<p>Iodinated contrast agents are essential for accurate diagnostics but pose a risk of contrast-induced acute kidney injury (CIAKI), primarily through oxidative stress. Current guidelines recommend intravenous hydration as the main preventive strategy. Targeted temperature management (TTM), which lowers core body temperature, has shown protective effects in ischemic conditions. However, its role in CIAKI remains unclear. This study investigated whether TTM at 33 and 36&#xa0;°C can mitigate CIAKI. Forty-two Sprague–Dawley rats were assigned to six groups (n = 7 per group): Control, TTM 33&#xa0;°C, TTM 36&#xa0;°C, CIAKI, CIAKI with TTM 33&#xa0;°C, and CIAKI with TTM 36&#xa0;°C. Body temperature was regulated using external cooling, and blood and tissue samples were collected after 24&#xa0;h. Serum creatinine, blood urea nitrogen, and markers of oxidative stress, apoptosis, inflammation, and renal injury were evaluated. Oxidative stress increased in the CIAKI group but decreased in both TTM groups. Superoxide dismutase levels declined in the CIAKI group but were restored with TTM. Apoptotic and inflammatory markers were elevated in the CIAKI group but reduced with TTM. Renal function was better preserved in the TTM at 36&#xa0;°C group than in the TTM at 33&#xa0;°C group. These findings suggest that TTM at 33 and 36 ℃ groups attenuates CIAKI by reducing oxidative stress, apoptosis, and inflammation. While TTM at 33 and 36℃ demonstrated protective effects, TTM at 36&#xa0;°C may provide a more pronounced functional benefit.</p>

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Targeted temperature management at 33 and 36 °C mitigates contrast-induced acute kidney injury

  • Hyewon Oh,
  • Jinho Beom,
  • June Park,
  • Ga Bin Park,
  • Je Sung You,
  • Yong Eun Chung

摘要

Iodinated contrast agents are essential for accurate diagnostics but pose a risk of contrast-induced acute kidney injury (CIAKI), primarily through oxidative stress. Current guidelines recommend intravenous hydration as the main preventive strategy. Targeted temperature management (TTM), which lowers core body temperature, has shown protective effects in ischemic conditions. However, its role in CIAKI remains unclear. This study investigated whether TTM at 33 and 36 °C can mitigate CIAKI. Forty-two Sprague–Dawley rats were assigned to six groups (n = 7 per group): Control, TTM 33 °C, TTM 36 °C, CIAKI, CIAKI with TTM 33 °C, and CIAKI with TTM 36 °C. Body temperature was regulated using external cooling, and blood and tissue samples were collected after 24 h. Serum creatinine, blood urea nitrogen, and markers of oxidative stress, apoptosis, inflammation, and renal injury were evaluated. Oxidative stress increased in the CIAKI group but decreased in both TTM groups. Superoxide dismutase levels declined in the CIAKI group but were restored with TTM. Apoptotic and inflammatory markers were elevated in the CIAKI group but reduced with TTM. Renal function was better preserved in the TTM at 36 °C group than in the TTM at 33 °C group. These findings suggest that TTM at 33 and 36 ℃ groups attenuates CIAKI by reducing oxidative stress, apoptosis, and inflammation. While TTM at 33 and 36℃ demonstrated protective effects, TTM at 36 °C may provide a more pronounced functional benefit.