Acute Kidney Injury Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: AKI is extremely common in our wards, complicating everything from sepsis and dengue to routine post-op care. Failure to identify and manage it promptly leads to high morbidity, mortality, and progression to chronic kidney disease (CKD).
High-Yield Definition (KDIGO 2012):
Acute Kidney Injury is defined by any of the following:
Increase in serum creatinine (SCr) by $\geq$26.5 $\mu$mol/L within 48 hours; OR
Increase in SCr to $\geq$1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; OR
Urine volume <0.5 mL/kg/hour for 6 hours.
Clinical One-Liner: "Patient's creatinine is climbing or they've stopped passing urine. Find out the cause—Pre-renal, Intra-renal, or Post-renal—and fix it, fast."
II. Etiology & Risk Factors
Etiology is classified by anatomical location.
Pre-renal (Hypoperfusion): Most common cause. The kidney structure is initially intact.
True Volume Depletion: Dehydration, haemorrhage, D&V, burns.
Reduced Effective Circulating Volume: Sepsis (vasodilation), Heart Failure (low cardiac output), Liver Cirrhosis (hepatorenal syndrome).
Renal Artery Stenosis/Thrombosis.
Intra-renal (Intrinsic): Direct damage to the kidney parenchyma.
Acute Tubular Necrosis (ATN): >80% of intrinsic cases.
Ischaemic: Prolonged pre-renal state (e.g., septic shock, prolonged hypotension).
Nephrotoxic: Exogenous (contrast dye, NSAIDs, gentamicin, amphotericin B) or Endogenous (myoglobin from rhabdomyolysis, uric acid from tumour lysis).
Acute Interstitial Nephritis (AIN): Allergic reaction. Classic causes are antibiotics (penicillins, cephalosporins), NSAIDs, PPIs.
Glomerulonephritis (GN): Rapidly progressive GN, post-infectious GN.
Post-renal (Obstruction): Blockage of urine flow.
Ureteric: Stones, tumours, external compression (e.g., nodes, retroperitoneal fibrosis).
Bladder Neck: Benign Prostatic Hyperplasia (BPH) (most common in men), prostate cancer, neurogenic bladder.
Urethral: Strictures, blocked urinary catheter.
Key Risk Factors (Malaysian Context):
Pre-existing CKD
Diabetes Mellitus (underlying diabetic nephropathy)
Hypertension
Sepsis
Volume depletion (e.g., dengue shock, severe gastroenteritis)
Nephrotoxic drug exposure (NSAIDs, traditional/herbal medications)
Age >65
Recent major surgery or IV contrast procedure
III. Quick Pathophysiology
Pre-renal: Reduced renal blood flow leads to a drop in glomerular filtration pressure (GFR). The kidney tries to compensate by retaining sodium and water (high urine osmolality, low urine sodium). If uncorrected, this ischaemia leads to ATN.
Intra-renal (ATN): Ischaemia or toxins cause direct damage and sloughing of the tubular epithelial cells. These dead cells form casts, obstructing the tubules. This leads to a back-leak of filtrate and a persistent drop in GFR, even if blood flow is restored. The kidney loses its ability to concentrate urine (low urine osmolality, high urine sodium).
Post-renal: Physical obstruction increases hydrostatic pressure in Bowman's space, opposing filtration and causing GFR to fall.
IV. Classification
Etiological: Pre-renal, Intra-renal, Post-renal. This dictates the diagnostic and management pathway.
Severity (KDIGO Staging): This dictates monitoring intensity, need for escalation, and prognosis.
StageSerum Creatinine (SCr)Urine Output (UO)
1
1.5–1.9x baseline OR $\geq$26.5 $\mu$mol/L increase
<0.5 mL/kg/h for 6–12 hours
2
2.0–2.9x baseline
<0.5 mL/kg/h for $\geq$12 hours
3
$\geq$3.0x baseline OR SCr $\geq$353.6 $\mu$mol/L OR initiation of RRT
<0.3 mL/kg/h for $\geq$24 hours OR Anuria for $\geq$12 hours
V. Clinical Assessment
🚩 Red Flags & Immediate Actions
Anuria (no urine output):
Action: Escalate to senior, perform immediate bladder scan, insert urinary catheter (if not in situ).
