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Nephrology
Critical Care
Internal Medicine
EMERGENCY

Acute Kidney Injury (AKI)

High EvidenceUpdated: 2025-12-27

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Red Flags

  • Anuria (Obstruction/Shock)
  • Hyperkalaemia >6.5 mmol/L (Arrhythmias)
  • Pulmonary Oedema (Refractory)
  • Severe Acidosis (pH <7.1)
  • Uraemic Encephalopathy/Pericarditis
Overview

Acute Kidney Injury (AKI)

1. Clinical Overview

Summary

Acute Kidney Injury (AKI) is a sudden decline in renal function occurring over hours to days, characterized by the retention of nitrogenous waste products (urea, creatinine) and disrupted homeostasis of fluid, electrolytes, and acid-base status. It is a defining medical emergency affecting up to 20% of all hospital admissions and >50% of ICU patients. [1] The updated KDIGO definition relies on sensitive criteria: a rise in creatinine of just 26.5 µmol/L within 48 hours is diagnostic. The "Three Pillars" of AKI classification—Prerenal (Perfusion failure), Intrinsic (Tissue damage), and Postrenal (Obstruction)—remain the foundational framework for management. Mortality remains high (10-30%), not from the renal failure itself (which dialysis can replace), but from the multi-organ consequences of the "Remote Organ Effects of AKI" (cytokine storm, lung injury, immune paralysis). [2]

Key Facts

  • Definition: Rise in Serum Creatinine (SCr) ≥26.5 µmol/L in 48h OR ≥1.5x baseline in 7 days OR Urine Output <0.5 ml/kg/h for 6h.
  • Incidence: 1 in 5 emergency admissions. 50-60% of critical care patients.
  • The "Silent Killer": Urine output is often preserved in "Non-Oliguric AKI" (common in drug toxicity), leading to missed diagnoses.
  • Prerenal Dominance: 60-70% of community-acquired AKI is prerenal (dehydration/sepsis) and reversible.
  • Intrinsic Shift: In ICU, Acute Tubular Necrosis (ATN) becomes the dominant cause (Sepsis-associated AKI).
  • Prognosis: A single episode of AKI doubles the 10-year risk of developing Chronic Kidney Disease (CKD) and End-Stage Renal Disease (ESRD). [3]

Clinical Pearls

[!TIP] Creatinine Lags Behind: Serum creatinine is a late marker of injury. By the time creatinine rises, GFR has already dropped by 50%. Trust Urine Output as the "Canary in the Coal Mine"—it drops hours before creatinine rises.

[!IMPORTANT] The "Fluid Challenge" Myth: In established ATN (Intrinsic AKI), the kidney cannot respond to fluids. Pumping litres of saline into an ATN patient causes "Salt Water Drowning" (Pulmonary/Tissue Oedema) without improving renal function. Know when to stop fluid Resuscitation and start fluid Removal.

[!WARNING] The "Nephrotoxic Hit": 30% of hospital-acquired AKI is preventable drug injury. The "DAMN" drugs (Diuretics, ACEi/ARBs, Metformin, NSAIDs) must be held in acute illness.

2. Epidemiology

Incidence & Demographics

  • Global Burden: AKI affects 13.3 million people annually, contributing to 1.7 million deaths. [4]
  • Hospital Prevalence: 10-20% of general ward admissions; approaches 60% in Sepsis.
  • Age: Incidence increases exponentially with age due to "Renal Reserve" loss (GFR loses 1ml/min/year after age 40).
  • Geography: High rates of community-acquired AKI in tropics (Malaria, Leptospirosis, Snake bite).

Risk Factors (The "Susceptible Kidney")

Patient Specific:

  • Age >65 (Reduced nephron mass).
  • CKD (The strongest predictor—"Acute on Chronic").
  • Heart Failure (Cardiorenal Syndrome Type 1).
  • Liver Disease (Hepatorenal risk).
  • Diabetes Mellitus.

Exposure Specific:

  • Sepsis (Endothelial dysfunction).
  • Major Surgery (Cardiac bypass >30% risk).
  • Contrast Media (Contrast-Induced Nephropathy).
  • Nephrotoxins (Aminoglycosides, Amphotericin, Chemo).
3. Pathophysiology

The Detailed Mechanism of Acute Tubular Necrosis (ATN)

ATN is the final common pathway for prolonged ischaemia or toxin exposure. Understanding the cellular biology is key to understanding why "fluid challenges" fail in established ATN.

Step 1: Initiation (The Prerenal Phase)

  • Haemodynamic Instability: The initiating event is often systemic hypotension (MAP <65 mmHg) or effective hypovolaemia (Sepsis/Heart Failure).
  • Autoregulation Failure: The kidney normally maintains GFR despite BP fluctuations via afferent dilation (Prostaglandins/NO) and efferent constriction (Angiotensin II).
  • Drug Interference: NSAIDs block afferent dilation; ACE inhibitors block efferent constriction. This renders the kidney defenseless against hypotension.
  • Result: GFR declines due to reduced filtration pressure, but tubular cells remain viable. This phase is reversible with rapid volume restoration.

Step 2: Extension (The Ischaemic Injury)

  • ATP Depletion: Proximal Tubule cells are strictly aerobic and high-energy consumers (due to active transport). Ischaemia leads to rapid ATP depletion.
  • Cytoskeletal Breakdown: Low ATP causes disassembly of the actin cytoskeleton.
  • Loss of Polarity (The Critical Step):
    • The Na+/K+ ATPase pump is normally anchored to the basolateral membrane (pumping sodium into the blood).
    • In ischaemia, the anchor proteins (Integrins) fail.
    • The pump translocates to the apical (luminal) membrane.
  • Consequence: Sodium is pumped into the urine instead of the blood. This explains the high Urine Sodium (>40 mmol/L) in ATN.
  • Tubuloglomerular Feedback: The Macula Densa senses this high distal sodium load. Interpreting this as "hyperfiltration", it releases Adenosine to potently constrict the afferent arteriole. This further obliterates GFR—a maladaptive "suicide" mechanism to prevent profound fluid loss.

Step 3: Maintenance (The "Muddy Brown" Phase)

  • Cell Necrosis & Apoptosis: Severe ischaemia leads to cell death, particularly in the S3 segment of the Proximal Tubule (most metabolically active) and the Thick Ascending Limb (medullary hypoxia).
  • Cast Formation: Dead epithelial cells detach and slough into the tubular lumen. They aggregate with Tamm-Horsfall Protein (uromodulin) to form obstructing granular casts ("Muddy Brown Casts").
  • Intratubular Obstruction: These casts physically block the flow of urine, raising intratubular pressure.
  • Backleak: The glomerular filtration pressure cannot overcome the obstruction. Filtrate leaks back through the denuded basement membrane into the renal interstitium.
  • Interstitial Oedema: This backleak causes interstitial swelling, which compresses the peritubular capillaries, worsening ischaemia (a vicious cycle).
  • Clinical: Established Anuria/Oliguria. Creatinine rises daily. Fluid challenges at this stage cause pulmonary oedema, not diuresis.

