Hypovitaminosis D Does Not Aggravate the Progression of Gentamicin-Induced Kidney Injury in Rats

<b>Background/Objectives</b>: Gentamicin is one of the most effective and widely used antibiotics to treat serious infections. In addition to its bactericidal properties, gentamicin has a nephrotoxic effect that results in acute kidney injury (AKI). AKI may be intensified by hypovitaminosis D. This study evaluated the effect of hypovitaminosis D in the progression of gentamicin-induced renal injury. <b>Methods</b>: Male Wistar Hannover rats received a standard (SD) or a vitamin D-free diet (VitD^-) before gentamicin treatment. After that, we divided the animals into four groups: Ctrl VitD, SD diet, and saline injection; Ctrl VitD^-, VitD^- diet, and saline injection; Genta VitD, SD diet, and gentamicin injection (40 mg/kg; IM); Genta VitD^-, VitD^- diet, and gentamicin injection (40 mg/kg; IM). After the end of gentamicin treatment, we followed the animals for 5 days (protocol 1) and 30 days (protocol 2). <b>Results</b>: The Genta VitD group (protocol 1) presented impaired renal function. Regarding morphological analyses, the Genta VitD group presented necrotic tubules (protocol 1) and atrophied tubules (protocol 2). In the inflammatory scenario, the Genta VitD group presented an increase in the number of CD68+ cells, as well as in the levels of interleukin 1β (protocols 1 and 2). In addition, gentamicin-treated animals (protocols 1 and 2) presented an increased renal expression of vimentin and fibronectin. Despite the notable changes in functional, inflammatory, and structural parameters induced by gentamicin, hypovitaminosis D did not aggravate the renal injury in this experimental model. <b>Conclusion</b>: Hypovitaminosis D did not aggravate the progression of gentamicin-induced renal injury in rats.