Pro-renin and Angiotensin I Are Elevated in Pediatric Sepsis

Monday, March 23, 2026

10:15 AM - 11:15 AM Central Time

Location: Connections Central - RST 14

SM

Shannon Moriarty-Loeper, MS, DO

New York University Langone Medical Center

Disclosure(s): No relevant financial relationship(s) to disclose.
RS

Rubab Sohail, MPH

Biostatistician
Cohen Children's Medical Center

Disclosure information not submitted.
April Slamowitz, MD (she/her/hers)

Nemours Childrens Hospital

Disclosure(s): No relevant financial relationship(s) to disclose.
MQ

Mei Qi, MD

Research Assistant
The Feinstein Institutes for Medical Research

Disclosure information not submitted.
AC

Andrea Connelly, BS

Research Assistant
Cohen Children's Medical Center

Disclosure information not submitted.
CD

Clifford Deutschman, MD, MS, MCCM

Professor of Pediatrics
Zucker School of Medicine at Hofstra/Northwell

Disclosure information not submitted.
MT

Matthew Taylor, MD

Attending Physician
Cohen Children's Medical Center

Disclosure information not submitted.
GF

Grace Fisler, MD

Assistant Professor of Pediatrics
Cohen Children's Medical Center

Disclosure information not submitted.

Introduction: Sepsis has been associated with both alterations in responses to the renin-angiotensin-aldosterone system (RAAS) and derangements in serum levels of RAAS components. A comprehensive understanding of how sepsis affects the RAAS is lacking. We hypothesized that components of RAAS in children with sepsis would be different from those measured in healthy children and that, in sepsis, RAAS protein levels would associate with degree of organ dysfunction.

Methods: This was a single-center, prospective observational cohort study of children (age 1 week to 18 years) admitted to a tertiary PICU who met Phoenix sepsis criteria within 24hrs of admission. Those with chronic renal failure, congestive heart failure, unrepaired congenital heart disease, or on home anti-hypertensive agents were excluded. Blood was collected in protease inhibitor-treated vials on hospital days 1, 2, and 3 and once for healthy patients. ELISAs quantified RAAS plasma protein levels. Data were analyzed with Wilcoxon rank-sum test and Spearman rank correlation.

Results: Eighty children (sepsis n=39, healthy n=41) were enrolled with no difference in sex between cohorts. The sepsis cohort was older (median age 8yrs [IQR 4-12] vs 2yrs [IQR 1-10]). Herein, we present data on four RAAS components. On Day 1, renin levels were 78.89 pg/mL in the sepsis cohort vs.118.80 pg/mL in the healthy cohort (p=0.32); and aldosterone levels were 370.92 pg/mL vs. 429.82 pg/mL respectively, (p = 0.77). Day 1 pro-renin was higher in children with sepsis compared to healthy children (3.92ng/mL, IQR 0.84-8.05, vs 1.01ng/mL, IQR 0.08-4.75, p=0.009). Day 1 angiotensin I was higher in children with sepsis compared to healthy children (1414pg/mL, IQR 650-3116 vs 808.7pg/mL, IQR 449-1788, p=0.03). Changes in angiotensin I over time correlated with Phoenix-8 scores, with more severe illness linked to increasing levels of angiotensin I (r=0.49, p=0.02).

Conclusions: Pro-renin is higher while renin levels remain unchanged in pediatric sepsis compared to healthy children, suggesting juxtaglomerular cell involvement. Angiotensin I is higher in children with sepsis compared to healthy children and correlates with degree of organ dysfunction. Further study will characterize additional RAAS components and may identify modifiable targets for future studies.