MORPHOLOGICAL AND MORPHOMETRIC CHANGES IN THE KIDNEYS IN EXPERIMENTAL ULCERATIVE COLITIS. LITERATURE REVIEW

Аннотация

Ulcerative colitis (UC) is a chronic inflammatory bowel disease that primarily affects the colon and rectum, but it is also associated with extra-intestinal manifestations, including renal dysfunction. The kidneys in experimental UC models, particularly those induced by dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS), exhibit several morphological and morphometric changes. These include inflammation, edema, glomerular damage, interstitial fibrosis, and altered renal blood flow, which can lead to impaired kidney function. The pathophysiological mechanisms behind renal involvement in UC are multifactorial, with systemic inflammation, oxidative stress, and ischemia playing key roles. The article provides a comprehensive review of the morphological and morphometric alterations in the kidneys observed in experimental UC models, discusses the potential underlying mechanisms, and highlights therapeutic interventions aimed at mitigating kidney damage. A better understanding of these changes is crucial for developing strategies to prevent renal complications inpatients with UC. Keywords: ulcerative colitis (UC), renal changes, experimental models, morphological alterations. morphometric changes, inflammation, kidney fibrosis, glomerular damage, oxidative stress, renal dysfunction, therapeutic interventions, systemic inflammation, kidney pathology Introduction. Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease (IBD) that primarily affects the colon and rectum. It is characterized by inflammation, ulceration, and mucosal damage of the gastrointestinal tract. Although UC primarily involves the digestive system, numerous studies have highlighted its extra-intestinal manifestations, affecting various organ systems, including the kidneys. Renal involvement in UC is increasingly recognized, and while its precise pathophysiology remains unclear, it has been postulated that both direct and indirect mechanisms contribute to renal dysfunction inthis disease. The Kidney-UC Link. Although the kidneys are not the primary target of UC, there is accumulating evidence suggesting that UC-associated inflammation has significant renal implications. Experimental studies in animals, particularly those using rodent models of UC, have demonstrated a variety of morphological and functional changes in the kidneys, some of which mimic those seen in human patients with UC (Gul et al., 2016). Animal models of UC, often induced by chemicals such as dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS), have proven invaluable in investigating these renal abnormalities and understanding theirunderlying mechanisms (Kant et al.,2018; Sharmaet al., 2019). 98,7:ROTCAFTCAPMI .SECNEICSLACIDEM,5202,yaM,5emuloV gro.srehsilbupcimedaca.www The systemic inflammation observed in UC patients is believed to be a major contributor to renal pathology. Pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6), which are elevated during UC flare-ups, can reach distant organs, including the kidneys, through the bloodstream (Torres et al., 2017). The kidneys, being highly vascular organs, are particularly susceptible to these systemic inflammatory signals. Moreover, UC-related renal abnormalities extend beyond inflammation alone. In experimental models, renal changes can range from glomerular damage, interstitial fibrosis, and tubular alterations to altered kidney size and function (Iglesias et al., 2020). Renal fibrosis, a key feature of chronic kidney disease (CKD), has been observed in UC-induced models, often as a result of the inflammatory cascade and oxidative stress (Sleiman et al., 2017). These structural changes can lead to kidney dysfunction, manifesting as proteinuria, impaired glomerularfiltration rate (GFR), andelectrolyte imbalances (Singh et al.,2021). Morphological and Morphometric Kidney Changes in UC. The kidneys in experimental UC models show a wide range of morphological changes, which are indicative of the kidney's response to chronic systemic inflammation. Studies have noted alterations inkidney size, glomerular architecture, and tubular structure, often characterized by glomerulosclerosis, tubulardilation, and interstitial fibrosis (Liu et al., 2018; Alimohammadi et al., 2019). Morphometric analysis, which quantifies these structural changes, is a valuable tool in assessing the severity of kidney damage in UC models (Gao et al., 2020). These alterations can be used as biomarkers of kidney injury and provide insight into the extent of renal involvement in UC. Ulcerative Colitis. Ulcerative colitis (UC) is a chronic inflammatory bowel disease primarily affecting the colon and rectum, characterized by recurrent symptoms and significant morbidity. The exact etiology of UC remains unknown, though it is thought to involve a complex interplay of genetic, environmental, and immunological factors[1][2]. The disease manifests through