Inflammatory Mediators of Acute Kidney Injury in Intensive Care

Prospective Studie of Inflammatory Markers in Urine, Plasma and Sputum Associated With Acute Kidney Injury

Status

Recruiting

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT03720860

Acronym

PronMed

Enrollment

100

Registered

2018-10-25

Start date

2018-01-01

Completion date

2026-05-31

Last updated

2026-01-12

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Acute Kidney Injury, Sepsis, Surgery

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.

Interventions

None listed

Study design

Observational model

COHORT

Time perspective

PROSPECTIVE

Eligibility

Sex/Gender

ALL

Age

18 Years to No maximum

Healthy volunteers

Yes

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

Design outcomes

Primary

Measure	Time frame	Description
Histones	Within 1 month	Correlation between levels of histones and degree of acute kidney injury

Secondary

Measure	Time frame	Description
Other inflammtory mediators	Within 1 month	Correlation between levels of other inflammtory mediators and degree of acute kidney injury

Countries

Sweden

Contacts

Primary ContactSara Bulow, MD

sara.bulow.anderberg@akademiska.se+46730247414

Outcome results