Figure Core mechanisms examiners expect in CICM/FFICM/EDIC answers. Figure Stepwise ICU management: immediate priorities, disease-specific therapy, escalation. Figure Classification and decision thresholds used in exam answers. Figure The AKI is staged by the creatinine rise and the urine fall (KDIGO 1-2-3); the prevention is the haemodynamics, the avoidance of the nephrotoxin, and the functional imaging. The biomarkers (the NGAL, the cystatin C) flag the injury before the creatinine; the RRT waits for the refractory hyperkalaemia, acidosis, fluid, and uraemia. AKI = abrupt kidney function reduction → urea/creatinine rise + fluid/electrolyte/acid-base derangement. KDIGO staging : Stage 1 (Cr ≥26.5 μmol/L in 48h OR 1.5-1.9x baseline; UO <0.5 mL/kg/hr × 6-12h), Stage 2 (Cr 2-2.9x; UO <0.5 × ≥12h), Stage 3 (Cr ≥3x OR RRT; UO <0.3 × ≥24h OR anuria ≥12h). Causes : PRE-renal (hypoperfusion — most common), INTRA-renal (ATN — ischaemia/toxins — most common intrinsic), POST-renal (obstruction). Prevention (mainstay — NO proven treatment): avoid nephrotoxins + optimise perfusion + monitor. RRT timing : AKIKI/STARRT-AKI — NO mortality benefit of EARLY RRT — wait for AEIOU. Mortality : Stage 1 10%, Stage 2 20%, Stage 3 40-50%.
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Clinical pearls
High-yield AKI points for CICM/FFICM exam
KDIGO staging — creatinine + urine output. (1) KDIGO (2012 — Kidney Disease: Improving Global Outcomes): international consensus definition + staging of AKI. (2) STAGING (based on creatinine AND/OR urine output — whichever is WORSE): (a) Stage 1 (MILD): creatinine ≥26.5 μmol/L (0.3 mg/dL) increase within 48h OR 1.5-1.9x baseline; urine output <0.5 mL/kg/hr for 6-12 hours. (b) Stage 2 (MODERATE): creatinine 2.0-2.9x baseline; urine <0.5 mL/kg/hr for ≥12 hours. (c) Stage 3 (SEVERE): creatinine ≥3.0x baseline OR ≥354 μmol/L (4.0 mg/dL) OR initiation of RRT; urine <0.3 mL/kg/hr for ≥24 hours OR anuria for ≥12 hours. (3) USE: (a) STAGE daily (track trajectory — worsening = worse prognosis; improving = recovering). (b) GUIDE management (Stage 3 → consider RRT; monitor closely). (c) RESEARCH (standardised definition — compare outcomes). (4) KEY: KDIGO staging requires KNOWING baseline creatinine (if unknown — estimate from MDRD formula assuming eGFR 75 — but this is imprecise). ALWAYS try to find baseline (previous blood tests). (5) URINE OUTPUT: need CATHETER (monitor hourly — calculate mL/kg/hr). Anuria (<50 mL/day) → suspect obstruction (catheter to exclude) OR bilateral renal artery occlusion OR severe ATN/cortical necrosis. (6) LIMITATIONS: creatinine is a LATE marker (doesn't rise until 25-50% of kidney function lost — by then significant injury has occurred) — biomarkers (NGAL, TIMP-2) may detect earlier (see below).[1] }Prevention is the mainstay — NO proven treatment. (1) THE KEY CONCEPT: there is NO drug that REVERSES established AKI. Once ATN (tubular necrosis) occurs → the tubular cells must REGENERATE → takes days-weeks → during this time → SUPPORTIVE care (manage fluid, electrolytes, acidosis, RRT if needed). (2) WHAT DOESN'T WORK (debunked treatments): (a) DIURETICS (frusemide): DON'T treat AKI — they manage fluid (may convert oliguric → non-oliguric — but DON'T improve renal recovery or mortality — CARRESSIC trial — high-dose frusemide in AKI — no outcome benefit). Use for FLUID MANAGEMENT only (if overloaded). (b) 'RENAL DOSE DOPAMINE' (2-5 mcg/kg/min): DEBUNKED — no renal benefit (Lee 2010 meta-analysis — no improvement in renal function or mortality — MORE arrhythmia). DON'T use. (c) FENOLDOPAM (dopamine-1 agonist): no proven