Midkine and ACE-Ang II Induced Endothelial Injury in Sepsis

Southeast University, China26 enrolled

Overview

Plasma midkine has reported to be elevated in infection and a regulator of angiotensin-converting enzyme (ACE). We aimed to investigate the plasma midkine in septic patients and its association with 28-day mortality and organ function, and also with plasma ACE and angiotensin II.

This study showed that Ang II induced endothelial injury in sepsis patients. Midkine has been shown to regulate the renin-angiotensin system and acts in the upstream signaling pathway of angiotensin (ANG) II. The investigators want to access the relationship between midkine level and ACE-Ang II induced endothelial injury in sepsis

Study Type

OBSERVATIONAL

Enrollment

Conditions

Sepsis

Eligibility

Sex: ALLMin age: 18 YearsMax age: 80 YearsHealthy volunteers:

Medical Language ↔ Plain English

The inclusive criteria were adult patients (age \> 18 years-old and \< 80 years-old) diagnosed with sepsis, according the definition of the Surviving Sepsis Campaign (2016) Exclusive criteria included: 1. age \< 18 years-old or \> 80 years-old; 2. pregnancy or breastfeeding; 3. malignancy; 4. patients with potentially elevated plasma midkine apart from sepsis including acute myocardial infarction, stroke, limb thrombosis, chronic renal dysfunction (baseline plasma creatine ≥2 mg/dL), autoimmune diseases and Alzheimer syndrome; 5. patients deceased or discharge from ICU within 24 hours; or, 6. written consents could not be obtained.

Locations (1)

Department of Critical Care Medicine

Nanjing, Jiangsu, China

Outcomes

Primary Outcomes

28-day mortality

All the patients were followed-up to 28 days and all-cause mortality was recorded.

Time frame: up to 28 days

Data from ClinicalTrials.gov

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