Lesson 1Urine studies and interpretation: urinalysis, urine sediment microscopy, urine electrolytes, fractional excretion of sodium and ureaThis section details how to obtain and interpret urine studies in AKI on CKD, including urinalysis, sediment microscopy, urine electrolytes, and fractional excretion indices, to differentiate prerenal, intrinsic, and postrenal causes and refine diagnosis.
Standard urinalysis and dipstick findingsSediment microscopy and key castsUrine sodium and osmolality patternsFENa, FEUrea, and their limitationsIntegrating urine data with clinical contextLesson 2Acute complications requiring urgent action: hyperkalemia, severe acidosis, pulmonary oedema, uremic manifestationsThis section addresses acute complications of AKI on CKD that require urgent action, including hyperkalemia, severe metabolic acidosis, pulmonary oedema, and uremic manifestations, with emphasis on stabilisation and indications for emergent dialysis.
Emergency management of hyperkalemiaTreatment of severe metabolic acidosisRecognition and therapy of pulmonary edemaIdentifying uremic symptoms and signsDialysis triggers in acute complicationsLesson 3Definitions and staging of AKI and CKD, KDIGO criteria and integrationThis section reviews definitions and staging of AKI and CKD, focusing on KDIGO criteria, integration of acute and chronic changes, and how staging informs prognosis, monitoring intensity, and thresholds for specialist consultation.
KDIGO AKI diagnostic criteriaKDIGO AKI staging and prognosisCKD definition, staging, and GFR categoriesIntegrating AKI on CKD classificationsImplications for follow-up and counselingLesson 4Pathophysiology of acute on chronic kidney injury: haemodynamic, intrinsic, and postrenal causesThis section explores the pathophysiology of acute on chronic kidney injury, distinguishing haemodynamic, intrinsic renal, and postrenal mechanisms, and linking these processes to clinical patterns, diagnostic tests, and targeted therapeutic strategies.
Hemodynamic causes and renal perfusionIntrinsic tubular and glomerular injuryPostrenal obstruction mechanismsNeurohormonal activation in CKD and AKIPathophysiology–guided treatment choicesLesson 5Identification and management of reversible precipitants: sepsis, nephrotoxins, volume depletion or overload, obstructionThis section reviews how to recognise and treat reversible AKI triggers in CKD, including sepsis, nephrotoxins, volume depletion or overload, and urinary obstruction, with emphasis on rapid correction and prevention of further kidney damage.
Recognizing sepsis and hemodynamic instabilityIdentifying and stopping nephrotoxic medicationsAssessing hypovolemia and fluid responsivenessManaging volume overload and decongestionDetecting and relieving urinary tract obstructionLesson 6Imaging indications and interpretation: renal ultrasound for obstruction, bladder scan, point-of-care ultrasound for volume statusThis section explains when and how to use imaging in AKI on CKD, including renal ultrasound for obstruction, bladder scanning for retention, and point-of-care ultrasound to assess volume status, cardiac function, and pulmonary congestion.
Indications for renal ultrasoundRecognizing hydronephrosis and obstructionBladder scan for retention and retention riskPOCUS for IVC and volume assessmentLung and cardiac POCUS in AKI on CKDLesson 7Key laboratory interpretation: creatinine kinetics, BUN/creatinine ratio, electrolytes, acid-base analysis, lactateThis section focuses on interpreting key laboratory data in AKI on CKD, including creatinine kinetics, BUN/creatinine ratio, electrolytes, acid–base status, and lactate, to distinguish acute from chronic changes and guide urgent management decisions.
Creatinine trends and baseline estimationUsing BUN/creatinine ratio in contextElectrolyte patterns in AKI on CKDAcid–base analysis and anion gap useLactate, perfusion, and tissue hypoxiaLesson 8Decision-making for renal replacement therapy in AKI: indications, timing, modality selection (intermittent haemodialysis vs CRRT vs SLED)This section covers decision-making for renal replacement therapy in AKI on CKD, including classic indications, timing debates, and selection among intermittent haemodialysis, CRRT, and SLED based on haemodynamics, resources, and goals of care.
Absolute and relative indications for RRTEarly versus delayed initiation strategiesChoosing intermittent HD versus CRRTWhen to use SLED and hybrid approachesAnticoagulation and access considerationsLesson 9Interdisciplinary communication with ICU, ED, primary teams and nursing for urgent AKI careThis section emphasises effective communication among ICU, ED, primary teams, and nursing in urgent AKI care, focusing on shared mental models, clear task delegation, escalation triggers, and standardised handoffs to improve safety and outcomes.
Essential data to share during handoffClarifying roles and responsibilitiesEscalation criteria and rapid responseCommunicating dialysis urgency and plansDocumentation and closed-loop communicationLesson 10Initial rapid bedside assessment: history, focused exam, volume status, haemodynamicsThis section outlines a structured bedside approach to AKI on CKD, integrating focused history, targeted physical examination, volume status assessment, and haemodynamic evaluation to rapidly identify life-threatening problems and likely AKI aetiology.
Key history elements in AKI on CKDFocused exam for perfusion and congestionBedside tools for volume status assessmentBlood pressure, MAP, and perfusion targetsRisk stratification for deterioration and ICU