benefit. (d) N-ACETYLCYSTEINE (NAC): for non-paracetamol AKI — no proven benefit (some use for contrast prophylaxis — but PRESERVE trial showed saline = bicarbonate + NAC no benefit). (e) ATRIAL NATRIURETIC PEPTIDE (ANP): mixed results — not standard. (f) ERYTHROPOIETIN, GROWTH FACTORS: experimental — not standard. (3) WHAT DOES WORK (PREVENTION): (a) AVOID NEPHROTOXINS (NSAIDs, aminoglycosides, contrast — stop/avoid if possible in at-risk). (b) OPTIMISE PERFUSION (fluids if hypovolaemic; vasopressors if vasodilated; inotropes if cardiac). (c) MONITOR (creatinine + urine output daily in ICU — detect early — intervene before ATN). (d) RISK STRATIFY (elderly, CKD, diabetes, sepsis, heart failure → higher risk → heightened vigilance). (4) KEY: AKI is PREVENTABLE (if recognised early + perfusion optimised + nephrotoxins stopped) but NOT TREATABLE once established (supportive care + time for healing). PREVENTION IS THE MAINSTAY.[1] }AKIKI + STARRT-AKI — EARLY vs LATE RRT. (1) THE QUESTION: when to START RRT in AKI — early (at some threshold — e.g., KDIGO Stage 3, BUN >80) vs late (wait for clinical indications — AEIOU)? (2) AKIKI (2016, NEJM): RCT — early RRT (within 6h of KDIGO Stage 3) vs delayed (RRT only if AEIOU indication developed) → NO mortality difference (48.5% vs 49.7% at 60 days). Early group had MORE RRT (some patients in delayed group RECOVERED without RRT — 49% never needed RRT). (3) STARRT-AKI (2020, NEJM): RCT — early (KDIGO Stage 2 → immediate RRT) vs delayed (AEIOU or no recovery after ≥72h) → NO mortality difference (43.9% vs 43.7% at 90 days). Early group had MORE adverse events (infection [catheter], bleeding [anticoagulation]). (4) IDEAL-ICU (2018): early vs late in septic shock AKI → NO difference. (5) CONCLUSION: NO MORTALITY BENEFIT of EARLY RRT → WAIT for clinical indications (AEIOU). Starting RRT EARLY: (a) EXPOSES patients to unnecessary RRT (those who would have recovered without). (b) INCREASES complications (catheter infection, bleeding from anticoagulation, haemodynamic instability). (c) COSTS more. (6) EXCEPTION: if clearly going to need RRT (rapidly rising creatinine + oliguria + fluid overloaded + trend suggests inevitable) → may start EARLIER (pre-emptive — daytime — planned — avoid emergency overnight RRT). (7) PRACTICE: DON'T rush to RRT for 'rising creatinine' alone → WAIT for AEIOU indications. Start when LIFE-THREATENING complications develop (or if trajectory clearly heading toward RRT — start pre-emptively during day).[2] }Biomarkers — NGAL, TIMP-2•IGFBP7 (NephroCheck). (1) PROBLEM with CREATININE: (a) LATE marker (doesn't rise until 25-50% of GFR lost — by then significant injury has occurred). (b) SLOW to change (takes 24-48h to rise after injury — can't detect REAL-TIME). (c) Dependent on MUSCLE MASS (elderly, cachectic → less creatinine → underestimate AKI severity). (2) NEW BIOMARKERS (detect injury EARLIER — BEFORE creatinine rises): (a) NGAL (neutrophil gelatinase-associated lipocalin): released from injured tubular cells → rises within 2-6 HOURS of AKI → EARLIER than creatinine. Urine + plasma NGAL. Useful for EARLY DETECTION (especially contrast-induced, post-cardiac surgery). (b) TIMP-2•IGFBP7 (NephroCheck — Sapphire/Bihorac 2014): cell cycle arrest markers — released by stressed tubular cells BEFORE necrosis. URINE test. PREDICTS AKI (KDIGO Stage 2-3) within 12 HOURS. If TIMP-2•IGFBP7 >0.3 → HIGH risk of moderate-severe AKI within 12h (sensitivity ~90%, specificity ~50%). SAPS trial (2019, NEJM) — NephroCheck-guided care (vs standard) → NO outcome benefit (but the biomarker PREDICTS AKI — it doesn't PREVENT it — interventions need to be