Jei-Wen Chang Taiwan

Professor Jei-Wen Chang, MD, PhD is a Professor of Pediatrics at National Yang Ming Chiao Tung University (NYCU) and Chief of the Division of General Pediatrics at Taipei Veterans General Hospital (Taipei VGH), Taiwan. She also serves as Vice Chair of the Department of Medicine and Chief of the Division of Pediatrics at the NYCU School of Medicine. Professor Chang earned her MD and PhD from National Yang Ming University and completed research training at the University of Miami Kidney Transplant Center and Imperial College London. Her clinical and research interests focus on pediatric nephrology, particularly pediatric kidney transplantation, chronic kidney disease, dialysis, congenital anomalies of the kidney and urinary tract (CAKUT), inherited kidney diseases, and precision medicine. She has established one of Taiwan's leading pediatric kidney transplant programs, achieving excellent graft outcomes, and has pioneered the application of genomic medicine in children with rare kidney diseases. Her research spans pediatric kidney transplantation, transplant-related complications, pediatric urology, autoimmune kidney diseases, and nationwide population-based studies aimed at improving outcomes for children with kidney and immune-mediated disorders.

20th September 2026 Sunday

Time	Session

10:45 12:30	New Horizons in Neonatal & Pediatric AKI-AKD Continuum Min-Hua TsengTaiwan Moderator Shotaro MatsumotoJapan Moderator The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside. The Missing Link: Navigating the Acute Kidney Disease (AKD) Window and Preventing CKD Jei-Wen ChangTaiwan Speaker The Missing Link: Navigating the Acute Kidney Disease (AKD) Window and Preventing CKDThe paradigm of acute kidney injury (AKI) has shifted dramatically over the past decade. Once regarded as a transient event, AKI is now recognized as the initiating step in a continuum that progresses through acute kidney disease (AKD) to chronic kidney disease (CKD). Representing the "missing link" in this spectrum, AKD—defined as persistent kidney dysfunction or injury lasting between 7 and 90 days after AKI—constitutes a critical, modifiable window during which timely intervention may interrupt disease progression and prevent irreversible kidney damage. This continuum is particularly pivotal in neonates and children. The developing kidney possesses unique developmental vulnerabilities, including incomplete nephrogenesis, reduced nephron endowment, and functional immaturity. Conditions such as prematurity, congenital anomalies of the kidney and urinary tract (CAKUT), hypoxic-ischemic injury, sepsis, congenital heart disease, and nephrotoxin exposure further compound the risk of maladaptive repair and incomplete recovery. Even following apparent clinical recovery, maladaptive repair and interstitial fibrosis may persist, increasing the lifelong risk of CKD, hypertension, and cardiovascular disease. This lecture will review the evolving concepts, epidemiology, and pathophysiological mechanisms of the AKI–AKD–CKD continuum, with an emphasis on neonatal and pediatric populations. Emerging biomarkers for the early detection of persistent kidney injury, risk stratification, and practical post-AKI management—including nephrotoxin stewardship, structured surveillance, and multidisciplinary follow-up—will be discussed. Recognizing AKD as a distinct clinical entity shifts the focus from treating AKI to promoting kidney recovery, offering a unique opportunity to preserve long-term kidney health and prevent CKD. Shotaro MatsumotoJapan Moderator The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside. Spotlight on Neonatal AKI: The AWAKEN Criteria, Unique Phenotypes, and Genetic Insights Chih-Chia ChenTaiwan Speaker Spotlight on Neonatal AKI: The AWAKEN Criteria, Unique Phenotypes, and Genetic InsightsNeonatal acute kidney injury (AKI) is a common and clinically significant complication in the neonatal intensive care unit (NICU), and is associated with increased mortality, prolonged hospitalization, and adverse long-term renal and neurodevelopmental outcomes. However, diagnosing AKI in neonates remains particularly challenging because the neonatal kidney is still undergoing maturation, and serum creatinine levels are influenced by maternal creatinine, gestational age, and the physiological postnatal decline in creatinine. This lecture will first review the evolution of neonatal AKI definitions, from early diagnostic approaches based on absolute serum creatinine values to the currently adopted modified KDIGO criteria. The limitations of current diagnostic criteria, including the delayed rise in serum creatinine and difficulties in establishing baseline renal function, will also be discussed. The second part of the lecture will focus on the clinical phenotypes of neonatal AKI. Rather than representing a single disease entity, neonatal AKI is a heterogeneous syndrome influenced by multiple factors, including prematurity, patent ductus arteriosus, and nephrotoxic medications. The differences between oliguric and non-oliguric AKI with also be discussed. Current evidence regarding the impact of neonatal AKI on both short-term outcomes and long-term renal health and neurodevelopment, together with the limitations of existing studies, will also be reviewed. Finally, the speech will highlight recent advances in the genetic susceptibility and precision medicine of neonatal AKI. Rapid developments in genomics and artificial intelligence are providing new insights into why neonates with similar clinical exposures develop markedly different degrees of kidney injury, while facilitating more accurate risk stratification and predictive modeling. By integrating clinical characteristics, biomarkers, and genetic information, the diagnosis and management of neonatal AKI are expected to evolve beyond traditional disease definitions toward phenotype-based classification and precision medicine. Shotaro MatsumotoJapan Moderator The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside. The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in Pediatrics Shotaro MatsumotoJapan Speaker The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside. Min-Hua TsengTaiwan Moderator Beyond Renal Replacement: Advanced Extracorporeal Blood Purification in Pediatric Sepsis I-Jung TsaiTaiwan Speaker Beyond Renal Replacement: Advanced Extracorporeal Blood Purification in Pediatric SepsisSepsis and hyperinflammatory syndromes remain leading causes of mortality in critically ill children, frequently complicated by multiorgan dysfunction syndrome and acute kidney injury. While continuous kidney replacement therapy (CKRT) is the cornerstone for managing fluid overload and solute clearance, standard modalities cannot adequately address the underlying dysregulated immune response driven by a profound cytokine storm. Recently, a significant paradigm shift has occurred in critical care nephrology, transitioning from conventional renal support toward advanced extracorporeal blood purification (EBP) techniques. Current literature emphasizes the clinical benefits of actively removing endotoxins and excessive cytokines to restore immune homeostasis. Modalities utilizing hemoadsorption membranes have demonstrated promising outcomes in adult studies, showing rapid hemodynamic stabilization and successful modulation of inflammatory markers in septic shock. However, literature regarding EBP in pediatric populations remains notably sparse. This knowledge gap is largely attributed to the physiological and technical challenges of pediatric care, particularly the high risks of hemodynamic instability associated with large extracorporeal circuit volumes in children weighing less than 10 kilograms. Standardized protocols for pediatric EBP are still lacking, necessitating cautious technical adaptations, such as targeted blood priming strategies. This presentation will review the current literature on EBP in sepsis, explore the physiological rationale behind targeted hemoadsorption, and discuss the practical challenges of applying these therapies in pediatrics. By moving beyond traditional renal replacement, we aim to highlight how integrating advanced blood purification into pediatric CKRT can safely modulate systemic inflammation, potentially improving clinical outcomes for vulnerable critically ill children. Min-Hua TsengTaiwan Moderator Q&A Room 103

