Mandarin Programme

• 08:00

  08:15
  會員報到、分組說明 Registration & Group Orientation
• 08:15

  11:30
  A. 偵探請就位！破解警報密碼，還原機器真相。-常見警報處理及醫囑開立 Detective Mode On ! Decoding Alarms and Restoring the Truth - Common Alarm Management and Medical Orders
  Yu-Shuan Fu Speaker 偵探請就位！破解警報密碼，還原機器真相-常見警報處理及醫囑開立
• 08:15

  11:30
  B. 強強聯手：解鎖CRRT+ECMO 進階照護力 Stronger Together: Advancing CRRT + ECMO Integrated Care
  Li-Rong Tseng Speaker 強強聯手：解鎖 CRRT＋ECMO 進階照護力
• 08:15

  11:30
  C. 精準吸附，淨化重症：吸附罐串接實戰全攻略 Precision Adsorption, Purifying the Critically ill : Comprehensive Guide to Adsorptive Therapy
  Hai-Hsi Chen Speaker CytoSorb療法臨床應用本教學主要說明 CytoSorb 血液吸附治療於臨床常見之適應症——敗血症、急性肝衰竭與橫紋肌溶解症—中的角色，重點在於藉由吸附過量發炎介質與中分子毒素，協助降低全身性發炎反應與器官負荷；同時說明其與CRRT 及 ECMO 串聯應用之實務原則，包括建議放置位置、血流方向與基本操作流程，協助臨床團隊在重症病人血液淨化與體外循環治療中，安全且有效地整合 CytoSorb 於既有治療架構中。

  Yu-Ning Chen Speaker 精準吸附，淨化重症：吸附罐串接實戰全攻略本教學主要說明 CytoSorb 血液吸附治療於臨床常見之適應症——敗血症、急性肝衰竭與橫紋肌溶解症—中的角色，重點在於藉由吸附過量發炎介質與中分子毒素，協助降低全身性發炎反應與器官負荷；同時說明其與CRRT 及 ECMO 串聯應用之實務原則，包括建議放置位置、血流方向與基本操作流程，協助臨床團隊在重症病人血液淨化與體外循環治療中，安全且有效地整合 CytoSorb 於既有治療架構中。
• 08:15

  11:30
  D. 關鍵決策，由你掌控：模擬CRRT療程中的實戰課 Critical Decisions in Your Hands: Simulation-Based CRRT Workshop -Case Discussion & Parameter Adjustment
  臨床照護情境討論、參數調整
  Shu-Ping Liu Speaker 關鍵決策，由你掌控:模擬CRRT療程中的實戰課提供模擬病人生理監測紀錄，學員以團體合作根據多變的生命徵象（如血壓下降、TMP過高）動態調整治療參數，訓練臨床應變力與醫護共同決策能力。
• 11:30

  12:00
  抽獎、合照 Lucky Draw & Group Photo
• 12:00

  12:00
  結業 Closing

• 14:00

  14:50
  創新教學導入CVVH訓練：PGY護理師臨床能力建構模式( Innovative Teaching Integration in CVVH Training: A Clinical Competency Development Model for PGY Nurses)
  Meng-Ling Shih Speaker 創新教學導入CVVH訓練：PGY護理師臨床能力建構模式運用創新教學之CVVH教學模式，結合情境教學、問題導向學習及臨床實務導入，設計分階段訓練架構。「從知識到行動」的轉化歷程，透過案例導入與即時回饋機制，強化PGY護理師之臨床決策能力與團隊合作能力。初步實施結果顯示，學員在CVVH操作熟練度、自我效能及臨床判斷能力上均有顯著提升。
• 14:50

  15:10
  Q&A
• 15:10

  16:00
  心腎症候群下 CKRT 護理決戰關鍵時刻
  Yun-Wen Yung Speaker 心腎症候群下 CKRT 護理決戰關鍵時刻探討加護病房因各種臨床因素導致的急性腎損傷（AKI），當臨床上啟動連續性腎臟替代治療（CKRT/CRRT）的臨床判斷與決策。在ICU常見的AKI主要的原因包括敗血症與休克，另外一個原因為心臟手術。臨床上可依據國際通用的 KDIGO 指引進行分期，並結合「BE SAFE」核心指標（如腦水腫、電解質失衡、血流動力學不穩定、酸中毒、體液超載等）精確評估啟動 CKRT 的時機，強調治療應視為提供腎臟輔助而非單純取代。其核心原理包含超濾、對流與擴散，實務操作上需精準控制處方劑量與過濾分率以降低凝管風險。最後，撤離治療需運用尿量及生化指標等客觀標準，藉由跨團隊合作優化預後並促進患者腎功能恢復。
• 16:00

