Genetic polymorphisms and acute kidney injury

Acute kidney injury (AKI) is one of the most serious complications of infectious diseases, occurring in 5% to 30—50% of hospitalized patients. Despite advances in the treatment of AKI, including renal replacement therapy, morbidity and mortality rates continue to rise. There is significant variability in the clinical manifestations of AKI among patients with identical pathology, highlighting the need to study additional factors that influence the severity and outcomes of the disease. Genetic variability, including gene polymorphisms that determine individual characteristics of regulatory mechanisms in kidney damage, may play an important role in this process. This article aims to analyze existing data on the impact of genetic factors on the development and outcomes of AKI, as well as gene polymorphisms that may serve as diagnostic criteria for early detection and risk of AKI. The focus is on genes associated with the inflammatory response, such as TNF-á, IL-1â, IL-6, IL-8, IFN-ã, TGF-â, and IL-10, and their potential role in predisposition to AKI and disease progression. The influence of genetic variations in vasomotor regulatory proteins, such as angiotensin-converting enzyme (ACE) and endothelial nitric oxide synthase (eNOS), on the development of AKI is also discussed. The relationship between polymorphisms in the BCL2 and SERPINA genes and AKI, as well as between polymorphisms in the SERPINA4 and SERPINA5 genes and the development of AKI in COVID-19 patients, is analyzed. Despite numerous studies and identified associations, data on genetic risk factors remain limited and contradictory, underscoring the need for further research. The identification of new genetic markers will help improve diagnosis and provide a personalized approach to the prevention and treatment of AKI, especially in children with a high predisposition to this condition.

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