Oxaluria in inflammatory bowel diseases (review)

   AIM: to analyse and synthesize Russian and foreign literature, to get acquainted with the concept of oxaluria, its types, transport mechanisms of oxalate transport in the intestine and the relationship between hyperoxaluria and inflammatory bowel diseases in order to identify possible options for therapeutic action on the mechanisms of development of these pathologies.   MATERIALS AND METHODS: the literature review was based on the Internet data, including bibliographic directories, books, journals, and original articles. The literature sources used for the article reflect the essence of the described problem to the fullest extent possible and can be useful for both practicing physicians and students of medical universities.   RESULTS: the gastrointestinal tract through epithelial transport of oxalate plays an exclusive role in oxalate homeostasis and hyperoxaluria. Metabolism of dietary oxalate and the formation of endogenous oxalate, its secretion, absorption, transport and biodegradation by intestinal microflora may influence the excretion of this compound by the kidneys. Knowledge of the interrelated relationships of the gut-kidney axis, mechanisms of transport, transport and biodegradation of oxalate, especially in inflammatory bowel disease, is of great importance for understanding the pathophysiology of hyperoxaluria as a risk factor for urinary stone formation with a point of pharmacological action in the gut. This literature review introduces the concept and forms of oxaluria, shows the classification of oxaluria, describes each form, and broadly explains the metabolism and mechanisms of oxalate transport in the human body. Special attention is given to intestinal hyperoxaluria and anion exchangers belonging to the large multifunctional SLC26 gene family, most of which are expressed throughout the gastrointestinal tract. The authors emphasise their current role in intestinal oxalate transport, as well as methods of possible drug action on the mechanisms of hyperoxaluria.   CONCLUSION: a multidisciplinary approach is needed to address the problems of intestinal hyperoxaluria and, consequently, the treatment of urolithiasis. The role of newly identified intestinal and renal anion exchangers is not fully understood, hence the targets and mechanisms of action on these types of exchangers with the possibility of preventing the development of urolithiasis are not fully understood. Further randomised studies on the problem under investigation are needed.