Step 4: The Recovery Phase (Differentiation)

  • Regeneration: If the basement membrane remains intact, surviving epithelial cells dedifferentiate into a mesenchymal state.
  • Proliferation: These cells migrate to cover denuded areas and undergo mitosis.
  • Differentiation: Cells re-express polarity markers and reassemble the cytoskeleton.
  • Polyuric Phase: The new cells are immature. They lack the concentrated gradient of the medulla and the full complement of aquaporin channels.
  • Clinical Consequence: The GFR recovers, but tubular reabsorption is poor. Patients may pass 3-5 Litres of urine per day. This puts them at high risk of dehydration, hypokalaemia, and hyponatraemia.

Step 5: Restoration

  • Functional Recovery: Over weeks to months, cellular function normalizes.
  • Hyperfiltration: In some cases, surviving nephrons hypertrophy and hyperfilter to compensate for lost nephrons.
  • Fibrosis: If injury was severe, incomplete repair leads to interstitial fibrosis and nephron loss—the genesis of Chronic Kidney Disease (CKD).

Classification by Pathophysiology

TypeMechanismKey DefectReversibility
PrerenalHypoperfusionDecreased GFR due to flowHigh (Immediate)
IntrinsicTissue InjuryTubular necrosis / GlomerulitisVariable (Days-Weeks)
PostrenalObstructionHigh intratubular pressureHigh (If relieved early)
4. Clinical Presentation

Clinical Scenarios

AKI presents in three distinct phenotypes, which guide immediate management. Identifying the phenotype is the first step in diagnosis.

1. The "Empty" Patient (Prerenal Phenotype)

2. The "Septic" Patient (Vasodilatory Phenotype)

3. The "Obstructed" Patient (Postrenal Phenotype)

4. The "Nephritic" Patient (Glomerulonephritis)

Atypical Presentations in the Elderly

Symptom Trajectory

Context
Community-acquired. History of Diarrhoea, Vomiting, Haemorrhage, or poor oral intake.
Symptoms
Thirst, Dizziness on standing (postural hypotension), Palpitations.
Signs
Tachycardia, Hypotension, Dry Mucous Membranes, Reduced Capillary Refill Time (>2 sec), Cool Peripheries, Sunken Eyes, Reduced Skin Turgor.
Urine
Concentrated, dark, low volume ("Tea coloured").
5. Clinical Examination Focus

Structured Assessment: The "Fluid & Flow" Exam

1. Volume Status (The "Goldilocks" Assessment)

  • Jugular Venous Pressure (JVP): The most useful bedside surrogate for Right Atrial Pressure.
  • Mucous Membranes: Look under the tongue (sublingual pool).
  • Axillae: Are they dry? (Specific for dehydration).
  • Chest: Crackles? (Fluid Overload).
  • Passive Leg Raise: Does BP/Pulse pressure improve? (Suggests fluid responsiveness).

2. The Kidney & Bladder

  • Palpate Bladder: A palpable bladder implies >300-500ml urine retention (Postrenal).
  • Renal Angle Tenderness: Punch gently. Positive in Pyelonephritis.
  • Bruits: Renal Artery Stenosis check.

3. Systemic Clues (Etiology Hunting)

  • Skin: Purpura (Vasculitis), Track marks (Hep C/HIV/Heroin nephropathy), Livedo Reticularis (Cholesterol Emboli), Butterfly rash (Lupus).
  • Eyes: Uveitis (Tubulointerstitial Nephritis), Retinopathy (Diabetes/Hypertension).

Procedural Skills: Essential for AKI Management

1. Male Urinary Catheterisation (The "Difficult" Catheter) AKI patients often have BPH necessitating catheterisation.

  • Indication: Monitoring output in shock, or Relieving obstruction.
  • Contraindication: Urethral trauma (blood at meatus).
  • Technique:
    • Use 12-14Fr (Silicon) for standard drainage. Use 16-18Fr (3-way) if clots present.
    • If resistance at prostate: Do NOT force. Use a Coudé tip (Tiemann) or call Urology.
    • Common error: Inflating balloon in the urethra (causes necrosis). Ensure return of urine before inflating.

2. Fluid Assessment via Passive Leg Raise (PLR) The most accurate bedside test for "Fluid Responsiveness".

  • Concept: Raising legs auto-transfuses ~300ml of venous blood from legs to heart.
  • Method:
    • Patient semi-recumbent (45 degrees).
    • Lay them flat and raise legs to 45 degrees.
    • Assess Cardiac Output (or Pulse Pressure) change within 1-2 mins.
    • Positive: Pulse Pressure increases >10%. Patient needs fluid.
    • Negative: No change. Patient is "Fluid Replete" or "Non-Responder". Giving fluid will just cause oedema.

3. Jugular Venous Pressure (JVP) Measurement

  • Position: 45 degrees, neck relaxed. Look between sternal and clavicular heads of SCM muscle.
  • Waveform: Double pulsation (a and v waves).
  • Distinction from Carotid: JVP is occludable, non-palpable, drops with inspiration, changes with position.
  • Measurement: Vertical height from Sternal Angle + 5cm (distance to RA). Normal <8cm H2O.

4. Renal Biopsy (Ultrasound Guided)

  • Role: Percutaneous needle biopsy (Tru-Cut) of the lower pole.
  • Preparation: Check Clotting (INR <1.4, Platelets >100). Stop Anticoagulants. Control BP (<140/90) to minimize bleeding.
  • Procedure: Prone position. Local anaesthetic. Spring-loaded gun. Take 2 cores (one for Light Microscopy/Immunofluorescence, one for Electron Microscopy).
  • Post-Care: Flat bed rest for 4-6 hours. Monitor BP and entry site/urine for haematuria.
  • Complications: Haematuria (Common), Perinephric Haematoma, AV Fistula, Infection.
6. Investigations
6. Investigations

Investigating AKI requires a "Sherlock Holmes" deductive approach to rule out reversible causes.

Step 1: The "Bedside" Screen (First 30 Mins)

1. Urinalysis (The Liquid Biopsy) Dipstick urine before the patient is catheterised if possible (to avoid trauma haematuria).

  • Blood + Protein (+++): Pathognomonic for Glomerulonephritis. This is a medical emergency. Urgent Microscopy required for "Red Cell Casts".
  • Blood only: Suggests Stones (Ureteric Colic), Tumour (Bladder Ca), or Trauma (Catheterisation).
  • Leucocytes + Nitrites: Pyelonephritis. Send for MC&S.
  • Protein only (+++): Heavy proteinuria (>1g/L) suggests Nephrotic Syndrome or Diabetic Nephropathy.
  • Normal Sediment: Suggests Prerenal failure (intact nephrons) or Postrenal obstruction.
  • "Muddy Brown" Casts: (Granular Casts) seen on microscopy. These are dead tubular cells + Tamm-Horsfall protein. Diagnostic of ATN.
  • Eosinophiluria: Suggests Acute Interstitial Nephritis (AIN), often drug-induced (Antibiotics/PPIs).

2. Fluid Balance Review

  • Calculate Cumulative Fluid Balance (Input minus Output over last 48h).
  • Weigh the patient. Is their current weight > Dry weight? (1kg weight gain ≈ 1L fluid retention).

Step 2: The "Biochemical" Screen (Laboratory)

1. Serum Creatinine (Kinetic Changes)

  • Baseline is key. A rise from 60 -> 120 (within range) is more significant than a stable 200.
  • Creatinine Kinase (CK): Mandatory in all elderly/fallers to rule out Rhabdomyolysis (CK >1000).
  • Urea: Disproportionate rise (Urea:Cr ratio >100:1) suggests:
    • Prerenal Dehydration (Slow flow allows urea reabsorption).
    • GI Bleed (Digested blood protein load).
    • Steroid use (Catabolism).