Time

Session

10:45

12:30

New Horizons in Neonatal & Pediatric AKI-AKD Continuum

Min-Hua TsengTaiwan Moderator

Shotaro MatsumotoJapan Moderator The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside.

The Missing Link: Navigating the Acute Kidney Disease (AKD) Window and Preventing CKD

Jei-Wen ChangTaiwan Speaker The Missing Link: Navigating the Acute Kidney Disease (AKD) Window and Preventing CKDThe paradigm of acute kidney injury (AKI) has shifted dramatically over the past decade. Once regarded as a transient event, AKI is now recognized as the initiating step in a continuum that progresses through acute kidney disease (AKD) to chronic kidney disease (CKD). Representing the "missing link" in this spectrum, AKD—defined as persistent kidney dysfunction or injury lasting between 7 and 90 days after AKI—constitutes a critical, modifiable window during which timely intervention may interrupt disease progression and prevent irreversible kidney damage. This continuum is particularly pivotal in neonates and children. The developing kidney possesses unique developmental vulnerabilities, including incomplete nephrogenesis, reduced nephron endowment, and functional immaturity. Conditions such as prematurity, congenital anomalies of the kidney and urinary tract (CAKUT), hypoxic-ischemic injury, sepsis, congenital heart disease, and nephrotoxin exposure further compound the risk of maladaptive repair and incomplete recovery. Even following apparent clinical recovery, maladaptive repair and interstitial fibrosis may persist, increasing the lifelong risk of CKD, hypertension, and cardiovascular disease. This lecture will review the evolving concepts, epidemiology, and pathophysiological mechanisms of the AKI–AKD–CKD continuum, with an emphasis on neonatal and pediatric populations. Emerging biomarkers for the early detection of persistent kidney injury, risk stratification, and practical post-AKI management—including nephrotoxin stewardship, structured surveillance, and multidisciplinary follow-up—will be discussed. Recognizing AKD as a distinct clinical entity shifts the focus from treating AKI to promoting kidney recovery, offering a unique opportunity to preserve long-term kidney health and prevent CKD.