  16:20
  Q&A
• 16:20

  17:10
  迎戰重症 AKI 的衰弱危機：從實證資料來審視臨床實務與未來復健策略
  Chia-Huan Yang Speaker 迎戰重症 AKI 的衰弱危機：從實證資料來審視臨床實務與未來復健策略 一、衰弱症 × AKI 雙向惡性循環 二、關鍵預後數據 — 短期死亡率 + 長期功能預後 三、CRRT 患者的衰弱挑戰 — 盛行率、死亡率比較 四、衰弱評估工具（CFS） —評分量表 +　要素 五、護理照護實務建議 　 未來展望與研究缺口 — 知識缺口 + 四大復健策略方向
• 17:10

  17:30
  Q&A

• 08:30

  09:10
  From AKI to Recovery: Medication Reconciliation and Polypharmacy Management
  Chia-Chi Chen Speaker From AKI to Recovery: Medication Reconciliation and Polypharmacy Management1. Overview of Kidney-Protective and Nephrotoxic Medications 2. Medication Reconciliation and Polypharmacy Management 3. Medication Assessment and Optimization During AKI 4. Medication Review After AKI Recovery; When to Resume Kidney-Protective Therapies

  Shu-Wen Lin Moderator
• 09:10

  09:50
  Cardio-Renal Syndrome in the ICU: Pharmacological Challenges in Multi-Organ Support
  Ya-Tzu Chang Speaker Cardio-Renal Syndrome in the ICU: Pharmacological Challenges in Multi-Organ SupportThis lecture will provide an overview of pharmacological management in cardiorenal syndrome and discuss its clinical application and therapeutic dilemmas through case-based discussion. Cardiorenal syndrome refers to a pathophysiological condition in which dysfunction of the heart or kidney induces acute or chronic dysfunction in the other organ. Pharmacological strategies include decongestion therapy and medications with cardiorenal protective effects, such as RAAS inhibitors, ARNIs, MRAs, and SGLT2 inhibitors. In clinical practice, treatment decisions must consider the patient’s hemodynamic status, renal function, electrolyte abnormalities, and overall clinical stability. The goal is to balance therapeutic benefits and potential harms while optimizing cardiac and renal protection in critically ill patients.

  Chian-Ying Chou Moderator
• 09:50

  10:10
  Coffee Break
• 10:10

  10:50
  Nephrotoxic Drug Stewardship (NDS): Leveraging Real-World Data for AKI Prevention
  Yi-Ming Hua Speaker Nephrotoxic Drug Stewardship (NDS): Leveraging Real-World Data for AKI Prevention藥物及腎毒性物質暴露是住院病人急性腎損傷（AKI）重要且可介入的危險因子。腎毒性藥物管理（NDS）並非單純停用腎毒性藥物，而是透過腎功能動態監測、腎毒性負荷評估、劑量調整、治療藥物監測、交互作用辨識、替代藥物選擇及用藥整合，在治療效益與腎臟安全之間取得平衡。電子病歷中的腎功能、用藥暴露、藥物濃度、共病及臨床結局等真實世界資料，可用於建立高風險分層與臨床決策支援。然而，單獨的電子警示未必能改善結果，必須結合具體可執行的建議、藥師介入及跨專業追蹤。本演講將以腎功能相關劑量調整及多重腎毒性藥物暴露為例，說明如何建立「風險辨識、即時介入、成效追蹤、回饋改善」的 NDS 模式，以降低藥物相關 AKI，同時維持必要治療的有效性。

  Hui-Chen Su Moderator
• 10:50

  11:30
  Optimizing Pre-ESRD Care: Impact of Pharmacist-Led Clinics
  Yen-Hao Liao Speaker Optimizing Pre-ESRD Care: Impact of Pharmacist-Led ClinicsChronic kidney disease (CKD) is associated with complex medication regimens, polypharmacy, and an increased risk of drug-related problems, particularly in patients with pre-end-stage renal disease (Pre-ESRD). This session will highlight the role of pharmacist-led clinics in optimizing medication therapy management within a multidisciplinary care model. Drawing on real-world clinical experience and research findings, the presentation will discuss how pharmacist interventions can improve medication adherence, identify and resolve drug-related problems, reduce inappropriate medication use, and support better clinical outcomes. The session will also explore the evolving role of clinical pharmacists in delivering patient-centered care and enhancing the quality of Pre-ESRD management.