2. Acid-Base (VBG/ABG)

  • Metabolic Acidosis: pH <7.35 with Low HCO3.
  • Anion Gap: Na - (Cl + HCO3).
    • High Gap (>12): Uraemia, Lactic Acidosis, Ketones, Toxins (MUDPILES).
    • Normal Gap: Renal Tubular Acidosis (RTA) or Diarrhoea.

3. The Immunology Panel (If Dipstick Positive)

  • ANCA (PR3/MPO): For Granulomatosis with Polyangiitis (Wegener's).
  • Anti-GBM: For Goodpasture's Syndrome.
  • ANA / dsDNA / C3, C4: For Lupus Nephritis (SLE).
  • Serum Free Light Chains: For Myeloma Kidney (Cast Nephropathy).
  • ASOT / Anti-DNase B: For Post-Streptococcal GN.

Step 3: The "Anatomical" Screen (Imaging)

1. Renal Ultrasound (US KUB) - Within 24 Hours Mandatory for all unexplained AKI.

  • Normal Size (9-12cm): Acute Disease.
  • Small (<9cm): Chronic Kidney Disease (Scarred).
  • Large (>13cm): Diabetic Nephropathy, HIV Nephropathy, or Infiltrative (Amyloid/Myeloma).
  • Hydronephrosis: Black dilated renal pelvis >10mm. Diagnostic of Obstruction.
  • Doppler: To rule out Renal Artery Stenosis or Renal Vein Thrombosis.

2. Non-Contrast CT KUB

  • Gold standard for Renal Stones (Calculi).
  • Avoid Contrast CT if possible (Contrast Nephropathy risk).

Step 4: The "Functional" Screen (Advanced)

Differentiating Prerenal vs ATN Useful when diagnosis is unclear (e.g., patient received fluids but Cr not improving).

IndexPrerenal (Intact Tubules)ATN (Dead Tubules)Physiology
Urine Sodium< 20 mmol/L> 40 mmol/LPrerenal preserves Na; ATN wastes Na
Urine Osmolality> 500 mOsm/kg< 350 mOsm/kgPrerenal concentrates; ATN isosthenuric
FeNa (%)< 1%> 2%Fractional Excretion of Sodium formula
FeUrea (%)< 35%> 50%Use this if patient is on Diuretics (which ruin FeNa)
BUN:Cr Ratio> 20:1< 10-15:1Urea reabsorbed in prerenal

Indications for Renal Biopsy

Biopsy is High Risk (Bleeding). Reserved for when it changes management:

  1. Unexplained AKI after excluding Prerenal/Postrenal causes.
  2. Suspected Rapidly Progressive Glomerulonephritis (RPGN) (Pulmonary-Renal Syndrome).
  3. Suspected AIN where drug culprit is unclear.
  4. Systemic Disease (Lupus, Vasculitis) to guide immunosuppression intensity.
  5. Non-recovery of ATN after 4 weeks.
7. Management

Management Algorithm

        AKI SUSPECTED (Cr Rise OR Oliguria)
                     ↓
┌──────────────────────────────────────────────┐
│       IMMEDIATE ASSESSMENT & SAFETY          │
│  1. ABCDE Assessment (Shock? Pulmonary Edema?)│
│  2. Exclude Obstruction (Bladder Scan)       │
│  3. Check Potassium & pH (VBG)               │
└──────────────────────────────────────────────┘
                     ↓
┌──────────────────────────────────────────────┐
│           DETERMINE FLUID STATUS             │
├───────────────────────┬──────────────────────┤
│      HYPOVOLAEMIC     │      EUVOLAEMIC      │
│ (Dry, Tachy, Low BP)  │   (Normal JVP/BP)    │
│          ↓            │          ↓           │
│   FLUID CHALLENGE     │    STOP & THINK      │
│ 500ml Balanced Cryst. │  Review Drugs        │
│          ↓            │  Review Sepsis       │
│    Re-assess (JVP)    │  Check Urine Na      │
└──────────┬────────────┴──────────────────────┘
           │
           ↓
┌──────────────────────────────────────────────┐
│         RESPONSE TO TREATMENT                │
├───────────────────────┬──────────────────────┤
│    URINE OUTPUT ↑     │    NO RESPONSE       │
│   (Prerenal Success)  │   (Established ATN)  │
│          ↓            │          ↓           │
│   Continue IVF Maintenance│ RESTRICT FLUIDS!     │
│                       │ Match Output + 500ml │
└───────────────────────┴──────────────────────┘

Renal Replacement Therapy (RRT) Modalities

When AEIOU criteria are met, the choice of modality depends on haemodynamic stability.

1. Intermittent Haemodialysis (IHD)

  • Mechanism: Rapid removal of solute and fluid via diffusion and ultrafiltration over 3-4 hours.
  • Indication: Stable patients. Rapid K+ removal needed.
  • Pros: Short duration (frees up patient for scans/physio), less anticoagulation.
  • Cons: Causes hypotension (Dysequilibrium syndrome). Not suitable for shocked patients.

2. Continuous Renal Replacement Therapy (CRRT)

  • Types: CVVH (Haemofiltration - Convection), CVVHD (Haemodialysis - Diffusion), CVVHDF (Diafiltration).
  • Mechanism: Slow, continuous removal (24/7).
  • Indication: Haemodynamically unstable patients (ICU). Sepsis. Cerebral Oedema (avoids rapid fluid shifts).
  • Pros: Excellent haemodynamic stability. Steady acid-base correction.
  • Cons: Patient strictly bedbound. Continuous anticoagulation needed (Heparin or Citrate). High nursing load (1:1).

3. Peritoneal Dialysis (PD)

  • Role in AKI: Rarely used in adults in developed world (slow clearance, infection risk, difficult to quantify). Used in Paediatrics or Low Resource settings.
  • Complication: Peritonitis.

4. Sustained Low Efficiency Dialysis (SLED)

  • Hybrid: 6-12 hours of dialysis. Slower than IHD, faster than CRRT.
  • Use: ICU patients who need stability but CRRT machines unavailable.

Anticoagulation for RRT

  • Regional Citrate: Gold standard for CRRT. Citrate chelates calcium in the circuit (preventing clots) and is metabolised to bicarbonate in the liver (buffer). Risk: "Citrate Lock" (Hypocalcaemia).
  • Unfractionated Heparin: Cheap, reversible (Protamine). Risk: HIT (Heparin Induced Thrombocytopenia) and bleeding.
  • Epoprostenol (Prostacyclin): Used if HIT or high bleed risk. Vasodilator (can cause hypotension).
  • No Anticoagulation: High flows needed, high risk of circuit clotting.

Access for RRT

  • Vas Cath: Non-tunnelled, large bore dual lumen catheter.
  • ** Sites**:
    1. Right Internal Jugular: Preferred (Straight path to RA).
    2. Femoral: High infection risk, DVT risk. Good for emergencies.
    3. Left Internal Jugular: Angled path (stenosis risk).
    4. Subclavian: AVOID. Stenosis ruins future fistula options for CKD.

