Plenary 1: Organ Dysfunction in the Critically Ill Patient: Emerging Concepts
Abstract List
19 Sep 2026
08:30
10:15
Room 101
Jay KoynerUnited States
Moderator
Special lecture: 2026 KDIGO AKI Guideline UpdateI will be updating the audience on the major conceptual updates of the 2026 KDIGO AKI Guidelines. I will focus on Chapter 1 and 2, including the evolving definition of AKI/AKD, AKI trajectories, biomarkers, and risk prediction, together with selected key updates from Chapter 4 on nephrotoxin-associated kidney injuryTargeting Persistent AKI and Promoting RecoveryI have been working with my co-moderators to develop a case based presentation looking at the use of biomarkers to predict outcomes in a patient with dialysis requiring AKI. and we will be discussing the intracicies of providing AKI-care to those receiving dialysis and how best to wean patients from dialysis and the long term outpatient managment of these patients
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08:30
08:50
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VinCent WuTaiwan
Speaker
AKD Care Redefined: Diabetes, Hypertension, and Strategies for Long-Term Health Traditional acute kidney injury (AKI) classifications, centered around semi-anatomical lines, no longer suffice in capturing the complexity of AKI. Subphenotyping, enriched with AKI biomarkers, holds insights into distinct risk profiles and tailored treatment strategies, redefining AKI and contributing to improved clinical management (Critical Care). Incorporating kidney biomarkers into strategies for early AKI detection and the initiation of AKI care bundles has shown greater effectiveness than using care bundles without these novel biomarkers. Our investigations have made notable advancements in identifying water-soluble regulatory iron hepcidin as a promising early biomarker for predicting postoperative acute kidney injury. Beyond hepcidin, our research extended into the exploration of predictive biomarkers, such as HJV, NGAL, and cFGF-23, uncovering their potential in prognosticating the occurrence and severity of AKI (Cell Death Dis, Antioxidants & redox signaling). The amalgamation of these biomarkers with existing clinical AKI scores holds immense promise in revolutionizing critical care and ushering in a new era of personalized patient management. Moreover, our endeavors have transcended theoretical advancements, with successful patent acquisition for AKI biomarkers attesting to our commitment. We were the inaugural contributors to the discourse on the effects of indoxyl sulfate on the tubulogenesis capability of endothelial progenitor cells and cell aging in acute kidney injury(Angiogenesis). A comprehensive review of the long-term prognosis of acute kidney injury, encompassing impacts on the heart, brain, bone lesions, gastrointestinal, and tissue carcinogenesis, was presented. (JASN, KI, cJASN, JAHA, ICM, CC). Our team posited that transferring post-AKI patients to nephrologists for care could reduce overall mortality and cardiovascular events (Value in Health). Through integrated analysis, we demonstrated that standard dialysis would increase the number of patients avoiding dialysis (CC), stimulating fervent discussions among AKI physicians at international conferences. Notably, we were global trailblazers in proposing that acute kidney disease, regardless of AKI presence, leads to mortality and end-stage kidney disease(eClinicalMedicine ).
Although the evidence for patients with acute kidney disease (AKD) is still lacking, several potential pharmacological agents may improve outcomes, including but not limited to angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists, sodium-glucose cotransporter 2 inhibitors, and glucagon-like peptide 1 receptor agonists (JAMA NO). In conclusion, accurate prognosis prediction and effective treatment for AKD are critical yet unmet clinical needs. Future studies are urgently needed to improve patient care in this complex and rapidly evolving field.
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08:50
09:05
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Kent DoiJapan
Speaker
Organ Crosstalk in AKIAcute kidney injury (AKI) is frequently complicated by distant organ dysfunction, significantly increasing patient morbidity and mortality. Recent clinical and experimental evidence highlights complex inter-organ crosstalk mechanisms, such as systemic cytokine release, oxidative stress, immune dysregulation, and damage-associated molecular patterns (DAMPs), that mediate extrarenal tissue injury. Experimental studies demonstrate distinct pathophysiological axes connecting the injured kidney with the heart and lungs. Specifically, mitochondrial dysfunction plays a critical role in acute cardiorenal syndrome. Furthermore, in AKI-induced acute lung injury, in addition to activation of the HMGB1–Toll-like receptor 4 (TLR4) pathway and formation of neutrophil extracellular traps (NETs), recent studies have reported a novel pathophysiological mechanism of impaired gas exchange mediated by neutrophil retention. This presentation provides an updated overview of the molecular pathways driving AKI-induced distant organ crosstalk, emphasizing key pathophysiology involving the heart and lungs, and discusses targeted therapeutic strategies to improve clinical outcomes in multi-organ failure.Heterogeneity and Future Direction of Major Adverse Kidney EventsThe "AKI/AKD/CKD axis" represents a critical continuum in nephrology, highlighting that acute kidney injury (AKI) is not merely a self-limiting episode but a potent driver of chronic kidney disease (CKD). Numerous clinical studies have reported the epidemiology of the AKI-to-CKD transition, demonstrating how recurrent or severe AKI accelerates renal decline. Crucially, methodological heterogeneity in defining Major Adverse Kidney Events (MAKE), as highlighted by our recent scoping review (Maeda et al., Intensive Care Med 2024), complicates the interpretation of clinical trial outcomes. To ensure the success of future clinical trials targeting AKI and the AKI-to-CKD transition, we must not only identify optimal therapeutic targets, but also establish standardized outcomes that directly align with improved patient care.Targeted Polymyxin B Hemadsorption in Sepsis: Lessons from Japanese Experience and Patient SelectionPolymyxin B haemadsorption (PMX-HA) has a long clinical history in Japan in the treatment of endotoxemia and septic shock. However, recent international randomized controlled trials and clinical guidelines have caused controversy regarding its routine use, citing inconsistent survival benefits in unselected populations. This presentation reviews the evolution of PMX-HA, from its origins in extensive Japanese clinical experience to modern precision medicine approaches in intensive care. Recent secondary analyses and real-world studies have highlighted significant heterogeneity in treatment effects, underscoring the necessity of appropriate patient selection. Subgroup analyses from the EUPHRATES trial demonstrated the potential efficacy of PMX-HA in patients with moderate-to-high endotoxin activity levels (EAA 0.6–0.9) and high severity of organ failure. Furthermore, machine learning applications such as causal forest modelling on large observational and trial cohorts have successfully identified specific biomarker profiles and clinical characteristics that define true responders.
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09:05
09:20
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Kathleen LiuUnited States
Speaker
How do I Manage Patients with Combined Kidney and Liver FailureKidney-Ventilator Interactions and Kidney Protective Ventilation /or Lung and Kidney CrosstalkHow Do I Care for the Patient with ARDS and AKIDe-escalating and Transitioning RRT: Best Practices
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09:20
09:35
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Mitra NadimUnited States
Speaker
Hepatorenal Syndrome: Recognition and Management or Disordered Physiology or Iatrogenic FailureManaging Patients With Combined Kidney and Liver FailureHow do I Manage Patients with Acute Liver Failure
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09:35
10:05
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Claudio RoncoItaly
Speaker
Hemoadsorption in the ICUSpecial Lecture: 50 Years of CRRT: A Journey Through InnovationRole of Renal Functional Reserve on AKI Risk and RecoveryHow Do I Use Hemadsorption in My PracticeManaging the Heart Failure Patient With Worsening Renal Function (WRF)
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10:05
10:15
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