  Hui-Yu Chen Moderator
• 11:30

  12:10
  Using Meta-Analysis to Evaluate the Risk of AKI Associated with IVI Drugs
  Shih-Chieh Shao Speaker Using Systematic Review and Meta-Analysis to Evaluate the Risk of AKI Associated with IVI DrugsIntravitreal anti-vascular endothelial growth factor (anti-VEGF) drugs are widely used to treat retinal diseases, but concerns remain regarding their potential systemic effects, including acute kidney injury (AKI). This presentation will demonstrate how systematic review and meta-analysis can be applied to evaluate rare safety outcomes associated with intravitreal therapies.

  Kai-Cheng Chang Moderator
• 12:10

  12:25
  Panel Discussion & Q&A

• 09:00

  09:50
  AKI跨領域團隊協作：結合院內警示系統與病人心理照護之整合模式
  Tzu-Chun Chen Speaker AKI跨領域團隊協作：結合院內警示系統與病人心理照護之整合模式急性腎損傷（Acute Kidney Injury, AKI）病人常因腎功能於短時間內惡化，面臨病情不確定、治療調整、可能接受腎臟替代療法及後續追蹤等壓力。AKI照護不僅需要即時醫療處置，更仰賴跨領域團隊透過資訊系統、臨床判斷與照護溝通，及早辨識高風險病人並啟動適切介入。 本次分享將以院內AKI警示系統推動經驗為核心，分享臨床如何運用燈號分級管理協助團隊掌握病人狀態。其中，黃色燈號代表系統出現AKI警示，提醒臨床團隊需提高警覺、追蹤腎功能變化並評估潛在風險；紅色燈號代表病人已有腎功能異常，但尚未由腎臟科收案，需進一步強化通報、評估與跨團隊銜接；綠色燈號則代表病人已由腎臟科收案，進入持續追蹤與專科共同照護流程。透過此分級機制，醫療團隊可更清楚掌握AKI病人之照護進程，降低風險辨識落差與照護延遲。 課程內容將進一步說明跨領域團隊在AKI照護中的合作角色，包括腎臟科醫師對腎功能異常與治療方向之評估，護理師於尿量、輸出入量、生命徵象、體液狀態與用藥安全之持續監測，藥師協助檢視腎毒性藥物與劑量調整，營養師提供符合腎功能狀態之營養建議，個案管理師協助追蹤、轉銜與衛教銜接，資訊團隊則透過警示系統支持臨床決策與照護流程優化。 除生理照護外，本課程亦將納入AKI病人的心理照護觀點。當病人得知腎功能異常、病況可能惡化或需接受透析評估時，常出現焦慮、害怕、失控感、對未來生活改變的擔憂，以及對家人造成負擔的壓力。護理人員可透過同理傾聽、清楚且一致的說明、評估病人與家屬的理解程度、提供可執行的照護建議，並在治療決策過程中融入共享決策與病人賦能，協助病人降低不確定感並提升治療參與感。 本課程期望透過院內AKI警示系統、紅黃綠燈號管理、跨領域團隊協作與心理照護經驗分享，強化醫療團隊對AKI病人之即時辨識、照護銜接、專科介入與人本支持能力，進一步提升AKI照護品質、病人安全與長期腎臟健康結果。
• 09:50

  10:15
  ​​重症 CRRT 照護的核心關鍵：適應症評估與警訊早期介入​
  Shu-Chen Wu Speaker ​​重症 CRRT 照護的核心關鍵：適應症評估與警訊早期介入​ 隨著重症醫學的進步，連續性腎替代療法（CRRT）已成為加護病房（ICU）救治多重器官衰竭與急性腎損傷（AKI）病患不可或缺的核心技術。本講座將引領與會者回顧 CRRT 的發展演進，從早期的基本血液淨化演進至當前精準的重症支持療法。內容將深入探討 CRRT 在加護病房中的關鍵臨床適應症，包括嚴重的體液過載、電解質與酸鹼失衡、以及敗血症引起的全身性發炎反應等處置決策。 此外，CRRT 治療過程中的機台警訊往往瞬息萬變，如何「早期發現、即時干預」是決定治療成敗與維持管路壽命的護理關鍵。本堂課將結合理論與近三十年的重症與透析臨床實務經驗，系統性解析常見的 CRRT 警訊（如跨膜壓高、動靜脈壓力異常等）之背後成因與臨床處置技巧。期能協助重症照護團隊建立預警思維，在警訊發生初期即能精準介入，優化重症病患的治療成效與照護品質。
• 10:15

