Background/Objectives: Acute kidney injury poses a significant public health concern, contributing to elevated rates of morbidity and mortality. In our study, we sought to explore the involvement of cation channels, known to influence renal physiology, in Rhabdomyolysis-Associated Acute Kidney Injury (RIAKI). Materials and Methods: A total of 32 Sprague–Dawley rats were divided into four groups for our study. All rats underwent 24 h of dehydration prior to experimentation. Subsequently, the control group received physiological saline, while the remaining groups (RIAKI-24, RIAKI-48, and RIAKI-72) were administered intramuscular injections of 5 mL/kg of 50% glycerol solution. The control and RIAKI-24 groups were euthanized 24 h post-injection, the RIAKI-48 group at 48 h, and the RIAKI-72 group at 72 h. Urine, blood, and renal tissue samples were collected for the assessment of renal function and histological damage. Results: Serum urea and creatinine levels exhibited a time-dependent increase, alongside reduced creatinine clearance. Moreover, kidney tissue analysis revealed elevated levels of TRPV1, TRPV4, and TRPC6 in the RIAKI-72 group compared to the control. The RIAKI-24 group displayed the most severe histological damage among the experimental groups. Conclusions: RIAKI was accompanied by changes in renal function and histopathology, as well as altered renal TRPV1, TRPV4, and TRPC6 protein levels. These findings suggest the potential involvement of TRP channels in RIAKI but do not establish their functional activity or whether the observed changes are harmful, protective, or compensatory. Further studies are needed to clarify the functional roles of these channels in renal injury.
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Kaya et al. (2026) studied this question.
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