Reason: Possible complete obstruction or vascular catastrophe (e.g., renal artery occlusion).
ECG changes of Hyperkalaemia (peaked T waves, wide QRS):
Action: IV CALCIUM GLUCONATE 10ml of 10% stat (cardioprotection), then IV insulin/dextrose.
Reason: Imminent risk of fatal arrhythmia.
Signs of Pulmonary Oedema (dyspnoea, bilateral crepitations, O2 desaturation):
Action: Sit patient up, high-flow O2, IV Frusemide 40-80mg stat.
Reason: Severe fluid overload, risk of respiratory failure.
Severe Metabolic Acidosis (e.g., pH <7.1, Bicarb <10):
Action: Escalate to senior, consider need for bicarbonate or urgent RRT.
Uraemic Encephalopathy (confusion, drowsiness) or Pericarditis (chest pain, rub):
Action: Escalate to senior, prepare for urgent RRT.
History
Key Diagnostic Clues:
Pre-renal: History of D&V, poor intake, fever/sepsis, known heart failure.
Intra-renal: Recent contrast scan, new "jamu" or NSAID, recent infection (sore throat, skin rash), classic triad for AIN (fever, rash, arthralgia - though rare).
Post-renal: Older male with poor stream, straining (BPH), lower abdominal pain, known pelvic malignancy.
Symptom Breakdown:
Common: Often asymptomatic and only detected on bloods. Oliguria (decreased UO) is a key sign but non-oliguric AKI is also common.
Less Common: Nausea, vomiting, lethargy.
Rare (Late/Uraemic): Confusion, shortness of breath (fluid overload), pruritus, pericarditic chest pain.
Pertinent Negatives:
No fever (less likely sepsis or AIN).
No urinary symptoms (less likely obstruction).
No new drugs or recent contrast (less likely toxic ATN/AIN).
No haemoptysis/rash (less likely vasculitis/GN).
Physical Examination (OSCE Approach)
General Inspection: Assess fluid status. Is the patient overloaded (pitting oedema, raised JVP) or depleted (dry mucous membranes, poor skin turgor)? Look for signs of uraemia (asterixis, drowsiness) or systemic disease (vasculitic rash).
Vitals:
Hypotension & Tachycardia: Suggests pre-renal cause (sepsis, dehydration).
Hypertension: Suggests fluid overload or intrinsic glomerular disease.
Disease-Specific Examination:
Abdomen: Palpate and percuss for a distended bladder (obstruction). Check for renal angle tenderness (pyelonephritis). Look for ascites (hepatorenal).
Cardiovascular: Check JVP. Auscultate for S3 gallop (fluid overload) or pericardial rub (uraemia).
Respiratory: Auscultate for bilateral basal crepitations (pulmonary oedema).
Skin: Check for rashes (AIN, vasculitis).
Pertinent Negatives: No palpable bladder (makes significant retention unlikely), JVP not raised, clear lung fields (argues against fluid overload).
Differentiating Disease Stage:
Early (Stage 1): Often just an abnormal lab value. Patient is haemodynamically stable, euvolaemic, good UO.
Late (Severe Disease, Stage 3): Patient is oliguric/anuric, fluid overloaded (pulmonary oedema, peripheral oedema), tachypnoeic (Kussmaul breathing from acidosis), and uraemic (confused, flapping tremor).
Clinical Pearl: First, assess fluid status (history, JVP, oedema). Second, review the drug chart (nephrotoxins). Third, rule out obstruction (bladder scan/USS). This will lead you to the cause in 80% of cases.
VI. Diagnostic Workflow
Differential Diagnosis
Pre-renal Azotaemia
Points For: History of dehydration/sepsis/HF. Responds to fluid challenge.
Points Against: No response to fluids. Evidence of renal damage (casts, proteinuria).
How to Differentiate: Cautious fluid challenge (if not overloaded). Urine studies (FENa <1%, FEUrea <35%) before diuretics.