  10:40
  重症 CRRT從異常警報排除到跨團隊支持協作
  Li-Ming Wu Speaker 重症 CRRT從異常警報排除到跨團隊支持協作一、 進階臨床實務訓練（Simulation Training）上一堂課學到的「警報定義」與「併發症」，轉化為床邊執行的直覺反應。 （一）高壓/低壓警報的即時處置模擬：模擬動靜脈壓力異常（Access/Return Pressure）的床邊排除技巧。超濾率（Ultrafiltration）偏差與跨膜壓（TMP）過高的應變處置。 （二）無預警斷電或機件故障危機處理自動回血功能失效時，如何切換為「手動回血」流程，確保病人血液不流失 。 （三）極致管路與濾器防凝血策略：針對容易凝血的高風險病人，深入演練抗凝劑（如 Heparin 或局部檸檬酸抗凝法 Regional Citrate Anticoagulation, RCA）的精準劑量調控與床邊監測 。 二、 CRRT 跨團隊照護協作（Multidisciplinary Collaboration）： （一）醫護共同決策 ──「早期啟動」與「動態撤離」：建立 ICU 重症醫師與護理師的共同語言，依據病人的血流動力學變化的關鍵指標，動態調整治療參數 。 （二）護藥聯手 ── 藥物劑量動態精準調整（重症藥師協作）：延續上一堂提到的「低分子量與游離態藥物易被清除」之痛點 。 核心訓練： 如何與重症藥師配合，針對抗生素（如 Vancomycin、Meropenem）在 CRRT 運作期間進行動態血中濃度監測（TDM）與劑量補償，避免治療濃度不足 。 （三）護營協作 ── 高流量透析下的營養支持（營養師協作）：針對簡報提及「確保足夠營養支持」 進行具體實作。 重症營養師如何評估 CRRT 清除掉的氨基酸與微量元素，精準計算並給予適當的靜脈/腸道營養配方（TPN/EN） 。 三、 跨團隊溝通與危急資源管理（CRM）重症團隊的關鍵溝通（Structured Communication）：運用 ISBAR 溝通工具，在病人血壓崩潰 、嚴重酸中毒 或大量漏血 的危急時刻，護理師如何向醫師團隊精確回報，引導團隊快速決策。 交班盲點與連續性照護品質（Quality Indicator）：制定 ICU 白班、夜班，以及血液透析室護理師之間的優化交班檢核表（Checklist），包含管路壽命評估、累積出入量平衡（Fluid Balance）的交接 。
• 10:40

  11:05
  AKI 病人血液透析期間照護決策
  Chiung-Yu Shih Speaker AKI病人血液透析期間照護決策急性腎損傷(Acute kidney injury, AKI)是住院病人(約5%~10%)中常出現的疾病，尤其是重症病人(約60%)伴隨有多重共病症者，其發生原因甚多，且會明顯增加病人的發病率和死亡率，不應被視為單一疾病；其臨床處置需更瞭解體液和電解質的平衡，給予評估及決策適當的透析治療模式；然其模式決策的選擇，應依血流動力學的穩定性進行評估。不穩定者優先採用連續性腎臟替代治療（CRRT）或緩慢低效率每日血液透析過濾術(SLEDD-f)，以降低心血管負荷；穩定者則可選用間歇性血液透析（IHD），避免透析中低血壓，造成腎臟再次缺血損傷；同時需每日評估並滾動式調整透析醫囑與電解質參數，維持治療穩定安全。 綜論，建立標準化的AKI預防處置，抉擇適當的透析治療策略及臨床照護，確保病人安全，在清除素毒與血流動力學穩定下，阻斷AKI的病程，以促進腎功能的恢復。 課程重點大綱:1.AKI病人透析適應症判斷 2.透析模式選擇 3.透析期間常見併發症 4.護理決策與即時處置
• 11:05