effective for benefit). (c) CYSTATIN C: small protein — freely filtered by glomerulus → measures GFR (better than creatinine in ICU — not affected by muscle mass). Useful for GFR estimation (especially in elderly, cachectic, cirrhosis). (3) CLINICAL USE (EMERGING — not yet routine): (a) EARLY DETECTION: if biomarker positive (NGAL/TIMP-2 elevated) + creatinine normal → SUBCLINICAL AKI (injury present but creatinine hasn't risen yet) → heighten vigilance + intensify prevention (stop nephrotoxins, optimise perfusion). (b) RISK STRATIFICATION: biomarker positive in ED/ICU admission → HIGH risk of AKI → closer monitoring + proactive prevention. (c) NOT yet STANDARD (biomarkers not universally available + SAPS showed no outcome benefit from biomarker-guided care — but research continues). (4) KEY: biomarkers (NGAL, TIMP-2) detect AKI EARLIER than creatinine — but NO proven outcome benefit from biomarker-guided care (SAPS) — emerging — may help in future (as effective AKI treatments are developed).[5] }Pre-renal → ATN — the progression. (1) THE SPECTRUM: pre-renal AKI → if untreated → progresses to ATN (intrinsic). (2) PRE-RENAL (compensated): (a) Reduced PERFUSION (hypovolaemia, shock, heart failure) → kidney HYPOPERFUSED. (b) KIDNEY COMPENSATES: (i) Afferent arteriole DILATES (prostaglandins — to maintain GFR despite low pressure). (ii) Efferent arteriole CONSTRICTS (angiotensin II — to maintain GFR despite low pressure). (iii) RAAS activated (retain Na + water — restore volume). (c) TUBULES INTACT (no necrosis — just 'stunned' from low perfusion). (d) URINE: concentrated (osm >500), Na <20, FENa <1%, bland sediment. (e) RAPIDLY REVERSIBLE: restore perfusion (fluids, vasopressors) → kidney recovers within HOURS-24h. (3) ATN (decompensated — tubular necrosis): (a) If pre-renal PERSISTS (perfusion not restored) → PROLONGED ISCHAEMIA → TUBULAR NECROSIS (tubular cells die). (b) ALSO: direct TOXIN (NSAIDs, aminoglycosides, contrast, myoglobin, haemoglobin) → direct tubular cell death. (c) TUBULES DAMAGED (necrosis — cells slough off → casts — 'muddy brown granular casts'). (d) URINE: isosthenuria (can't concentrate — osm <350), Na >40, FENa >2%, muddy brown casts. (e) NOT rapidly reversible (takes DAYS-WEEKS to regenerate tubular cells — supportive care during healing). (4) THE TRANSITION: pre-renal → ATN occurs when ischaemia PERSISTS (typically >6-12h of severe hypoperfusion) → tubular cell injury → necrosis. ONCE ATN → the course is prolonged (days-weeks — even if perfusion restored — the necrotic cells must be replaced). (5) CLINICAL IMPLICATION: TREAT PRE-RENAL EARLY (before it progresses to ATN) → rapid recovery. If already ATN → supportive (no treatment — time). (6) FENa: pre-renal <1% (retaining Na); ATN >2% (can't retain Na — tubular damage). BUT: FENa is confounded by DIURETICS (frusemide causes Na loss → FENa high even in pre-renal) → if patient on diuretics → FENa unreliable → use FENa <1% is supportive of pre-renal but not definitive if diuretics given. (7) PRACTICE: assess volume status (clinical + ultrasound) → if hypovolaemic → fluids (restore before ATN). Check FENa/urine Na (if available — helps distinguish pre-renal from ATN — but clinical assessment is more important).