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

Abstract List

20 Sep 2026 10:45 11:05
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.