  11:30
  急性腎損傷病人血液透析的照護缺口：第一線護理師的臨床決策與實務分享
  Li-Hwa Tsai Speaker 急性腎損傷病人血液透析的照護缺口：第一線護理師的臨床決策與實務分享臨床實務上，發對於急性腎損傷（AKI）病人血液透析的照護缺乏系統化的指引，導致前、中、後期的照護決策流於破碎與被動執行醫囑。本次報告將從第一線臨床實務出發，分享如何建構「三階段全期護理照護決策地圖」。內容橫跨三核心階段：(1) 啟動期扮演安全守門員，結合生理數據給予個體化透析處方建議；(2)透析中利用早期預警指標，在低血壓發生前主動決策介入，嚴防二次腎損傷；(3)返家/出院期透過結構化照護，延續病人自我管理。期盼藉由本次現狀分享與交流，推動標準化照護共識，彰顯護理人員在動態決策中的關鍵價值，進而優化AKI病人的臨床預後。
• 11:30

  11:45
  AKI-to-CKD 智能照護流程建構與實務成效
  I-Chen Lee Speaker AKI-to-CKD 智能照護流程建構與實務成效急性腎損傷（Acute Kidney Injury, AKI）為住院病人常見且高風險之臨床問題，若未及早辨識與介入，可能進展為急性腎臟病（AKD）甚至慢性腎臟病（CKD），增加透析、再住院及死亡風險。本院透過資訊系統整合，建立 AKI E-alert System，利用住院、急診及門診血清肌酸酐（Serum Creatinine）變化，自動比對基準值，依據 KDIGO 標準進行 AKI 分期與警示，提升臨床團隊對 AKI 病人的即時辨識能力。進一步結合台灣健保 AKD 與 CKD 照護條件，建置 CKD MAP，並導入 One Team 住院個案管理系統，整合腎臟科醫師、個管師、護理師、藥師及營養師跨團隊照護流程。系統可自動篩選符合收案條件之病人，協助個案管理介入、腎毒性藥物檢視、營養與衛教評估，以及出院後 AKD/CKD 門診追蹤轉介，建立完整 AKI-to-CKD 照護鏈結。本次分享將介紹本院 AKI 智能警示系統架構、AKD照護流程設計、跨團隊照護模式及資訊整合策略，並呈現導入後之收案率、腎臟科會診率、個案追蹤率及照護效益成果。期望透過數位轉型與精準照護模式，提升 AKI 病人早期介入與長期腎臟保護成效，作為未來 AKI-to-CKD 整合照護之實務參考。
• 11:45

  12:00
  急性腎損傷個案管理策略
  Chiao-Chuan Huang Speaker 急性腎損傷個案管理策略本院推行以病人為中心之急性腎損傷個案管理策略，落實跨團隊衛教機制，強化病人對疾病進程的認知，以提升定期接受腎臟專科追蹤之遵從性。護理師教導AKD惡化因子及日常照護，並建立用藥安全觀念，如：避免自行服用 NSAIDs 等腎毒性藥物。導入智能化資訊系統主動篩選符合條件病人，即時提示醫療團隊進行AKD照護，本照護模式透過「病人自主、醫護精準、資訊智能」期能達到早期發現、即時介入，以降低 AKD惡化為慢性腎臟病（CKD）之風險。
• 12:00

  12:15
  衛教師經驗分享：衛教師的角色與實務觀點
  Tsung-Lin Wu Speaker
• 12:15

  12:20
  Q&A

• 08:30

  09:10
  Micronutrient Strategy in Critically Ill AKI Patients: Balancing Oxidative Stress, Inflammation, and CRRT Losses
  Yin-Yi Han Speaker Micronutrient Strategy in Critically Ill AKI Patients: Balancing Oxidative Stress, Inflammation, and CRRT LossesAcute kidney injury is common in critically ill patients and is frequently accompanied by systemic inflammation, oxidative stress, mitochondrial dysfunction, immune dysregulation, and metabolic instability. In this context, micronutrients are not merely supportive supplements; they serve as essential cofactors for antioxidant defense, immune competence, endothelial integrity, energy metabolism, and tissue repair. However, micronutrient management in critically ill patients with AKI is challenging because of increased requirements, difficulty in assessing deficiency, impaired renal clearance, and substantial losses during continuous renal replacement therapy (CRRT). This lecture will discuss practical micronutrient strategies for critically ill patients with AKI, focusing on key nutrients such as thiamine, vitamin C, vitamin D, selenium, zinc, copper, and other trace elements. Their biological roles, potential CRRT-related losses, clinical relevance, and safety considerations will be reviewed. Based on current evidence and clinical experience, a risk-adapted, phase-based approach will be proposed to balance deficiency correction, metabolic resilience, and avoidance of excessive supplementation in this vulnerable population.
• 09:10