[1] }Drug dosing in AKI — adjust ALL medications. (1) AKI reduces CLEARANCE of renally excreted drugs → accumulation → toxicity. (2) ADJUST DOSE based on eGFR (estimated from creatinine — but in AKI, eGFR is CHANGING — use CURRENT creatinine — and reassess daily). (3) COMMONLY OVERDOSED DRUGS in AKI: (a) VANCOMYCIN: renally cleared → accumulates in AKI → nephrotoxic + ototoxic. TDM (trough or AUC) — adjust based on levels + renal function. (b) BETA-LACTAMS (pip-tazo, meropenem, cefepime): renally cleared → accumulate → neurotoxicity (seizures — especially cefepime). Adjust dose for eGFR. Consider extended/continuous infusion (maintains time above MIC without high peaks). (c) GABAPENTIN/PREGABALIN: renally cleared → accumulates → somnolence, ataxia, respiratory depression. Reduce dose or hold. (d) MORPHINE: active metabolites (M6G) renally cleared → accumulates → prolonged narcosis. Use FENTANYL (no active renal metabolites) or reduce morphine dose. (e) DIGOXIN: renally cleared → accumulates → toxicity (arrhythmia). TDM + dose-adjust. (f) ENOXAPARIN (LMWH): renally cleared → accumulates → bleeding. Reduce dose or switch to UFH (shorter half-life — easier to reverse). (g) METFORMIN: renally cleared → accumulates → LACTIC ACIDOSIS (especially in AKI — STOP metformin in AKI). (4) PHARMACIST REVIEW: every AKI patient → pharmacist reviews ALL medications → adjusts for renal function → prevents toxicity. (5) MONITOR: drug levels (vancomycin, aminoglycosides, digoxin) — trend — adjust. (6) KEY: AKI changes drug clearance → adjust ALL renally cleared drugs (or the patient develops toxicity from standard doses). Pharmacist review is essential.[1] }Diuretics in AKI — DON'T treat but manage fluid. (1) DIURETICS (frusemide) in AKI: (a) DON'T TREAT AKI (no evidence of improved renal recovery or mortality). (b) DON'T PREVENT progression (don't stop pre-renal → ATN). (c) CARRESSIC trial (2017): high-dose frusemide in AKI with fluid overload → NO difference in renal recovery or mortality (but did increase urine output + reduced fluid). (2) WHAT DIURETICS DO IN AKI: (a) MANAGE FLUID OVERLOAD: if AKI + fluid overloaded (pulmonary oedema) → frusemide → offload volume → improves oxygenation. (b) CONVERT OLIGURIC to NON-OLIGURIC: may help (easier to manage electrolytes — if still producing urine, less likely to need urgent RRT for hyperkalaemia). (c) But: if the kidney is SEVERELY damaged (ATN) → frusemide won't work (no tubular function to stimulate). (3) WHEN TO USE: (a) FLUID OVERLOAD (pulmonary oedema, effusion) → frusemide IV (start 20-40 mg → titrate to response — may need high doses in AKI — 250 mg infusion — if resistant). (b) HYPERKALAEMIA (frusemide promotes K+ excretion — but less effective than RRT in severe AKI). (c) TRIAL: if oliguric → trial of frusemide (if responds → non-oliguric → easier to manage — but no survival benefit). (4) WHEN NOT TO USE: (a) If NOT fluid overloaded (diurese → hypovolaemia → worse AKI). (b) If pre-renal (diurese → further hypovolaemia → worse pre-renal — fluids instead). (5) KEY: frusemide DOESN'T treat AKI — manages fluid — use for fluid overload (if overloaded) — DON'T use for 'treating' AKI (no benefit — may harm if makes patient hypovolaemic).[1] }Contrast-associated AKI — PRESERVE trial. (1) DEFINITION (CA-AKI): creatinine rise >26.5 μmol/L (0.3 mg/dL) within 48-72h of contrast — no other cause. (2) RISK FACTORS: CKD (eGFR <45), diabetes, age >75, heart failure, hypovolaemia, high contrast volume, intra-arterial injection. (3) PREVENTION — PRESERVE trial (2018, NEJM): (a) Isotonic saline = sodium bicarbonate (no difference — saline standard). (b) NAC = placebo (NO benefit). (c) CONCLUSION: ISOTONIC SALINE is the only proven prevention (1 mL/kg/hr for 6-12h pre/post). (d) Minimise contrast volume. (e) Use low/iso-osmolar contrast (iodixanol). (f) Hold diuretics + metformin (if eGFR <60). (g) Hold nephrotoxins (NSAIDs, aminoglycosides). (4) KEY: PRESERVE debunked bicarbonate + NAC — saline remains standard. (5) PRACTICE: for high-risk patient needing contrast → saline + minimise contrast volume + low-osmolar agent + hold metformin. Consider alternative imaging (ultrasound, MRI without contrast).