Background <p>Feline infectious peritonitis (FIP) is a fatal, immune-mediated disease caused by the mutagenic variants of feline coronavirus and manifests as effusive (wet) and non-effusive (dry) clinical forms with distinct pathological features. Although necrosis is a common histopathological finding in FIP, the contribution of specific regulated cell death (RCD) pathway-associated protein expression patterns to tissue injury across different clinical forms remains poorly understood. This study aimed to concurrently and comparatively evaluate apoptosis, necroptosis, autophagy-associated cell death, and ferroptosis in the renal tissues of cats with effusive and non-effusive FIP.</p> Methods <p>Archival kidney samples from cats diagnosed with effusive (<i>n</i> = 18) and non-effusive (<i>n</i> = 18) FIP were included in the study. Immunohistochemistry on tissue sections was performed to assess markers associated with apoptosis by Caspase-3 and Caspase-8, necroptosis-associated signaling by RIP3, autophagy-associated activity by LC3-II, and ferroptosis-associated lipid metabolic susceptibility by ACSL-4. Necrosis was evaluated histomorphologically using a semi-quantitative scoring system, and immunohistochemical expression levels were digitally quantified and statistically compared between the groups.</p> Results <p>Histopathological evaluation revealed widespread tubular degeneration and necrosis in both clinical forms, with no significant difference in necrosis scores between the effusive and the non-effusive FIP. In contrast, quantitative differences in RCD-associated marker expression were identified. The non-effusive form exhibited significantly higher Caspase-3, Caspase-8, and LC3-II immunoreactivity, suggesting a higher prevalence of markers associated with caspase-dependent apoptosis and autophagy-associated activity. Conversely, RIP3 and ACSL-4 immunoreactivity were significantly increased in the effusive form, indicating increased expression of markers associated with necroptosis-related and ferroptosis-related processes. All evaluated markers were detected in both disease forms, indicating overlapping expression profiles rather than mutually exclusive pathway involvement.</p> Conclusion <p>Collectively, these findings indicate that RCD-associated proteins are differentially expressed in the effusive and the non-effusive FIP, reflecting quantitative differences in marker expression rather than definitive evidence of pathway-specific activation. While the non-effusive form showed higher expression of markers associated with caspase-dependent apoptosis and autophagy-associated activity, the effusive form exhibited increased expression of proteins related to proinflammatory and oxidative cell death-associated pathways. These findings provide a descriptive immunohistochemical profile of cell death-associated markers in renal lesions of FIP and highlight the need for future studies using complementary molecular and protein-based approaches to further clarify their functional significance.</p>