Complications of RRT

  • Catheter Related Bloodstream Infection (CRBSI): Staph aureus/epidermidis.
  • Hypotension: "Intradialytic Hypotension".
  • Disequilibrium Syndrome: Rapid urea removal causes cerebral edema (favours water movement into brain cells).
  • Air Embolism.

1. The "STOP AKI" Care Bundle (Standard of Care)

Every patient with AKI must have these 4 steps enacted within 6 hours.

  1. Sepsis Screen: Blood Cultures, Urine Cultures, Lactate. Start Antibiotics within 1h if Sepsis suspected.
  2. Toxins Stopped: Deprescribe NSAIDs, ACEi, ARBs, Diuretics (unless overloaded), Metformin (risk of Lactic Acidosis), Aminoglycosides.
  3. Optimise Volume: Assess fluid status. If hypovolaemic, resuscitate. If euvolaemic, maintain.
  4. Prevent Harm: Monitor Creatinine daily. Review drug doses (Renally adjust antibiotics like Vancomycin/Gentamicin).

2. Pharmacology of Key Agents

DrugIndicationDoseMechanismCautions
FurosemideFluid Overload only40-80mg IVLoop Diuretic (Na/K/2Cl blocker)Ototoxicity. Do NOT use to "kick start" kidneys in ATN (no benefit).
Calcium GluconateHyperkalaemia30ml 10% IVStabilises Cardiac MembraneDoes not lower Potassium. Effect lasts 30-60 mins.
Insulin (Actrapid)Hyperkalaemia10 Units IVShifts K+ intracellularlyMust give with 50ml 50% Dextrose to prevent Hypoglycaemia.
SalbutamolHyperkalaemia10-20mg NebulisedBeta-2 Agonist (Shifts K+)Causes tachycardia. High dose required (4x asthma dose).
Sodium BicarbonateSevere Acidosis (pH <7.1)1.26% or 8.4% IVBufferEvidence weak. Risk of hypernatraemia/fluid overload.

3. Comprehensive Renal Drug Database

In AKI, drug accumulation leads to toxicity. Dosage adjustment is critical.

Drug ClassAgentAKI Adjustment StrategyConsequences of Accumulation
AnalgesicsMorphineAVOID. Active metabolites (M6G) accumulate.Narcosis, Respiratory Depression, Seizures.
OxycodoneAVOID / Use caution.Similar to Morphine.
FentanylSAFE. Hepatic clearance.Drug of choice in AKI.
CodeineAVOID.Severe drowsiness.
NSAIDsCONTRAINDICATED.Causes prerenal vasoconstriction and AIN.
ParacetamolSafe. No adjustment.Hepatotoxic in overdose (causes Hepatorenal).
AntibioticsGentamicinHIGH RISK. One-off dose usually safe. Avoid maintenance. TDM mandatory.Direct Tubular Toxicity (ATN). Ototoxicity.
VancomycinHIGH RISK. Load normally. Extend interval (e.g. q48h). Monitor Trough.Nephrotoxic. Red Man Syndrome.
AmoxicillinSafe in mild AKI. Reduce dose in severe (accumulates).Seizures at very high levels.
Co-AmoxiclavReduce dose (risk of cholestasis?).Seizures.
Piperacillin-TazoReduce dose (Renal clearance of both).Seizures, Sodium load.
MeropenemReduce dose (e.g. 500mg BD vs 1g TDS).Seizures.
DoxycyclineSAFE. Hepatic excretion.None.
NitrofurantoinINEFFECTIVE. Contraindicated.Peripheral Neuropathy.
TrimethoprimCaution. Increases Creatinine (blocks secretion) without changing GFR. Causes Hyperkalaemia.Hyperkalaemia.
CardiacACE InhibitorsWITHHOLD. Unless AKI is stable/recovering.Reduces GFR (efferent dilation). Hyperkalaemia.
DigoxinHIGH RISK. Avoid or reduce dose massively.Arrhythmias, Nausea, Yellow vision.
Beta BlockersAtenolol (Renal) - Reduce. Bisoprolol/Carvedilol (Hepatic) - Safer.Bradycardia.
StatinsAtorvastatin (Safe). Rosuvastatin (Start low).Rhabdomyolysis risk increases in AKI.
DiureticsFurosemideHigh doses needed (160-240mg) to overcome tubular resistance.Ototoxicity. Hypokalaemia.
SpironolactoneCONTRAINDICATED.Life-threatening Hyperkalaemia.
ThiazidesIneffective if GFR <30.Hyponatraemia.
AnticoagulantsLMWH (Enoxaparin)Accumulates. Reduce to prophylactic dose (20mg) or switch to Unfractionated Heparin.Major Haemorrhage.
WarfarinMonitor INR closely (Protein binding changes).Bleeding.
DOACsCONTRAINDICATED in severe AKI. No reversal agent readily available (historically).Major Haemorrhage.
DiabetesMetforminWITHHOLD.Lactic Acidosis (MALA).
SulphonylureasAVOID (Gliclazide). Accumulate.Prolonged Hypoglycaemia.
InsulinInsulin half-life increases (renally cleared).Hypoglycaemia (reduce dose).
SGLT2 InhibitorsWITHHOLD. Not effective for glucuresis. Risk of Euglycaemic DKA.DKA.

4. Contrast Prescribing Protocol

Contrast-Induced Nephropathy (CIN) risk reduction.

  1. Risk Stratify: eGFR <45 or AKI causes high risk.
  2. Volume Expansion: The only proven prevention.
    • Protocol: 1 mL/kg/hour of 0.9% Saline for 12 hours before and 12 hours after procedure.
  3. Use Isosmolar Contrast: Lowest nephrotoxicity.
  4. Withhold Nephrotoxins: Stop ACEi/NSAIDs/Metformin 24h before.

5. Nutrition in AKI

AKI is a catabolic state. Malnutrition increases mortality.

  • Energy: 25-30 kcal/kg/day.
  • Protein:
    • Non-Catabolic (Conservative): 0.8-1.0 g/kg/day (to reduce urea generation).
    • Catabolic (Sepsis/Dialysis): 1.5-1.7 g/kg/day (Dialysis removes amino acids, need to replace).
  • Electrolytes: Restrict Potassium and Phosphate intake.

2. Fluid Management: The "Goldilocks" Principle

  • Hypovolaemia: Give Fluid (Hartmann's/Plasmalyte preferred over 0.9% Saline to prevent Hyperchloraemic Acidosis).
    • Challenge: 250-500ml bolus over 15 mins. Assess response (HR, BP, Urine).
  • Euvolaemia (ATN): If "filled" but oliguric, DO NOT continue forcing fluids. You will cause pulmonary oedema.
    • Action: Restriction. Match Output + 500ml (Insensible loss).
  • Furosemide Stress Test (FST):
    • Indication: Euvolaemic patient with Oliguria.
    • Dose: 1.0-1.5 mg/kg IV bolus.
    • Result: If <200ml urine in 2 hours -> Likely progression to RRT.

3. Hyperkalaemia Management (Detailed)

Potassium >6.5 or ECG changes (Tented T waves, Wide QRS).

  1. Protect (Myocardium): 30ml 10% Calcium Gluconate IV over 10 mins.
  2. Shift (Intracellular): 10 units Actrapid + 50ml 50% Dextrose over 15 mins. Salbutamol 10-20mg Nebs.
  3. Eliminate: Calcium Resonium (slow), Loop Diuretics (if passing urine), Dialysis (Definitive).