Acute-on-Chronic Kidney Disease (AoCKD)
Points For: Known history of DM/HTN, anaemia, abnormal Ca/PO4.
Points Against: Normal Hb, normal kidney size on USS, previously normal creatinine.
How to Differentiate: Check old creatinine results. Renal ultrasound showing small, echobright kidneys confirms CKD.
Obstructive Uropathy (Post-renal)
Points For: Older male, anuria or fluctuating polyuria/oliguria, palpable bladder.
Points Against: Normal renal ultrasound.
How to Differentiate: Renal/Bladder Ultrasound is the key investigation.
Investigations Plan
Bedside / Initial (First 15 Mins):
UFEME (Urine Full Examination & Microscopy): Look for:
Blood/Protein: Suggests glomerular disease.
WBC/Leukocytes/Nitrites: Suggests UTI/pyelonephritis.
Casts: Muddy brown casts (pathognomonic for ATN), WBC casts (AIN, pyelonephritis), RBC casts (GN).
ECG: CRITICAL. To rule out life-threatening hyperkalaemia.
Bladder Scan: To rule out retention. If >200ml, insert catheter.
First-Line Labs & Imaging:
RP/BUSE: Check creatinine (to stage), Urea, Potassium, Bicarbonate (for acidosis).
FBC: Check Hb (anaemia of CKD?), TW (sepsis?).
Renal Ultrasound (USS KUB): MANDATORY for almost all AKI patients to rule out post-renal obstruction (hydronephrosis) and assess kidney size (CKD vs. AKI).
Confirmatory / Gold Standard / Second-Line:
Urine Electrolytes (FENa, FEUrea): Can help differentiate pre-renal from ATN, but must be interpreted before diuretics are given. (FENa <1% suggests pre-renal; >2% suggests ATN).
Septic Workup: Blood C&S, Urine C&S (if infection suspected).
Specialised Tests (for intrinsic disease, discuss with senior):
Autoimmune screen (ANA, ANCA), Complement (C3, C4) for suspected GN.
CK/Myoglobin: For suspected rhabdomyolysis.
Renal Biopsy: Gold standard for diagnosing intrinsic renal disease (GN, AIN, vasculitis).
VII. Staging & Severity Assessment
Staging is via the KDIGO criteria (see Section IV). The stage dictates management:
Stage 1: Monitor closely. Find and treat cause. Avoid nephrotoxins.
Stage 2: Escalate to senior. Actively manage (e.g., fluid challenge, hold drugs). Needs nephrology input if not improving.
Stage 3: Escalate immediately. Needs nephrology review. High likelihood of requiring Renal Replacement Therapy (RRT).
VIII. Management Plan
A. Principle of Management
Treat the underlying cause.
Correct fluid, electrolyte, and acid-base imbalances.
Avoid further nephrotoxic insults.
Provide supportive care until renal function recovers.
B. Immediate Stabilisation (The "STOP AKI" Bundle)
S - Sepsis: Treat underlying sepsis aggressively with antibiotics as per CPG.
T - Toxins: STOP all nephrotoxic drugs.
NSAIDs (diclofenac, mefenamic acid).
ACE-inhibitors (perindopril) & ARBs (losartan) - temporarily hold.
Aminoglycosides (gentamicin) - review dosing.
Avoid IV contrast.
O - Optimise: Optimise haemodynamics and fluid balance.
If Hypovolaemic: IV fluid challenge (e.g., Hartmann's or Normal Saline 250-500ml stat, then reassess). Do not "drown" the patient.
If Hypervolaemic (fluid overloaded): Fluid restrict, give IV frusemide challenge (e.g., 40-80mg).
If Euvolaemic: Maintain euvolaemia. Strict input/output chart.
P - Prevent: Prevent complications.
Hyperkalaemia: Treat immediately (Section V).
Obstruction: Relieve (e.g., urinary catheter).
Monitoring: Strict hourly urine output (may need catheter), repeat BUSE/RP in 4-6 hours.
C. Definitive Treatment (The Ward Round Plan)
Pre-renal: Continue optimising volume status (fluids for dehydration, diuretics/inotropes for cardiorenal syndrome).