Shotaro MatsumotoJapan Moderator The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside.
Spotlight on Neonatal AKI: The AWAKEN Criteria, Unique Phenotypes, and Genetic Insights

Chih-Chia ChenTaiwan Speaker Spotlight on Neonatal AKI: The AWAKEN Criteria, Unique Phenotypes, and Genetic InsightsNeonatal acute kidney injury (AKI) is a common and clinically significant complication in the neonatal intensive care unit (NICU), and is associated with increased mortality, prolonged hospitalization, and adverse long-term renal and neurodevelopmental outcomes. However, diagnosing AKI in neonates remains particularly challenging because the neonatal kidney is still undergoing maturation, and serum creatinine levels are influenced by maternal creatinine, gestational age, and the physiological postnatal decline in creatinine. This lecture will first review the evolution of neonatal AKI definitions, from early diagnostic approaches based on absolute serum creatinine values to the currently adopted modified KDIGO criteria. The limitations of current diagnostic criteria, including the delayed rise in serum creatinine and difficulties in establishing baseline renal function, will also be discussed. The second part of the lecture will focus on the clinical phenotypes of neonatal AKI. Rather than representing a single disease entity, neonatal AKI is a heterogeneous syndrome influenced by multiple factors, including prematurity, patent ductus arteriosus, and nephrotoxic medications. The differences between oliguric and non-oliguric AKI with also be discussed. Current evidence regarding the impact of neonatal AKI on both short-term outcomes and long-term renal health and neurodevelopment, together with the limitations of existing studies, will also be reviewed. Finally, the speech will highlight recent advances in the genetic susceptibility and precision medicine of neonatal AKI. Rapid developments in genomics and artificial intelligence are providing new insights into why neonates with similar clinical exposures develop markedly different degrees of kidney injury, while facilitating more accurate risk stratification and predictive modeling. By integrating clinical characteristics, biomarkers, and genetic information, the diagnosis and management of neonatal AKI are expected to evolve beyond traditional disease definitions toward phenotype-based classification and precision medicine.

Shotaro MatsumotoJapan Moderator The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside.
The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in Pediatrics