4. Indications for Dialysis (RRT)

Mnemonic: AEIOU

  • Acidosis: pH <7.15 refractory to bicarbonate.
  • Electrolytes: Hyperkalemia >6.5 refractory to medical therapy.
  • Ingestion: Dialyzable toxins (Lithium, Aspirin, Ethylene Glycol).
  • Overload: Pulmonary Oedema refractory to diuretics.
  • Uraemia: Encephalopathy, Pericarditis, Neuropathy.
8. Complications

Uraemic Complications

  • Pericarditis: Inflammation of the pericardial sac. Requires Urgent Dialysis.
  • Encephalopathy: Asterixis, confusion, seizures.
  • Platelet Dysfunction: Uraemia inhibits platelet aggregation -> Bleeding risk.

Metabolic

  • Metabolic Acidosis: High Anion Gap (Retention of H+ and Sulphates/Phosphates).
    • Consequence: Myocardial depression, Kussmaul respiration.
  • Hyperphosphataemia: Cannot excrete phosphate. Causes reciprocal Hypocalcaemia.

Fluid Overload

  • Pulmonary Oedema: The "Salt Water Drowning" of iatrogenic overload.
  • Tissue Oedema: Delayed wound healing, abdominal compartment syndrome.

Viva Points

Scenario: The Oliguric Patient "You are called to a patient passing 10ml urine/hour. They have had 2L of fluid. JVP is raised. What do you do?" Response: "Do NOT give more fluid. This is likely established ATN. Assess volume status carefully. If fluid overloaded, try Furosemide Stress Test. If no response, restrict fluid."

Specific Clinical Syndromes

1. Rhabdomyolysis

  • Definition: Skeletal muscle breakdown releasing Myoglobin.
  • Diagnosis: CK >1000 U/L (often >10,000). Urine Dipstick Positive for Blood (Myoglobin) but Microscopy Negative for RBCs.
  • Mechanism: Myoglobin is directly toxic to tubules and precipitates in acidic urine.
  • Treatment: Aggressive Volume Expansion (Target 3ml/kg/hr urine). Urinary Alkalinization (Bicarbonate) is controversial but commonly used for CK >5000 to prevent cast formation.
  • Complications: Hyperkalaemia (released from muscle), Hyperphosphataemia, Hypocalcaemia (calcium deposits in muscle), Compartment Syndrome.

2. Hepatorenal Syndrome (HRS)

  • Definition: Functional renal failure in advanced Liver Cirrhosis (portal hypertension).
  • Mechanism: Splanchnic vasodilation causes effective hypovolaemia -> Intense RAAS activation -> Renal Vasoconstriction.
  • Diagnosis: Diagnosis of exclusion. No response to 2 days of Albumin withdrawal.
  • Treatment: Terlipressin (Splanchnicoconstrictor) + 20% Albumin. Definitive treatment is Liver Transplant.

3. Cardiorenal Syndrome (Type 1)

  • Definition: Acute Heart Failure leading to AKI.
  • Mechanism: "Congestive Kidney Failure". High Central Venous Pressure (CVP) transmits to Renal Veins, reducing perfusion gradient (MAP - CVP).
  • Treatment: Diuresis. Despite rising Creatinine, offloading fluid often improves GFR by reducing renal venous congestion. "Permissive AKI" is acceptable if decongestion is achieved.

4. Acute Interstitial Nephritis (AIN)

  • Trigger: Drugs (PPI, Penicillins, NSAIDs) > Infection.
  • Clinical: ~2 weeks after exposure. Sterile Pyuria (WBCs in urine with negative culture).
  • Management: Stop culprit. Prednisolone 1mg/kg if no recovery in 1 week.

5. Abdominal Compartment Syndrome

  • Trigger: Trauma, Pancreatitis, Ruptured AAA repair.
  • Mechanism: Intra-abdominal Pressure (IAP) >20 mmHg compresses renal veins.
  • Diagnosis: Measure bladder pressure via catheter.
  • Treatment: Laparostomy (Decompression).
9. Prognosis & Outcomes

Risk Prediction Scores

Several scoring systems exist to predict AKI severity and mortality.

  • Renal Angina Index (RAI): Used in Paediatrics/ICU to predict severe AKI. Based on change in Cr and fluid overload %.
  • SHARF Score: (Surviving Hospital Acute Renal Failure).
  • APACHE II / SOFA: General ICU scores included Renal components.
  • Biomarkers: NGAL (Neutrophil Gelatinase-Associated Lipocalin) and TIMP-2*IGFBP7 (NephroCheck) are FDA approved to predict AKI risk ("Renal Stress") before Creatinine rises.

Natural History

  • Prerenal: Excellent prognosis if reversed in 24-48h.
  • ATN: "Maintenance Phase" lasts 7-21 days (time for tubular regeneration). Patient may require dialysis support during this bridge.
  • Recovery: 90% of ATN survivors recover renal function, but many have residual CKD.

Long Term Risks

  • CKD: AKI is a major risk factor for future CKD.
  • Recurrence: "Once an AKI, always an AKI risk".
  • Mortality: ICU mortality for AKI requiring dialysis is 50-60%.
  • Cardiovascular: AKI survivors have higher risk of Heart Failure and Stroke (Cardio-Renal Syndrome Type 4).

Discharge Planning

  • Medication Review: Re-start ACEi/ARB only when Cr is stable and patient euvolaemic. (Usually withhold for 2-3 days post-discharge).
  • Monitoring: Repeat U&Es in 1 week.
  • Education: "Sick Day Rules" (Stop DAMN drugs if vomiting/diarrhoea).

Nursing Care Plan

  • Strict Fluid Balance: Hourly urine output. Report <30ml/hr.
  • Daily Weights: Essential for fluid status.
  • Skin Care: Oedematous skin is fragile. Pressure area care.
  • Mouth Care: Uraemia causes metallic taste and dryness.
  • Diet: Low Potassium if hyperkalaemic.
10. Evidence & Guidelines

Evolution of AKI Definitions (Classification Comparison)

The definition of AKI has evolved from "RIFLE" to "AKIN" to the current "KDIGO" standard.

ClassificationYearCriteriaLimitations
RIFLE2004Risk (1.5x Cr), Injury (2x Cr), Failure (3x Cr), Loss, ESRD.Required baseline Cr (often unknown). "Loss" and "ESRD" were outcome measures, not severity stages.
AKIN2007Added "Absolute rise of >26.5 µmol/L". Removed "Loss/ESRD".Small rises in Cr (26.5) found to be associated with mortality. Timeframe 48h.
KDIGO2012Stage 1: 1.5-1.9x baseline OR >26.5 rise.
Stage 2: 2.0-2.9x baseline.
Stage 3: 3.0x baseline OR Cr >354 OR Dialysis.		Consolidated RIFLE and AKIN. The current gold standard.

KDIGO 2012 Guidelines

The global standard.

  • Definitions: See table above.
  • Recommendation: Use Isotonic Crystalloids for volume expansion. Avoid Starches (HES).
  • Vasopressors: Suggests Noradrenaline to maintain MAP >65 mmHg in vasomotor shock (Level 2C).
  • Diuretics: Do not use diuretics to prevent or treat AKI, except for fluid overload (Level 1B).
  • Dopamine: "Renal dose dopamine" is ineffective and harmful (arrhythmias). Do NOT use.
  • Nutrition: 20-30 kcal/kg/day. Do not restrict protein to prevent dialysis.