[1] }AKI epidemiology — AKI-EPI. (1) AKI-EPI (Hoste 2015, Intensive Care Medicine): multicentre observational study — AKI prevalence in ICU. RESULT: (a) 57% of ICU patients develop AKI (any stage — KDIGO). (b) 14% need RRT. (c) AKI associated with INCREASED mortality (even Stage 1 — 10% vs no AKI — 5%). (d) Stage 3 + RRT mortality ~40-50%. (2) WHY SO COMMON IN ICU: (a) CRITICALLY ILL patients → multiple kidney insults (sepsis, shock, nephrotoxins, contrast, rhabdomyolysis). (b) Inflammation (cytokines → kidney dysfunction). (c) Haemodynamic instability (hypoperfusion). (d) Nephrotoxic drugs (antibiotics, vasopressors, contrast). (3) KEY: AKI is UBIQUITOUS in ICU (over half of patients) — EVERY ICU patient should have creatinine + urine output monitored daily — PREVENTION is the mainstay.[4] }Recovery — polyuric phase + CKD risk. (1) POLYURIC PHASE of recovery: (a) As tubules REGENERATE (ATN healing — new tubular cells) → they initially CANNOT CONCENTRATE urine (the concentrating mechanism hasn't fully recovered) → POLYURIA (high urine output — 3-5 L/day). (b) This is a GOOD sign (kidney recovering — producing urine) BUT: risk of ELECTROLYTE loss (K+, Mg2+, phosphate — washed out in high output). (c) Monitor electrolytes DAILY during polyuric phase — replace losses. (d) The polyuria RESOLVES over days-weeks (as concentrating mechanism recovers). (2) CREATININE FALLING: (a) During recovery → creatinine falls (kidney clearing). (b) If on RRT: creatinine falls between sessions (if kidney recovering — clearing some independently of RRT). (c) If creatinine is ONLY cleared by RRT (doesn't fall between sessions) → kidney NOT recovering yet → continue RRT. (3) WEANING RRT: (a) Signs: urine output >500 mL/day without diuretics + creatinine stable/falling (between sessions). (b) Reduce RRT (reduce CRRT effluent rate; increase IHD interval; reduce SLED frequency). (c) Trial off (stop RRT — monitor creatinine + urine + electrolytes). (d) If stable without RRT → decannulate (remove access). (e) If creatinine rises again → resume RRT. (4) AKI → CKD: (a) 10-30% of severe AKI (Stage 3 + RRT) survivors develop CKD (especially: elderly, diabetes, pre-existing CKD, prolonged AKI, recurrent AKI). (b) EACH AKI episode increases CKD risk (cumulative — recurrent AKI → progressive CKD → ESKD). (c) FOLLOW-UP: nephrology referral + renal function monitoring (creatinine + eGFR + proteinuria) at 3 months — if CKD developing → manage (ACEi/ARB for proteinuria, BP control, glycaemic control). (d) PREVENT recurrence (avoid nephrotoxins — especially NSAIDs in CKD patients). (5) KEY: AKI recovery involves polyuric phase (monitor electrolytes) → creatinine falls → wean RRT → 10-30% develop CKD (follow-up).[1] }Crush injury / rhabdomyolysis AKI — myoglobin. (1) RHABDOMYOLYSIS: muscle breakdown (trauma/crush, statins, prolonged immobilisation, seizures, heat stroke, malignant hyperthermia, drugs) → myoglobin released → filtered by kidney → TOXIC to tubules (direct injury + cast obstruction + free iron + volume depletion) → AKI. (2) DIAGNOSIS: (a) CREATINE KINASE (CK) >5x normal (>1000 U/L — often >10,000-100,000 in severe). (b) URINE: dark/red-brown ('tea-coloured') — positive for blood on dipstick (myoglobin) BUT NO RBC on microscopy (false positive — myoglobin cross-reacts with dipstick blood). (c) Metabolic: hyperkalaemia (K+ released from muscle), hyperphosphataemia, hypocalcaemia (Ca binds to damaged muscle), metabolic acidosis. (3) MANAGEMENT: (a) AGGRESSIVE FLUIDS (the main treatment — crystalloid — 10-12 L/day in severe crush — maintain high urine output [200-300 mL/hr] — flush myoglobin through kidneys + prevent cast formation + correct volume depletion). (b) ALKALINISE URINE (bicarbonate — pH >6.5 — keeps myoglobin more soluble — less precipitation in tubules — controversial — some use, some don't — but fluids are the key). (c) TREAT hyperkalaemia (calcium gluconate [BUT: hypocalcaemic from rhabdo — calcium may worsen tissue calcification — controversial — use for cardiac protection only if K+ cardiac toxicity]). (d) TREAT compartment syndrome if present (fasciotomy — relieve pressure — prevent ongoing muscle injury). (e) RRT if severe (AKI from myoglobin — may need RRT for hyperkalaemia/fluid overload). (4) KEY: rhabdomyolysis AKI → AGGRESSIVE FLUIDS (the treatment — flush myoglobin) + alkaline urine (controversial) + electrolyte management.[1] }Hepatorenal syndrome (HRS) — special AKI. (1) HRS: AKI in CIRRHOSIS + ASCITES — from severe splanchnic vasodilation (NO) → reduced effective circulating volume → RAAS/SNS activation → intense renal vasoconstriction → low GFR → AKI. (2) TYPES: (a) Type 1 (HRS-AKI — acute): rapid deterioration (creatinine doubles in <2 weeks) — high mortality (80% at 2 weeks without treatment). (b) Type 2 (HRS-AKD — chronic): slower — associated with refractory ascites. (3) DIAGNOSIS (ICD-AKI criteria — International Club of Ascites): (a) Cirrhosis + ascites. (b) AKI (creatinine rise — KDIGO). (c) NO response to ALBUMIN challenge (albumin 1 g/kg/day x2 days — no improvement → suggests HRS [not volume-responsive pre-renal]). (d) NO shock, no nephrotoxins, no structural kidney disease (normal urine sediment + no proteinuria). (4) MANAGEMENT: (a) ALBUMIN (1 g/kg/day x2 days — as challenge [to exclude volume-responsive pre-renal] + as treatment [colloid — expand intravascular volume]). (b) VASOCONSTRICTORS (reverse splanchnic vasodilation): (i) TERLIPRESSIN + albumin (CONFIRM trial 2021, NEJM — terlipressin improved renal function — first FDA-approved for HRS — but risk of respiratory failure in some — monitor). (ii) NORADRENALINE + albumin (alternative — IV — continuous infusion — ICU setting). (iii) OCTREOTIDE + midodrine (less effective — third-line). (c) TREAT ASCITES (paracentesis + albumin replacement). (d) LIVER TRANSPLANT (definitive — HRS resolves with transplant — new liver stops producing vasodilators → splanchnic vasoconstriction normalises → renal perfusion restored). (e) RRT (bridge to transplant — or if not transplant candidate — poor prognosis). (5) KEY: HRS = AKI in cirrhosis/ascites from splanchnic vasodilation → albumin challenge (exclude pre-renal) + terlipressin/noradrenaline (reverse vasodilation) + liver transplant (definitive).[1] }Cardiorenal syndrome — dual organ failure. (1) CARDIORENAL SYNDROME: heart + kidney dysfunction — one organ's failure worsens the other (bidirectional). (2) TYPES: (a) Type 1 (ACUTE cardiorenal — ADHF → AKI — from low cardiac output → renal hypoperfusion + venous congestion). (b) Type 2 (CHRONIC cardiorenal — chronic HF → CKD). (c) Type 3 (ACUTE renocardial — AKI → cardiac dysfunction — from fluid overload + electrolytes [hyperkalaemia → arrhythmia] + uraemia [pericarditis]). (d) Type 4 (CHRONIC renocardial — CKD → cardiac — from volume overload + HTN + vascular calcification). (e) Type 5 (SYSTEMIC — sepsis → both heart + kidney). (3) CLINICAL DILEMMA (Type 1 — ADHF + AKI): (a) Patient has HF (needs diuretics to offload) + AKI (creatinine rising). (b) Diuretics → reduce preload → improve HF BUT may worsen AKI (from hypovolaemia). (c) Fluids → improve AKI (perfusion) BUT worsen HF (overload). (d) THE KEY: VENOUS CONGESTION is the main driver of cardiorenal AKI (not low output — raised renal venous pressure → reduced GFR). So: DIOURESE (even if creatinine rises slightly — the congestion is causing the AKI). Once decongested → renal function IMPROVES (despite initial creatinine rise). (e) DON'T stop diuretics for rising creatinine if patient is CONGESTED (the congestion is causing the AKI — diurese more, not less). (f) EXCEPTION: if creatinine rises + patient is DRY (not congested — over-diuresed) → reduce diuretics (hypovolaemia → AKI). (4) KEY: cardiorenal syndrome Type 1 → DIOURESE if congested (even if creatinine rises — congestion is the problem) — DON'T stop diuretics for rising creatinine if still congested. Assess volume status (clinical + ultrasound).[1] }Outcomes + long-term. (1) MORTALITY: Stage 1 ~10%, Stage 2 ~20%, Stage 3 ~40-50% (AKI is a MARKER of illness severity — mortality is from the underlying cause [sepsis, MODS], not AKI per se — but AKI CONTRIBUTES [fluid overload, electrolytes, acidosis, drug toxicity]). (2) RECOVERY: most recover renal function within 1-4 weeks (ATN heals — tubular cells regenerate). Some take longer (months). Some DON'T recover (→ CKD/ESKD). (3) AKI → CKD: 10-30% of severe AKI (Stage 3 + RRT) survivors → CKD. Risk factors: elderly, diabetes, pre-existing CKD, prolonged AKI, recurrent AKI. EACH AKI episode increases CKD risk (cumulative). (4) FOLLOW-UP: nephrology referral + renal function monitoring at 3 months — if CKD developing → manage (ACEi/ARB for proteinuria, BP control, glycaemic control). (5) PREVENTION: (a) AVOID nephrotoxins (especially in at-risk — elderly, CKD, diabetes, sepsis). (b) OPTIMISE perfusion (fluids + vasopressors — goal-directed — avoid prolonged hypoperfusion). (c) MONITOR (creatinine + urine output daily in ICU — detect early — intervene before ATN). (d) BIOMARKERS (NGAL, TIMP-2 — emerging — may allow earlier detection). (e) ANTIBIOTIC STEWARDSHIP (reduce unnecessary antibiotics → less nephrotoxic exposure). (f) CONTRAST AVOIDANCE (if possible — or pre-hydrate — PRESERVE — saline). (6) KEY: AKI is COMMON (57% ICU) + SERIOUS (Stage 3 mortality 40-50%) → PREVENTION is the mainstay (avoid nephrotoxins + optimise perfusion + monitor) → NO proven treatment (supportive + RRT when indicated) → 10-30% develop CKD (follow-up).[1] } Red flags
KDIGO staging (creatinine + urine output) — stage daily.[1] }PREVENTION is the mainstay — NO proven TREATMENT for established AKI.[1] }AVOID nephrotoxins (NSAIDs, aminoglycosides, contrast, ACEi/ARB if hypoperfused).[1] }AKIKI/STARRT-AKI : NO mortality benefit of EARLY RRT — wait for AEIOU indications.[2] }RRT indications (AEIOU) : Acidosis, Electrolytes, Ingestion, Overload, Uraemia.[1] }Mortality : Stage 1 10%, Stage 2 20%, Stage 3 40-50%.[4] }AKI → CKD : 10-30% of severe AKI survivors — nephrology follow-up.[1] }Diuretics DON'T treat AKI (manage fluid only — don't use routinely).[1] }'Renal dose dopamine' DEBUNKED — don't use.[1] }Drug dosing : adjust ALL renally cleared drugs (pharmacist review).[1] } Prognosis
AKI evidence and outcomes [4]
Exam practice — SAQs
SAQ — Applying the KDIGO 2012 AKI definition and staging at the bedside 10 minutes · 10 marks
Reveal all A 71-year-old man (weight 75 kg) is admitted to ICU with community-acquired pneumonia and septic shock. A creatinine taken 6 weeks earlier by his GP was 95 micromol/L. On ICU day 2 his creatinine is 210 micromol/L, and over the last 18 hours his urine output has averaged 0.4 mL/kg/h. He is catheterised and received furosemide 40 mg six hours ago.
