Inflammatory Mediators of Acute Kidney Injury in Intensive Care
This study examines why sepsis (a serious blood infection) causes acute kidney injury in critically ill patients. Researchers are investigating the inflammatory substances in the body that may damage the kidneys during sepsis to better understand and potentially prevent this complication.
Key Objective:This research could lead to new treatments that prevent or reduce kidney damage in sepsis patients by targeting the inflammatory processes that harm kidney function.
Who to Consider:Critically ill patients with sepsis who have developed acute kidney injury or are at high risk for developing it should consider discussing participation with their medical team.
Trial Parameters
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Brief Summary
Acute kidney injury (AKI) affects more than 50% of patients admitted to the intensive care unit. The most common underlying cause is sepsis. Severe AKI in combination with sepsis is associated with high mortality. The mechanisms for sepsis-induced AKI are largely unknown. Our hypothesis is that the inflammatory response to an infection cause collateral damage to host tissue and contributes to the development of AKI. In this study we want to investigate the presence of novel inflammatory mediators in patients with sepsis, patients subjected to major surgery (sterile inflammation) and non-inflamed patients and correlate their levels with the risk for AKI.
Eligibility Criteria
Inclusion Criteria: Patients admitted to the intensive/post operative care unit * with septic shock or * post major surgery or * after intoxication with a chemical compund Exclusion Criteria: * Pregnancy or * Breast feeding or * Chronic kidney disease or * intoxication with nephrotoxic compund or * lack of informed consent