Landmark Trials Summary

TrialYearQuestionInterventionResultImpact
SAFE2004Fluid Choice in ICUAlbumin vs SalineNo difference in mortality. Subgroup: Albumin harmful in Traumatic Brain Injury.Demonstrated Albumin is safe in renal failure but expensive.
CHEST2012HES vs SalineHydroxyethyl Starch (6%) vs SalineStarch increased risk of AKI and RRT.Banned Starches in ICU.
6S2012HES vs Ringer'sHES vs Ringer's AcetateStarch increased death and RRT.Confirmed HES is nephrotoxic.
SPLIT2015Saline vs Buffered0.9% NaCl vs PlasmalyteNo difference in AKI.Single centre, low risk patients.
SMART2018Saline vs Buffered0.9% NaCl vs PlasmalyteBalanced crystals REDUCED AKI and Death (Composite).Shifted practice to Balanced Crystalloids (Hartmann's/Plasmalyte).
AKIKI2016Dialysis TimingEarly vs DelayedNo survival benefit to early start.Validated "Wait and See" (Conservative).
ELAIN2016Dialysis TimingEarly vs DelayedEarly start reduced mortality.Contradicted AKIKI. But ELAIN was single-centre, mostly surgical.
STARRT-AKI2020Dialysis TimingAccelerated vs StandardNo benefit to early start. Higher adverse events.Definitively ended the "Start Early" debate.

"STOP-AKI" Trial (2015)

  • Question: Does a care bundle reduce AKI?
  • Result: Implementing a bundle (as described above) significantly reduced the incidence and severity of AKI in cardiac surgery.

STARRT-AKI (2020)

  • Question: Accelerated (early) vs Standard initiation of RRT?
  • Finding: Early dialysis (prophylactic) showed NO benefit and higher risk of adverse events.
  • Practice: Wait for solid indications (AEIOU) rather than "starting early".

AKIKI Trial (2016)

  • Question: Timing of Dialysis in ICU.
  • Result: Immediate RRT in severe AKI (Stage 3) showed no mortality benefit over delayed strategy (waiting for complications).
  • Impact: Confirmed "Wait and See" is safe if no emergency indications exist.

BICAR-ICU Trial (2018)

  • Question: Sodium Bicarbonate for Metabolic Acidosis (pH <7.2).
  • Result: No overall mortality benefit, BUT in the subgroup with AKI (AKIN stage 2-3), bicarbonate REDUCED mortality and need for dialysis.
  • Practice: Consider Bicarb in severe acidosis with AKI.

SMART Trial (2018)

  • Question: Balanced Crystalloids (Plasmalyte/Hartmann's) vs Saline (0.9% NaCl).
  • Result: Balanced crystalloids resulted in Lower rates of AKI and death/dialysis (MAKE30 composite outcome).
  • Mechanism: Saline causes Hyperchloraemic Metabolic Acidosis, which causes renal vasoconstriction.
  • Practice: Prefer Balanced Crystalloids for resuscitation.
11. Patient/Layperson Explanation

What is AKI?

"Acute Kidney Injury means your kidneys have suddenly stopped filtering waste from your blood properly. It is usually temporary, unlike Chronic Kidney Disease."

Why did this happen?

"It usually happens for one of three reasons:

  1. Dehydration: Not enough blood getting to the kidneys (like a pump running dry).
  2. Effect: A medication or infection has temporarily stunned the kidney cells.
  3. Blockage: Something is stopping urine from coming out (like a prostate issue)."

Will I need Dialysis?

"Most patients do NOT need dialysis. We treat it with fluids and medication changes. Dialysis is only used as a temporary 'life-support' machine for the kidneys if they shut down completely, to do their job while they heal."

12. References
  1. KDIGO. Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2:1-138.
  2. Bellomo R, Kellum JA, Ronco C. Acute kidney injury. Lancet. 2012;380(9843):756-766. [PMID: 22617274]
  3. Coca SG, Singanamala S, Parikh CR. Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis. Kidney Int. 2012;81(5):442-448. [PMID: 22113526]
  4. Mehta RL et al. Spectrum of acute renal failure in the intensive care unit: the PICARD experience. Kidney Int. 2004;66(4):1613-1621. [PMID: 15458458]
  5. Hoste EA et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med. 2015;41(8):1411-1423. [PMID: 26162677]
  6. Gaudry S et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit. N Engl J Med. 2016;375(2):122-133. [PMID: 27181456]
  7. STARRT-AKI Investigators. Timing of Initiation of Renal-Replacement Therapy in Acute Kidney Injury. N Engl J Med. 2020;383(3):240-251. [PMID: 32668114]
  8. Chawla LS et al. Acute kidney injury and chronic kidney disease as interconnected syndromes. N Engl J Med. 2014;371(1):58-66. [PMID: 24988558]
  9. Uchino S et al. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005;294(7):813-818. [PMID: 16106006]
  10. Bagshaw SM et al. Timing of initiation of renal-replacement therapy in acute kidney injury. N Engl J Med. 2020.
  11. Gronich N et al. Acute kidney injury induced by contrast media. Nat Rev Nephrol. 2021.
  12. Ostermann M et al. Diagnosis and management of acute kidney injury: a physician's primer. Postgrad Med J. 2015.
  13. Lewington AJ et al. New KDIGO guidelines on the management of blood pressure in acute kidney injury. Lancet. 2013.
  14. Perazella MA. Drug-induced acute kidney injury. Am J Kidney Dis. 2018.
  15. Ronco C et al. The concept of acute kidney injury. Nat Rev Nephrol. 2019.
  16. Semler MW et al. Balanced Crystalloids versus Saline in Critically Ill Adults (SMART). N Engl J Med. 2018;378:829-839. [PMID: 29485925]
  17. Jaber S et al. Sodium Bicarbonate Therapy for Patients with Severe Metabolic Acidosis in the ICU (BICAR-ICU). Lancet. 2018;392:31-40. [PMID: 29910040]
  18. Gaudry S et al. Initiation Strategies for Renal-Replacement Therapy (AKIKI). N Engl J Med. 2016;375:122-133. [PMID: 27181456]
  19. Kellum JA et al. Recovery after Acute Kidney Injury. Am J Respir Crit Care Med. 2017;195:847-857. [PMID: 27726410]
  20. NICE Guideline NG148. Acute kidney injury: prevention, detection and management. 2019.
  21. Angeli P et al. Diagnosis and management of acute kidney injury in patients with cirrhosis. J Hepatol. 2015. [PMID: 25638527]
  22. House AA et al. Definition and classification of Cardio-Renal Syndromes. Kidney Int. 2010. [PMID: 20593458]
  23. Bosch X et al. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med. 2009. [PMID: 19571281]
  24. Davenport A et al. Hyperkalaemia treatment guidelines. Resuscitation. 2016.
  25. Moledina DG et al. Phenotyping of Acute Interstitial Nephritis. J Am Soc Nephrol. 2019. [PMID: 31061139]
13. Examination Focus

Glossary of Terms

TermDefinitionClinical Significance
Acute Tubular Necrosis (ATN)Death of tubular epithelial cells due to ischaemia or toxins.The most common cause of intrinsic AKI. Reversible but requires time (weeks).
AnuriaUrine output <100 ml/24 hours (or effectively zero).Suggests complete obstruction, vascular catastrophe, or cortical necrosis.
AzotaemiaElevation of blood urea nitrogen (BUN) and creatinine.Biochemical term; "Uraemia" is the clinical syndrome.
Fractional Excretion of Sodium (FeNa)Percentage of filtered sodium that is excreted in urine.Differentiates Prerenal (<1%) from Intrinsic (>2%).
Glomerulonephritis (GN)Inflammation of the glomeruli.Causes nephritic syndrome (haematuria, hypertension).
HydronephrosisDilation of the renal pelvis and calyces.Hallmark of postrenal obstruction seen on Ultrasound.
Interstitial Nephritis (AIN)Inflammation of the renal interstitium (spaces between tubules).Often drug-induced (allergic). presents with eosinophiluria.
UraemiaThe clinical syndrome of renal failure (nausea, pericarditis, encephalopathy).Indication for dialysis.