  09:50
  Energy and Protein Prescription in AKI During CRRT: Precision Nutrition Support vs Predictive Estimation
  Chih-Yi Hsu Speaker Energy and Protein Prescription in AKI During CRRT: Precision Nutrition Support vs Predictive Estimation急性腎損傷（AKI）合併連續性腎臟替代治療（CRRT）患者常處於高度代謝壓力與蛋白質分解狀態，且CRRT過程中會增加胺基酸、葡萄糖及微量營養素流失，使能量與蛋白質需求更加複雜。傳統以預測公式進行營養處方，於此族群可能產生顯著誤差，無法反映個別病人的動態代謝變化。近年來，精準營養支持概念逐漸受到重視，強調依據間接熱量測定、氮平衡及臨床病程進行個別化調整。本演講將比較預測估算與精準營養策略於CRRT病人中的應用，並探討其臨床可行性與實務整合，以提升重症營養照護品質。
• 09:50

  10:10
  Coffee Break
• 10:10

  10:50
  Preoperative Metabolic Optimization: Can Amino Acid Supplementation Reduce Postoperative AKI?
  Tsui-Yin Tung Speaker Preoperative Metabolic Optimization: Can Amino Acid Supplementation Reduce Postoperative AKI?研究與統合分析證實，手術中靜脈輸注胺基酸顯著降低AKI風險。機制為激發腎儲備功能、優化腎臟灌注。此方案安全且具成本效益，縮短住院天數。雖未降低死亡率，仍是Level 1實證的可行方式。
• 10:50

  11:30
  Nutrition in Hepato-Renal Syndrome: Protein Restriction, Keto-Analogues, and Metabolic Modulation
  Hong Kai-Yi Speaker
• 11:30

  12:10
  Post-AKI Nutritional Recovery: Preventing Sarcopenia and Slowing AKI-to-CKD Transition
  Shu-Tzu Chen Speaker Post-AKI Nutritional Recovery: Preventing Sarcopenia and Slowing AKI-to-CKD TransitionIt is a misconception that patients recovering from acute kidney injury should avoid a high-protein diet that may increase the risk of sarcopenia. However, this concept is not supported by current evidence. Adequate protein intake helps preserve lean body mass by reducing muscle protein breakdown, but high protein intake alone does not stimulate muscle hypertrophy. Excessive protein consumption may only increase nitrogenous waste production and impose an unnecessary metabolic burden on the recovering kidneys. The most effective strategy for increasing muscle mass is resistance exercise combined with appropriate nutritional supplement. Carbohydrate intake before exercise helps reduce muscle protein breakdown, while adequate carbohydrate with a small amount of protein after exercise effectively stimulates muscle protein synthesis and promotes muscle growth. This lecture will review the physiological mechanisms underlying skeletal muscle hypertrophy and discuss evidence-based exercise and nutritional strategies for the prevention and treatment of sarcopenia in patients with kidney disease, with particular emphasis on those recovering from acute kidney injury. 若需中文摘要 如下 急性腎損傷恢復期的病人不適合攝取高蛋白質飲食可能導致肌少症發生是錯誤的觀念，因為增加蛋白質攝取才能增加肌肉量避免肌少症發生並不正確。足夠的蛋白質可避免肌肉分解，但不會增加肌肉量。增加肌肉量不需要大量的蛋白質，過多的蛋白質只會產生較多的含氮廢物增加腎臟負擔。增加肌肉量需要阻力運動與運動前、後正確的營養補充;運動前補充糖類可避免肌肉耗損，運動後補充足夠的糖與少量蛋白質就能有效增加肌肉量。本次演講內容以增加肌肉組成的生理機制為基礎，重點說明預防或治療腎臟病人肌少症的運動營養補充策略。Panel Discussion: From ICU to Community – Building a Renal Nutrition Care ContinuumPatients with acute kidney injury (AKI), especially those requiring intensive care and kidney replacement therapy, are at high risk of malnutrition, muscle wasting, and functional decline. However, nutritional care is often fragmented during the transition from acute illness to recovery and long-term kidney care. This panel will discuss strategies to establish a continuum of renal nutrition care from ICU to community, including individualized nutrition support during AKI, protein and energy management , post-AKI nutritional recovery , and multidisciplinary approaches to improve long-term outcomes and quality of life.
• 12:10

