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

Abstract

Acute kidney injury (AKI) is defined as an increase greater than 0.3 mg/L of serum creatinine within 48 hours and is a major cause of 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 by aminoglycoside administration and dehydration implementation. The animals in the Deh+Genta group exhibited the lowest average weight and feed intake after the fifth day of the experiment. In this same period, water consumption by the Genta group was lower than the Control group, but in the following days of the experiment, polydipsia was noted for this group. The Deh+Genta group displayed the highest mean serum urea after the fifth day. The gentamicin-treated groups exhibited higher means than the Control group 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 dehydration can mask the results by indicating false negative values. The urinary GGT enzyme did not act as an early AKI biomarker. Decreased glomerular filtration rates enhanced the concentration of blood components and masked urinary and tissue components.