Inflammatory Mediators of Acute Kidney Injury in Intensive Care

N/ARecruitingNCT03720860

Uppsala University100 enrolled

Overview

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.

Study Type

OBSERVATIONAL

Enrollment

100

Conditions

Sepsis Surgery Acute Kidney Injury

Eligibility

Sex: ALLMin age: 18 YearsHealthy volunteers:

Medical Language ↔ Plain English

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

Locations (1)

Outcomes

Primary Outcomes

Histones

Correlation between levels of histones and degree of acute kidney injury

Time frame: Within 1 month

Secondary Outcomes

Other inflammtory mediators

Correlation between levels of other inflammtory mediators and degree of acute kidney injury