August 15, 2026 at 1:00 PM ET on Microsoft Teams

Pediatric AKI and immunomodulation without immunosuppression

Join leading ICU intensivists, nephrologists, and clinical nurse managers for a focused discussion on emerging approaches to sepsis-induced acute kidney injury in pediatric patients.

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August 15, 2026 at 1:00 PM ET on Microsoft Teams

What you’ll learn

QUELIMMUNE in Practice: Navigating Pediatric AKI and ICU Integration

In this session, viewers will explore the clinical burden of sepsis-induced pediatric AKI and the limitations of current treatment approaches. Participants will receive a clear, accessible overview of QUELIMMUNE’s mechanism of action and discover exactly where it fits within the pediatric care pathway.

Through real-world clinical insights covering patient selection, optimal timing, and practical ICU workflow integration, attendees will be equipped with the key considerations needed to evaluate their current CRRT programs and determine if this therapy is appropriate for their institution

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Why attend

QUELIMMUNE in Practice: Navigating Pediatric AKI and ICU Integration

In this session, viewers will explore the clinical burden of sepsis-induced pediatric AKI and the limitations of current treatment approaches. Participants will receive a clear, accessible overview of QUELIMMUNE’s mechanism of action and discover exactly where it fits within the pediatric care pathway.

Through real-world clinical insights covering patient selection, optimal timing, and practical ICU workflow integration, attendees will be equipped with the key considerations needed to evaluate their current CRRT programs and determine if this therapy is appropriate for their institution

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About QUELimmune

QUELIMMUNE in Practice: Navigating Pediatric AKI and ICU Integration

In this session, viewers will explore the clinical burden of sepsis-induced pediatric AKI and the limitations of current treatment approaches. Participants will receive a clear, accessible overview of QUELIMMUNE’s mechanism of action and discover exactly where it fits within the pediatric care pathway.

Through real-world clinical insights covering patient selection, optimal timing, and practical ICU workflow integration, attendees will be equipped with the key considerations needed to evaluate their current CRRT programs and determine if this therapy is appropriate for their institution

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Meet the experts

Leading clinicians sharing clinical experience and evidence

Headshot of Dr. Stuart Goldstein MD, FAAP, FNKF

Dr. Stuart Goldstein MD, FAAP, FNKF

Cincinnati Children’s Hospital

Headshot of Theresa Mottes APRN-NP, CPNP-AC, CDN

Theresa Mottes APRN-NP, CPNP-AC, CDN

Lurie Children’s Hospital

Headshot of Katie Plomaritas BSN, RN

Katie Plomaritas BSN, RN

Mott Children’s Hospital

Headshot of Dr. Stephen Gorga MD, MSC, FAAP

Dr. Stephen Gorga MD, MSC, FAAP

University of Michigan

Headshot of Dr. Kevin Chung, MD

Dr. Kevin Chung, MD

Chief Medical Officer, SeaStar Medical

Integration

Seamless CRRT Integration

QUELIMMUNE™ is not a standalone machine; it is designed as a simple adjunct therapy. It connects directly in-line to an existing continuous renal replacement therapy (CRRT) circuit (such as Prismaflex or PrisMax), creating a low-shear extracorporeal pathway for the patient’s blood.

Chemistry

A Low-Calcium Environment

The therapy relies on standard Regional Citrate Anticoagulation (RCA) to maintain a strictly controlled, low-ionized calcium environment (<0.40 mmol/L) within the circuit. This specific chemistry is required for the device’s immunomodulatory process to function.

Cellular deactivation

Selective Cellular Deactivation

Within this low-shear, low-calcium environment, the device’s synthetic hollow fiber membranes selectively target and bind highly activated, pro-inflammatory neutrophils and monocytes. This acts as a temporary “timeout” for the hyperactive white blood cells driving the cytokine storm, calming them down without permanently removing them from the body.

Resolution

Restoring Systemic Homeostasis

Once deactivated, the targeted neutrophils undergo apoptosis, while the monocytes are reprogrammed into an anti-inflammatory, reparative phenotype. These calmed cells are then released back into systemic circulation, signaling the body to halt multi-organ damage and restore immune homeostasis—crucially achieving this without causing systemic immunosuppression.

Secure your spot today

August 2026. Live webinar. Expert faculty. Clinical insights you can implement immediately.