Role of mitochondrial function in the transition from Acute to Chronic Kidney Injury

• Grant number: 23/14011-6
• Support Opportunities: Scholarships in Brazil - Program to Stimulate Scientific Vocations
• Start date: January 08, 2024
• End date: February 27, 2024
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Niels Olsen Saraiva Câmara
• Grantee: Ashelley Kettyllem Alves de Sousa
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Acute kidney injury (AKI) is defined by a sudden loss of renal excretory function lasting up to seven days, which can be determined based on the assessment of serum creatinine levels and oliguria. ARF is considered a global public health problem, affecting approximately 20% of hospitalized patients and is associated with 50% of mortality rates in patients admitted to intensive care units (1,2). Common causes leading to AKI include a variety of clinical conditions, including: sepsis, hypoperfusion, obstruction, parenchymal renal disease, toxicity from iodinated radiological contrast, and to a greater extent toxicity from nephrotoxic drugs. Among nephrotoxic agents, the use of cisplatin, one of the most used and potent chemotherapy drugs, is associated with high incidence rates of nephrotoxicity, affecting between 20-41% of patients who use this antineoplastic. Mitochondria, which are present in abundance in nearby tubular cells, have been widely experimental and their dysfunction has been identified as an initiating factor for AKI. Proximal tubular cells are metabolically very active due to their important role in the reabsorption of approximately 70% of all glomerular filtrate. However, the contribution of mitochondrial dysfunction in the transition from ARF to DRC has not yet been completely elucidated and, given the high rates of progression from ARF to DRC, the search for understanding the cellular and molecular mechanisms involved in this process becomes increasingly important. most necessary. Therefore, the study of mitochondrial dysfunction in the transition process from AKI to DRC may raise new mechanisms as well as serve as a basis for the elucidation of new therapeutic strategies with the aim of delaying the development or progression of ARF to DRC and initial projects of kidney disease. (AU)