  12:25
  Panel Discussion: From ICU to Community – Building a Renal Nutrition Care Continuum
  Shu-Tzu Chen Speaker Post-AKI Nutritional Recovery: Preventing Sarcopenia and Slowing AKI-to-CKD TransitionIt is a misconception that patients recovering from acute kidney injury should avoid a high-protein diet that may increase the risk of sarcopenia. However, this concept is not supported by current evidence. Adequate protein intake helps preserve lean body mass by reducing muscle protein breakdown, but high protein intake alone does not stimulate muscle hypertrophy. Excessive protein consumption may only increase nitrogenous waste production and impose an unnecessary metabolic burden on the recovering kidneys. The most effective strategy for increasing muscle mass is resistance exercise combined with appropriate nutritional supplement. Carbohydrate intake before exercise helps reduce muscle protein breakdown, while adequate carbohydrate with a small amount of protein after exercise effectively stimulates muscle protein synthesis and promotes muscle growth. This lecture will review the physiological mechanisms underlying skeletal muscle hypertrophy and discuss evidence-based exercise and nutritional strategies for the prevention and treatment of sarcopenia in patients with kidney disease, with particular emphasis on those recovering from acute kidney injury. 若需中文摘要 如下 急性腎損傷恢復期的病人不適合攝取高蛋白質飲食可能導致肌少症發生是錯誤的觀念，因為增加蛋白質攝取才能增加肌肉量避免肌少症發生並不正確。足夠的蛋白質可避免肌肉分解，但不會增加肌肉量。增加肌肉量不需要大量的蛋白質，過多的蛋白質只會產生較多的含氮廢物增加腎臟負擔。增加肌肉量需要阻力運動與運動前、後正確的營養補充;運動前補充糖類可避免肌肉耗損，運動後補充足夠的糖與少量蛋白質就能有效增加肌肉量。本次演講內容以增加肌肉組成的生理機制為基礎，重點說明預防或治療腎臟病人肌少症的運動營養補充策略。Panel Discussion: From ICU to Community – Building a Renal Nutrition Care ContinuumPatients with acute kidney injury (AKI), especially those requiring intensive care and kidney replacement therapy, are at high risk of malnutrition, muscle wasting, and functional decline. However, nutritional care is often fragmented during the transition from acute illness to recovery and long-term kidney care. This panel will discuss strategies to establish a continuum of renal nutrition care from ICU to community, including individualized nutrition support during AKI, protein and energy management , post-AKI nutritional recovery , and multidisciplinary approaches to improve long-term outcomes and quality of life.

• 14:00

  14:30
  SGLT-2 抑制劑於慢性腎臟病之臨床應用與保護機轉
  Chung-Kuan Wu Speaker SGLT-2 抑制劑於慢性腎臟病之臨床應用與保護機轉 The role of SGLT2 inhibitors in the treatment of diabetic and non-diabetic kidney disease Diabetic kidney disease is a major cause of chronic kidney disease and end-stage kidney disease. In addition to hyperglycemia and metabolic abnormalities, its pathophysiology involves glomerular hyperfiltration, increased intraglomerular pressure, excessive tubular workload, and renal inflammation. Sodium-glucose cotransporter-2 inhibitors (SGLT2 inhibitors) reduce glucose and sodium reabsorption in the proximal tubule, restore tubuloglomerular feedback, lower intraglomerular pressure, decrease tubular workload, and may attenuate renal inflammation. These mechanisms contribute to cardiovascular and kidney protection beyond their glucose-lowering effects. In addition, the sustained beneficial effects extend to non-diabetic kidney disease. Large clinical trials and meta-analyses have demonstrated that SGLT2 inhibitors reduce albuminuria, slow kidney function decline, and decrease cardiovascular and renal adverse events. These benefits were observed in addition to standard treatment with renin–angiotensin system inhibitors. Key topics of the presentation include: 1. The physiological roles of SGLT1 and SGLT2 in the intestine and proximal renal tubule 2. The mechanisms by which SGLT2 inhibition reduces intraglomerular pressure, tubular workload, and renal inflammation 3. Cardiovascular and renal outcomes from the clinical trial, and relevant meta-analyses 4. The role of SGLT2 inhibitors in the comprehensive management of patients with type 2 diabetes and chronic kidney disease according to the KDIGO guideline Overall, SGLT2 inhibitors have evolved from glucose-lowering agents into a fundamental component of cardiovascular and kidney risk management in diabetic kidney disease. Their timely use, based on kidney function, albuminuria, cardiovascular risk, and the overall comorbidity profile, may help delay kidney disease progression and improve long-term clinical outcomes. The role of SGLT2 inhibitors in the treatment of diabetic and non-diabetic kidney disease Diabetic kidney disease is a major cause of chronic kidney disease and end-stage kidney disease. In addition to hyperglycemia and metabolic abnormalities, its pathophysiology involves glomerular hyperfiltration, increased intraglomerular pressure, excessive tubular workload, and renal inflammation. Sodium-glucose cotransporter-2 inhibitors (SGLT2 inhibitors) reduce glucose and sodium reabsorption in the proximal tubule, restore tubuloglomerular feedback, lower intraglomerular pressure, decrease tubular workload, and may attenuate renal inflammation. These mechanisms contribute to cardiovascular and kidney protection beyond their glucose-lowering effects. In addition, the sustained beneficial effects extend to non-diabetic kidney disease. Large clinical trials and meta-analyses have demonstrated that SGLT2 inhibitors reduce albuminuria, slow kidney function decline, and decrease cardiovascular and renal adverse events. These benefits were observed in addition to standard treatment with renin–angiotensin system inhibitors. Key topics of the presentation include: 1. The physiological roles of SGLT1 and SGLT2 in the intestine and proximal renal tubule 2. The mechanisms by which SGLT2 inhibition reduces intraglomerular pressure, tubular workload, and renal inflammation 3. Cardiovascular and renal outcomes from the clinical trial, and relevant meta-analyses 4. The role of SGLT2 inhibitors in the comprehensive management of patients with type 2 diabetes and chronic kidney disease according to the KDIGO guideline Overall, SGLT2 inhibitors have evolved from glucose-lowering agents into a fundamental component of cardiovascular and kidney risk management in diabetic kidney disease. Their timely use, based on kidney function, albuminuria, cardiovascular risk, and the overall comorbidity profile, may help delay kidney disease progression and improve long-term clinical outcomes.
• 14:30