a Define AKI using the KDIGO 2012 criteria, stage this patient showing your reasoning, and explain how the furosemide affects your staging.
b Explain how you would establish a baseline creatinine if no recent value were available, and the pitfalls of each method.
c State the approximate mortality associated with each KDIGO stage and explain the implications for monitoring and prognosis.
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SAQ — KDIGO Stage 3 AKI: staging, aetiological classification, and biomarkers 10 minutes · 10 marks
Reveal all A 58-year-old woman (weight 60 kg) is in ICU on day 3 of severe acute pancreatitis. Her creatinine has risen from a baseline of 80 to 360 micromol/L and she is anuric, producing under 10 mL of urine per hour for the last 14 hours despite a bladder scan showing under 50 mL residual. She is on noradrenaline 0.3 mcg/kg/min. Urine sodium is 45 mmol/L, fractional excretion of sodium (FENa) is 2.8%, and urine microscopy shows muddy brown granular casts.
a Stage this AKI, justify your aetiological classification, and explain why FENa and the urine indices can be misleading in critically ill patients.
b Describe the role of cell-cycle arrest biomarkers (TIMP-2 x IGFBP7, NephroCheck) in AKI, including their advantage over creatinine, and cite the key trial. State whether they change this patient and her management.
c Outline your immediate management priorities for this patient.
[1]
Densification notes for fellowship revision
This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.
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Revision checkpoint 1 (1_definition): KDIGO 2012 definition of AKI.
Revision checkpoint 2 (2_staging): Stage 1/2/3 thresholds.
Revision checkpoint 3 (3_aetiology): Pre-renal vs ATN vs post-renal.
Revision checkpoint 4 (4_prevention): Stop nephrotoxins.
Revision checkpoint 5 (5_biomarkers): Creatinine late marker.
Revision checkpoint 6 (6_rrt_timing): AEIOU indications.
Revision checkpoint 7 (7_modality): CRRT if unstable.
Revision checkpoint 8 (8_complications): HyperK, acidosis, overload, uraemia.
Revision checkpoint 9 (9_evidence): AKI-EPI epidemiology.
Revision checkpoint 10 (10_traps): Early RRT for rising Cr alone.
Revision checkpoint 11 (11_special): Rhabdomyolysis fluids.
Revision checkpoint 12 (12_icu): Hourly UO catheter.
Revision checkpoint 13 (13_prognosis): Stage mortality gradient.
Revision checkpoint 14 (14_boards): CICM SAQ staging cases.
Revision checkpoint 15 (15_saq): Stage this patient.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute kidney injury kdigo prevention biomarkers rrt timing.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
[1] References [1] Kellum JA, et al. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical care (London, England) , 2013.PMID 23394211 [2] Gaudry S, et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit. The New England journal of medicine , 2016.PMID 27181456 [3] STARRT-AKI Investigators, et al. Timing of Initiation of Renal-Replacement Therapy in Acute Kidney Injury. The New England journal of medicine , 2020.PMID 32668114 [4] Hoste EA, et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive care medicine , 2015.PMID 26162677 [5] Bihorac A, et al. Validation of cell-cycle arrest biomarkers for acute kidney injury using clinical adjudication. American journal of respiratory and critical care medicine , 2014.PMID 24559465 [6] Ralib AM, et al. The clinical utility window for acute kidney injury biomarkers in the critically ill. Critical care (London, England) , 2014.PMID 25366893 