Common Exam Questions

1. "Differentiate Prerenal from Intrinsic Renal Failure."

  • Answer: Look at Urine Sodium and Osmolality. Prerenal = Avid retention (Na <20, Osm >500). Intrinsic = Tubules cannot reabsorb (Na >40, Osm <350).

2. "What are the indications for Urgent Dialysis?"

  • Mnemonic: AEIOU (Acidosis, Electrolytes/HyperK, Intoxication, Overload, Uraemia).

3. "What is Contrast Induced Nephropathy?"

  • Answer: A rise in Cr 24-48h after contrast.
  • Prevention: Hydration (IV 0.9% Saline) 12h pre and post (Though SMART suggested Plasmalyte, guidelines often say Saline). N-Acetylcysteine is NO LONGER recommended (Evidence weak).

Common Mistakes

  • Failing to check bladder: Always palpate/scan for retention!
  • Fluid Overloading ATN: Treating "Low Urine" with "More Fluid" in a patient who is already wet.
  • Missing Obstruction: Assuming "No pain = No obstruction" (Silent obstruction in elderly/diabetics).
  • Ignoring Creatinine Trends: A "Normal" Cr of 90 is abnormal if it was 50 yesterday.

Advanced Clinical Reasoning

1. The "Sodium Paradox" Question: "Why is Urine Sodium LOW in Prerenal failure but HIGH in ATN?" Explanation:

  • In Prerenal states (hypovolaemia), the body tries to hold onto every drop of water. Aldosterone is maximal, stimulating aggressive Sodium reabsorption in the DCT/Collecting Duct. Water follows sodium. Thus, little sodium appears in urine (<20 mmol/L).
  • In ATN, the tubular cells are dead. The pump that normally reclaim sodium (Na+/K+ ATPase) are broken or misplaced. Sodium cannot be reabsorbed and flows straight into the urine (>40 mmol/L).

2. "Why does Hyperkalaemia Kill?" Explanation:

  • High extracellular Potassium lowers the resting membrane potential of cardiomyocytes (making them "less negative").
  • This makes them initially excitable, then refractory (unable to repolarize).
  • Result: Asystole or Ventricular Fibrillation.
  • Calcium Gluconate works by raising the threshold potential, restoring the gap between resting and threshold, stabilizing the membrane.

Further Advanced Cases (MCQ Bank)

Case 4: The "Septic" Interpretation A 70-year-old male is treated for Pneumonia. Cr rises 80 -> 150. BP 110/70. Urine output 40ml/hr. Question: Which mechanism best explains his AKI?

  • A) Prerenal Hypovolaemia
  • B) Acute Tubular Necrosis
  • C) Post-infectious GN
  • D) Septic Vasodilation Correct: D. Sepsis causes "Distributive" defects.

Case 5: The "Contrast" Conundrum A 60-year-old diabetic (Cr 140) needs a Coronary Angiogram. Question: What is the most effective preventative measure?

  • A) N-Acetylcysteine Oral
  • B) Sodium Bicarbonate IV
  • C) 0.9% Sodium Chloride IV
  • D) Furosemide IV Correct: C. The only intervention with strong Evidence (Level 1A) is volume expansion.

Case 7: The "False" AKI A 25-year-old male bodybuilder. Creatinine 160. Normal Urea. Normal urine. Question: What is the diagnosis?

  • A) Steroid Nephropathy
  • B) Dehydration
  • C) High Muscle Mass (Pseudo-AKI)
  • D) Rhabdomyolysis Correct: C. Creatinine is a breakdown product of muscle creatine. High muscle mass = High baseline Cr. Urea is normal, suggesting GFR is fine. Cystatin C would be a better test (unaffected by muscle).

Case 8: The "Triad" A patient presents with Fever, Rash, and Eosinophilia after starting Omeprazole. Cr 250. Question: Diagnosis?

  • A) Acute Interstitial Nephritis (AIN)
  • B) ATN
  • C) Pyelonephritis
  • D) Vasculitis Correct: A. The classic triad of AIN (Fever, Rash, Eosinophilia) is only present in 10-15% of cases, but when present, strongly suggests it. Stop the drug. steroids (Prednisolone) are often given.

Case 9: The "Pulmonary-Renal" Syndrome A 60-year-old female with Haemoptysis and AKI (Cr 400). CXR shows diffuses alveolar haemorrhage. Question: Which antibody is most likely positive?

  • A) Anti-核 (ANA)
  • B) Anti-GBM or ANCA
  • C) Rheumatoid Factor
  • D) Anti-Cardiolipin Correct: B. Anti-GBM (Goodpasture's) and ANCA (Vasculitis) are the two main causes of Pulmonary-Renal Syndrome. Urgent Plasma Exchange (PLEX) is needed for Anti-GBM.

Case 10: The "Myeloma" Kidney An elderly man with Back pain, Hypercalcaemia, and AKI. Dipstick is Negative for protein. Question: Why is the dipstick negative?

  • A) The protein is Albumin
  • B) The protein is Immunoglobulin Light Chains
  • C) The kidneys are not leaking protein
  • D) The dipstick is faulty Correct: B. Urine Dipstick detects Albumin only. It does NOT detect Bence-Jones Proteins (Light chains). You must request "Urine Protein Electrophoresis" or "Serum Free Light Chains".

Spot Diagnosis (Pathology Descriptions)

1. "Muddy Brown Casts"

  • Diagnosis: Acute Tubular Necrosis (ATN).
  • Composition: Necrotic tubular epithelial cells + Tamm-Horsfall Protein.
  • Significance: Pathognomonic for ATN. Predicts non-responsiveness to fluids.

2. "Red Cell Casts"

  • Diagnosis: Glomerulonephritis (e.g., IgA, Lupus, Vasculitis).
  • Composition: RBCs trapped in protein matrix.
  • Significance: Indicators of active glomerular inflammation. Urgent biopsy.

3. "White Cell Casts"

  • Diagnosis: Pyelonephritis or Interstitial Nephritis.
  • Composition: WBCs (neutrophils/eosinophils).
  • Significance: Infection or Allergy.

4. "Dyslineated / Eosinophilic Casts"

  • Diagnosis: Myeloma Kidney (Cast Nephropathy).
  • Description: Fractured, hard, glassy casts.