  15:00
  GLP-1 受體促效劑在腎臟與心血管代謝保護的新進展
  Ming-Tso Yen Speaker
• 15:00

  15:30
  新型鉀離子結合劑 Lokelma 的應用
  Kuang-Yu Wei Speaker 新型鉀離子結合劑 Lokelma 的應用Over the past decade, treatment of chronic kidney disease (CKD) and heart failure has evolved towards an integrated approach to cardiorenal protection that includes renin–angiotensin–aldosterone system (RAAS) inhibitors, mineralocorticoid receptor antagonists (MRAs), sodium–glucose cotransporter 2 (SGLT2) inhibitors and more individualized strategies for dietary potassium intake. RAAS inhibitors remain a cornerstone of treatment, and clinical trials have generally demonstrated the greatest benefits when these drugs are prescribed at maximally tolerated doses. However, the risk of hyperkalaemia frequently limits their initiation, dose optimization and continued use, thereby reducing the potential kidney and cardiovascular benefits of treatment. Hyperkalaemia should therefore be regarded as a manageable complication of cardiorenal therapy rather than an automatic indication to reduce or discontinue RAAS inhibition. Contemporary management includes correction of reversible causes together with individualized dietary interventions, diuretics, SGLT2 inhibitors and potassium-lowering therapies. The aim of these strategies is not merely to achieve a transient reduction in blood potassium, but to enable patients to initiate and maintain guideline-directed treatment. When further inhibition of the RAAS pathway is indicated, an MRA can be added to a maximally tolerated angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. In individuals at increased risk of hyperkalemia, the non-steroidal MRA may offer a more favorable potassium profile than steroidal MRAs. Beyond their established cardiorenal benefits, SGLT2 inhibitors reduce the risk of serious hyperkalemia and could therefore facilitate continued treatment with RAAS inhibitors and MRAs. Novel potassium binders, including sodium zirconium cyclosilicate and patiromer, effectively reduce blood potassium levels and prevent recurrent hyperkalaemia, thereby enabling sustained or intensified RAAS inhibitor therapy in patients with CKD and heart failure. Sodium zirconium cyclosilicate has also been shown to control predialysis hyperkalaemia in patients receiving haemodialysis. Emerging evidence suggests that potassium binders may have additional effects, including reductions in aldosterone levels, systolic blood pressure and urinary albumin excretion with patiromer, and increased serum bicarbonate concentrations with sodium zirconium cyclosilicate. By mitigating the risk of hyperkalemia, potassium binders could also enable some patients with CKD to adopt healthier potassium-rich, plant-predominant dietary patterns.