Laboratory changes inherent to acute kidney injury induced by aminoglycosides in wistar rats

• Autor(a) principal: Queiroz Lima, Ana Carolina
• Data de Publicação: 2022
• Outros Autores: Freitas Rodrigues Godinho, Ana Bárbara, Bueno Dias, Caio Vitor, Novaes Rocha, Vinícius, Jerdy, Hassan
• Tipo de documento: Artigo
• Idioma: por; eng
• Título da fonte: Ciência animal brasileira (Online)
• Texto Completo: https://revistas.ufg.br/vet/article/view/70110

Acute kidney injury (AKI) is defined as an increase greater than 0.3 mg/dL of serum creatinine within 48 hours and is a major causeof death in patients in intensive care units. Twenty-four Wistar rats were divided into three groups: Control (0.9% saline), Genta(gentamicin 50 mg.kg-1 BID) and Deh+Genta (gentamicin 50 mg.kg-1 BID + water restriction) and tested in an AKI model byaminoglycoside administration and dehydration implementation. The animals in the Deh+Genta group exhibited the lowest averageweight and feed intake after the fifth day of the experiment. In this same period, water consumption by the Genta group was lowerthan the Control group, but in the following days of the experiment, polydipsia was noted for this group. The Deh+Genta groupdisplayed the highest mean serum urea after the fifth day. The gentamicin-treated groups exhibited higher means than the Controlgroup for serum creatinine, which proved to be a late renal marker for AKI. Serum GGT was higher in the Deh+Genta group,whereas urinary GGT was higher in the groups that received gentamicin, characterizing enzymuria, although severe dehydrationcan mask the results by indicating false negative values. The urinary GGT enzyme did not act as an early AKI biomarker. Decreasedglomerular filtration rates enhanced the concentration of blood components and masked urinary and tissue components.Keywords: Gentamycin; Rodents; Biochemical change.