Intra-renal (ATN): Primarily supportive. Maintain euvolaemia. Nutrition is important. Wait for tubules to recover (can take days to weeks).
Intra-renal (AIN/GN): Specifics. Requires nephrology input. Usually involves steroids or other immunosuppression.
Post-renal: Relieve the obstruction.
Bladder neck: Urinary catheter (CBD).
Ureteric: Needs urology input for JJ stent or percutaneous nephrostomy.
D. Indications for Renal Replacement Therapy (RRT / Dialysis)
This is a nephrology decision. Escalate if you see:
A: Acidosis (severe, refractory, pH <7.1)
E: Electrolyte (refractory hyperkalaemia >6.5 or with ECG changes)
I: Intoxication (specific drugs e.g., lithium, metformin-associated lactic acidosis)
O: Overload (refractory pulmonary oedema)
U: Uraemia (encephalopathy, pericarditis)
E. Long-Term & Discharge Plan
Follow-up: Repeat creatinine 1-2 weeks post-discharge to ensure resolution.
Medication Review: Restart renoprotective drugs (e.g., ACEi/ARBs) after AKI has resolved and patient is stable, if indicated.
Counselling: Advise on "sick day rules" (i.e., to temporarily hold ACEi/ARBs, diuretics, and NSAIDs if they have fever, D&V).
Referral: Refer to Nephrology clinic if creatinine does not return to baseline (i.e., new AKI-on-CKD).
IX. Complications
Immediate: Hyperkalaemia, Fluid Overload (Pulmonary Oedema), Severe Metabolic Acidosis.
Short-Term: Uraemia (encephalopathy, pericarditis, bleeding), Infection (sepsis), Malnutrition.
Long-Term: Progression to CKD, End-Stage Renal Disease (ESRD) requiring permanent dialysis, increased long-term cardiovascular risk and mortality.
X. Prognosis
Prognosis is highly dependent on the cause, severity (KDIGO stage), and patient's baseline health.
AKI with full recovery (e.g., young patient with pre-renal AKI from gastroenteritis) has a good prognosis.
AKI in the context of sepsis, multi-organ failure, or on a background of advanced CKD has a very high in-hospital mortality (>30-50%).
Key Prognostic Factors: Baseline CKD, severity of AKI, need for RRT, presence of sepsis, advanced age.
XI. How to Present to Your Senior
"Doctor, referring patient [Name, Age, Ward].
S: Patient has developed AKI Stage [Stage]. The creatinine today is [today's value], up from [baseline value or admission value] yesterday. The urine output for the past [X] hours has been [e.g., <0.5ml/kg/h].
B: Patient was admitted for [reason]. Key risk factors are [e.g., sepsis, recent contrast, on NSAIDs].
A: On assessment, the patient is [fluid status - e.g., overloaded, with bilateral crepitations and JVP up 4cm]. Vitals are [BP, HR, O2 Sat]. ECG shows [e.g., no hyperkalaemic changes]. Bladder scan shows 50ml.
R: I suspect the cause is [e.g., ATN secondary to sepsis]. I have stopped the [nephrotoxic drug] and given a stat dose of IV frusemide. My plan is to monitor UO hourly, fluid restrict to 1L/day, and repeat the BUSE in 6 hours. Requesting your review for further management."
XII. Summary & Further Reading
Top 3 Takeaways:
AKI is a clinical emergency defined by SCr rise or UO drop (KDIGO).
Your first steps are to assess fluid status, review the drug chart, and rule out obstruction with a bladder scan/USS.
Management is "STOP AKI": Treat Sepsis, stop Toxins, Optimise haemodynamics, and Prevent complications (especially hyperkalaemia). Escalate based on "AEIOU" criteria.
Key Resources:
KDIGO (2012) Clinical Practice Guideline for Acute Kidney Injury: (The foundational international guideline).
UpToDate: "Definition and staging of acute kidney injury in adults" and "Etiology and diagnosis of acute kidney injury in adults".
Amboss: "Acute Kidney Injury"
