPC <0.5. Of the 76 dogs evaluable at last follow-up, 48% were classified as responders. Compared to nonresponders, responders exhibited significantly lower median DCS, BP, and TD, suggesting that better overall disease control—even at lower trilostane doses—correlates with proteinuria resolution. Notably, 52% of proteinuric dogs did not respond adequately, highlighting that trilostane alone may be insufficient to resolve proteinuria in a substantial proportion of HC patients. These findings suggest that while trilostane can induce sustained proteinuria reduction in some dogs with HC beginning at approximately 3 months of treatment, concurrent management of hypertension and clinical signs remains critical. Additional therapies targeting proteinuria may be warranted in nonresponders.

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