Shotaro MatsumotoJapan Speaker The Ultimate Support: Heart-Lung-Kidney Crosstalk and ECMO-CRRT Integration in PediatricsExtracorporeal membrane oxygenation (ECMO) and continuous kidney replacement therapy (CKRT) support pediatric cardiopulmonary failure complicated by acute kidney injury (AKI) and fluid overload (FO). AKI and multiorgan dysfunction are increasingly viewed through bidirectional kidney-lung-heart crosstalk, extending in ECMO/CKRT patients to artificial organs: oxygenator, blood pump, and hemofilter. Kidney-lung crosstalk shares pathways of vascular rigidity, neurohormonal activation, tissue hypoxia, and aberrant immune signaling. Ventilator-induced biotrauma impairs renal function, while AKI worsens lung injury via fluid, acid-base, and cytokine derangements; positive-pressure ventilation further raises right-ventricular afterload and central venous pressure, reducing renal perfusion. Kidney-heart crosstalk (cardiorenal syndrome type 3) involves analogous inflammatory and neuroendocrine mechanisms and carries a high mortality risk in children. Beyond native organs, the oxygenator activates complement/inflammatory cascades via blood-biomaterial contact, and non-pulsatile pump flow causes shear-induced hemolysis, with free hemoglobin/iron contributing to AKI. CKRT-ECMO circuit connection requires attention to circuit pressures, embolism risk, and altered drug pharmacokinetics-challenges framed by the multiple organ support therapy (MOST) concept. Key management priorities include early correction of FO, standardized CKRT-ECMO integration per PCRRT-ICONIC and ADQI/ELSO consensus recommendations, lung-protective ventilation and conservative fluid management, and long-term renal/blood-pressure surveillance after ECMO. Research has evolved from single-center FO-mortality studies to consensus statements, the extracorporeal organ support concept, and the multicenter WE-ROCK registry, with recent work clarifying molecular mechanisms of sepsis-associated lung-kidney crosstalk. Future work should pursue biomarker-driven endotyping and integrated MOST platforms.Core Decisions: Modality Selection (CVVH / CVVHD / CVVHDF) & PrescriptionModality selection and dose prescription remain unresolved in pediatric continuous kidney replacement therapy (CKRT). Pediatric trials are scarce, so practice extrapolates from adult evidence, while 2026 KDIGO and Surviving Sepsis Campaign updates have reopened debate. Ronco's 2000 trial established an "at least 35 mL/kg/h" paradigm after showing improved survival with higher ultrafiltration, later refuted by the large ATN and RENAL trials, which found no survival benefit from higher intensity and more complications. KDIGO 2012 therefore recommended a delivered dose of 20-25 mL/kg/h, unchanged in the 2026 draft, which additionally now recommends against high-volume hemofiltration (HVHF) in adult septic AKI, reflecting negative IVOIRE trial and Cochrane review findings. For modality, CVVHDF has become dominant in the WE-ROCK pediatric registry, rising from 30% to 76% of prescriptions, though some favor CVVH for convective clearance; no modality shows a survival advantage. For dose, the 2026 KDIGO draft newly defines pediatric practice points: weight- rather than surface-area-based prescription to avoid inadvertent infant overdosing, initial effluent of 25-30 mL/kg/h, augmented dosing to 200 mL/kg/h for hyperammonemia, and an ultrafiltration-rate of maximal 2.5ml/kg/h. WE-ROCK data show prescribed doses far exceeding these targets without an observed dose-outcome association. Adding to this uncertainty, the 2026 pediatric Surviving Sepsis Campaign guideline newly recommends HVHF (>35 mL/kg/h) in septic shock, conditionally and with low certainty, reversing its 2020 position on a fragile three-trial meta-analysis (Fragility Index=1)-contrasting with adult evidence and the concurrent adult KDIGO recommendation against HVHF. Given risks such as dialytrauma and drug underdosing, this fragile signal warrants cautious application. This session invites participants to weigh this evidence and build a practical framework for individualizing modality and dose decisions at the bedside.

Min-Hua TsengTaiwan Moderator
Beyond Renal Replacement: Advanced Extracorporeal Blood Purification in Pediatric Sepsis

I-Jung TsaiTaiwan Speaker Beyond Renal Replacement: Advanced Extracorporeal Blood Purification in Pediatric SepsisSepsis and hyperinflammatory syndromes remain leading causes of mortality in critically ill children, frequently complicated by multiorgan dysfunction syndrome and acute kidney injury. While continuous kidney replacement therapy (CKRT) is the cornerstone for managing fluid overload and solute clearance, standard modalities cannot adequately address the underlying dysregulated immune response driven by a profound cytokine storm. Recently, a significant paradigm shift has occurred in critical care nephrology, transitioning from conventional renal support toward advanced extracorporeal blood purification (EBP) techniques. Current literature emphasizes the clinical benefits of actively removing endotoxins and excessive cytokines to restore immune homeostasis. Modalities utilizing hemoadsorption membranes have demonstrated promising outcomes in adult studies, showing rapid hemodynamic stabilization and successful modulation of inflammatory markers in septic shock. However, literature regarding EBP in pediatric populations remains notably sparse. This knowledge gap is largely attributed to the physiological and technical challenges of pediatric care, particularly the high risks of hemodynamic instability associated with large extracorporeal circuit volumes in children weighing less than 10 kilograms. Standardized protocols for pediatric EBP are still lacking, necessitating cautious technical adaptations, such as targeted blood priming strategies. This presentation will review the current literature on EBP in sepsis, explore the physiological rationale behind targeted hemoadsorption, and discuss the practical challenges of applying these therapies in pediatrics. By moving beyond traditional renal replacement, we aim to highlight how integrating advanced blood purification into pediatric CKRT can safely modulate systemic inflammation, potentially improving clinical outcomes for vulnerable critically ill children.

Min-Hua TsengTaiwan Moderator
Q&A

Room 103