Viva Points

1. "Tell me about the indications for Renal Biopsy." Model Answer: "Renal biopsy is an invasive procedure with bleeding risk (Native kidney ~1% risk of major bleed). I would reserve it for cases where the histology changes management. Specifically:

  1. Unexplained AKI: Where Prerenal (Fluid) and Postrenal (US) causes are excluded.
  2. Nephrotic Syndrome: To distinguish Minimal Change from FSGS/Membranous.
  3. Pulmonary-Renal Syndrome (Vasculitis/Anti-GBM): To confirm diagnosis and assess 'activity vs chronicity' (Active crescents treat with Cyclophosphamide; Sclerotic scars do not).
  4. Transplant Dysfunction: Rejection vs ATN vs Drug toxicity."

2. "How do you adjust drug dosing in AKI?" Model Answer: "Renal drug handling is critical.

  1. Loading Dose: Usually unchanged (e.g., Digoxin/Vancomycin loading), as Volume of Distribution is unchanged or increased (oedema).
  2. Maintenance Dose: Must be reduced. Either lower the dose (e.g., LMWH 20mg instead of 40mg) or extend the interval (e.g., Vancomycin every 48h instead of 12h).
  3. Monitoring: TDM (Therapeutic Drug Monitoring) for Vancomycin/Gentamicin."

3. "What is Tumour Lysis Syndrome?" Model Answer: "It is massive oncological emergency caused by the rapid lysis of malignant cells (usually Haematological like Burkitt's or ALL) after chemotherapy.

  • Pathophysiology: Release of intracellular contents: Potassium, Phosphate, Uric Acid.
  • Renal Impact: Uric Acid crystals precipitate in tubules (Obstructive Uropathy). Calcium-Phosphate stones.
  • Prevention: Aggressive Hydration (3L/day). Allopurinol (Xanthine oxidase inhibitor) or Rasburicase (Recombinant Urate Oxidase - breaks down Uric acid).
  • Treatment: Acute Dialysis if Hyperkalaemia/Oliguria occurs."

Advanced MCQ Bank (Challenge Questions)

Case 11: The "Muddy" Urine A patient with Sepsis develops oliguria. Urine microscopy shows "Granular Casts". Question: What is the pathophysiology of these casts?

  • A) Glomerular leakage of RBCs
  • B) Bacterial aggregation
  • C) Sloughing of necrotic tubular epithelial cells
  • D) Precipitation of Uric Acid Correct: C. Muddy brown casts are hallmark of ATN, representing dead tubular cells mixed with Tamm-Horsfall protein.

Case 12: The High Gap An alcoholic is found collapsed. Cr 300. pH 7.1. Anion Gap 24. Question: Which is the most likely additional toxin?

  • A) Ethanol
  • B) Isopropyl Alcohol
  • C) Ethylene Glycol
  • D) Benzodiazepines Correct: C. Ethylene Glycol (Antifreeze) causes profound High Anion Gap Metabolic Acidosis and AKI (Calcium Oxalate stones). Ethanol causes ketosis but rarely severe AKI alone.

Case 13: The "Blue Toe" A 75-year-old male has a coronary angiogram. 2 weeks later, he develops AKI, Eosinophilia, and Blue Toes. Question: Diagnosis?

  • A) Contrast Nephropathy
  • B) Cholesterol Embolization Syndrome
  • C) AIN
  • D) Pyelonephritis Correct: B. The triad of AKI + Embolic signs (Livedo/Blue toe) + Eosinophilia after vascular manipulation suggests Cholesterol Emboli (showered from aorta).

Case 14: The "Sting" A hiker is stung by multiple wasps. Develops dark urine and AKI. CK 50,000. Question: Diagnosis?

  • A) Anaphylaxis
  • B) Rhabdomyolysis
  • C) Pigment Nephropathy (Haemoglobin)
  • D) Direct Venom Toxicity Correct: B. Wasp venom is a potent myotoxin causing Rhabdomyolysis.

Case 15: The "Hepatorenal" Choice A cirrhotic patient has AKI (Cr 200) not responding to volume. Question: What is the first-line drug treatment?

  • A) Noradrenaline
  • B) Octreotide
  • C) Terlipressin
  • D) Midodrine Correct: C. Terlipressin (+ Albumin) is the gold standard for Type 1 HRS. It causes splanchnic vasoconstriction, improving renal perfusion.

Case 16: The "Fluid Responder" A patient with AKI has a JVP of 2cm. Passive Leg Raise increases Pulse Pressure by 15%. Question: What is the next step?

  • A) Give 500ml Hartmann's Bolus
  • B) Give Furosemide
  • C) Start Noradrenaline
  • D) Do nothing Correct: A. The patient is Fluid Responsive (PLR positive). Fluid resuscitation is indicated.

Case 17: The "Hyperkalaemic" Arrest A patient arrests with K+ 8.5. Question: What is the first drug to give during CPR?

  • A) Adrenaline 1mg
  • B) Calcium Chloride 10ml 10%
  • C) Insulin/Dextrose
  • D) Amiodarone Correct: B. Membrane stabilization is the priority in hyperkalaemic arrest. (Adrenaline is given too, but Calcium addresses the specific cause).

Case 18: The "Post-Renal" Trap An elderly man has Anuria. Bladder scan shows 0ml. Question: Does this rule out obstruction?

  • A) Yes
  • B) No, it could be bilateral ureteric obstruction
  • C) No, the scanner is inaccurate
  • D) Yes, suggest Prerenal Correct: B. An empty bladder only rules out urethral/prostatic obstruction. Bilateral ureteric obstruction (e.g. malignancy) would cause empty bladder but dilated kidneys (Hydronephrosis). US KUB is mandatory.

Case 19: The "Dialysis" Decision A patient has pH 7.25, K+ 5.8, Fluid overload (manageable on oxygen). Question: Is immediate dialysis indicated?

  • A) Yes (Acidosis)
  • B) Yes (Overload)
  • C) No
  • D) Yes (Hyperkalaemia) Correct: C. None of these are refractory or life-threatening yet. Medical management (Diuretics, Bicarb, Insulin) should be tried first.

Case 20: The "Recovery" danger A patient recovering from ATN starts passing 4L urine/day. Question: What is the main risk?

  • A) Hyperkalaemia
  • B) Hypokalaemia and Dehydration
  • C) Pulmonary Oedema
  • D) Hypernatraemia Correct: B. The Polyuric recovery phase risks massive washout of electrolytes (HypoK) and volume depletion.

Last updated: 2025-12-27

At a Glance

EvidenceHigh
Last Updated2025-12-27
Emergency Protocol

Red Flags

  • Anuria (Obstruction/Shock)
  • Hyperkalaemia >6.5 mmol/L (Arrhythmias)
  • Pulmonary Oedema (Refractory)
  • Severe Acidosis (pH &lt;7.1)
  • Uraemic Encephalopathy/Pericarditis

Clinical Pearls

  • **The "Nephrotoxic Hit"**: 30% of hospital-acquired AKI is preventable drug injury. The "DAMN" drugs (Diuretics, ACEi/ARBs, Metformin, NSAIDs) must be held in acute illness.
  • 65 (Reduced nephron mass).
  • 2 sec), Cool Peripheries, Sunken Eyes, Reduced Skin Turgor.
  • 100ml/hr. Risk of electrolyte washout.
  • 300-500ml urine retention (Postrenal).

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines