Scholarlink

<p>Sepsis-associated acute kidney injury (SA-AKI) is a serious complication in critically ill patients and contributes significantly to mortality. However, the mechanisms underlying SA-AKI remain incompletely understood, and experimental models vary considerably in severity. This study investigated a rat model of SA-AKI induced by cecal ligation and puncture (CLP) using different numbers of perforations. Male Wistar rats were assigned to Sham, CLP 2P, CLP 5P, and CLP 10P groups and evaluated 72 h after surgery. Mortality, clinical signs, renal function, histopathology, inflammatory mediators, kidney injury biomarkers, and systemic parameters were analyzed. Mortality increased with the number of perforations and was highest in the CLP 10P group. Clinical scores and creatinine clearance indicated greater disease severity in CLP 10P animals. All CLP groups exhibited reduced sodium and potassium clearance, whereas tubular and interstitial injury increased progressively with the number of perforations. Renal expression of pro-inflammatory mediators and kidney injury biomarkers, including IL-18, IL-1β, KIM-1, and NGAL, was significantly elevated in the CLP 10P group. These animals also showed reduced blood glucose levels, increased C-reactive protein concentrations, lower pCO₂ values, and alterations in bicarbonate and base excess consistent with severe systemic inflammation and metabolic disturbances. Histological analysis confirmed more pronounced tubular and inflammatory injury in the CLP 10P group. These findings demonstrate that the CLP 10P protocol produces a reproducible model of severe sepsis-associated renal injury characterized by marked systemic inflammation, renal structural damage, and activation of kidney injury biomarkers, providing a useful platform for investigating pathophysiological mechanisms and evaluating novel therapeutic strategies.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Characterization of acute kidney injury induced by a cecum ligation and puncture model

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年8月5日

查看全文
  • Caroline Muiler Barbosa Nogueira,
  • Carolina Monteiro de Lemos Barbosa,
  • Carla Medeiros da Silva,
  • Felipe Mateus dos Santos Ornellas,
  • Débora dos Santos Ornellas,
  • Sergio Augusto Lopes de Souza,
  • Patricia Rieken Macedo Rocco,
  • Fernanda Ferreira Cruz,
  • Christina Maeda Takiya,
  • Marcelo Marcos Morales

摘要

Sepsis-associated acute kidney injury (SA-AKI) is a serious complication in critically ill patients and contributes significantly to mortality. However, the mechanisms underlying SA-AKI remain incompletely understood, and experimental models vary considerably in severity. This study investigated a rat model of SA-AKI induced by cecal ligation and puncture (CLP) using different numbers of perforations. Male Wistar rats were assigned to Sham, CLP 2P, CLP 5P, and CLP 10P groups and evaluated 72 h after surgery. Mortality, clinical signs, renal function, histopathology, inflammatory mediators, kidney injury biomarkers, and systemic parameters were analyzed. Mortality increased with the number of perforations and was highest in the CLP 10P group. Clinical scores and creatinine clearance indicated greater disease severity in CLP 10P animals. All CLP groups exhibited reduced sodium and potassium clearance, whereas tubular and interstitial injury increased progressively with the number of perforations. Renal expression of pro-inflammatory mediators and kidney injury biomarkers, including IL-18, IL-1β, KIM-1, and NGAL, was significantly elevated in the CLP 10P group. These animals also showed reduced blood glucose levels, increased C-reactive protein concentrations, lower pCO₂ values, and alterations in bicarbonate and base excess consistent with severe systemic inflammation and metabolic disturbances. Histological analysis confirmed more pronounced tubular and inflammatory injury in the CLP 10P group. These findings demonstrate that the CLP 10P protocol produces a reproducible model of severe sepsis-associated renal injury characterized by marked systemic inflammation, renal structural damage, and activation of kidney injury biomarkers, providing a useful platform for investigating pathophysiological mechanisms and evaluating novel therapeutic strategies.