Acute Kidney Injury – MBBS Final Medicine Exam Notes

Definition and Diagnostic Criteria (KDIGO)

AKI is diagnosed when ANY ONE of the following occurs: 1, 2

Serum creatinine rises ≥0.3 mg/dL within 48 hours, OR
Serum creatinine rises to ≥1.5× baseline within 7 days, OR
Urine output <0.5 mL/kg/h for ≥6 consecutive hours 1, 2

Critical point: Even a modest 0.3 mg/dL creatinine rise carries approximately 4-fold increased in-hospital mortality—patients die "from AKI," not merely "with AKI." 2, 3

KDIGO Staging System

Stage	Serum Creatinine Criterion	Urine Output Criterion
Stage 1	1.5–1.9× baseline OR ≥0.3 mg/dL rise within 48h	<0.5 mL/kg/h for >6 hours
Stage 2	2.0–2.9× baseline	<0.5 mL/kg/h for >12 hours
Stage 3	≥3.0× baseline OR ≥4.0 mg/dL (with acute rise ≥0.3 mg/dL) OR initiation of dialysis	<0.3 mL/kg/h for ≥24h OR anuria ≥12h

1, 2, 4, 3

Prognostic significance: Progressive advancement through stages correlates with incrementally higher mortality; Stage 3 requiring dialysis carries approximately 4-fold mortality risk. 2, 3

Etiological Classification

Prerenal AKI (Functional)

Volume depletion: hemorrhage, GI losses, burns, third-spacing 5, 6
Decreased effective circulating volume: heart failure, cirrhosis, nephrotic syndrome 5, 6
Medications altering glomerular hemodynamics: ACE inhibitors, ARBs, NSAIDs 2, 4

Intrinsic Renal AKI

Acute tubular necrosis (ATN): ischemic or nephrotoxic (aminoglycosides, contrast, myoglobin) 5, 6
Acute interstitial nephritis: drug-induced (β-lactams, PPIs, NSAIDs), infection 5, 6
Glomerulonephritis: post-infectious, vasculitis, lupus nephritis 5, 6
Vascular: renal artery thrombosis, atheroemboli, malignant hypertension 5, 6

Postrenal AKI (Obstructive)

Bilateral ureteral obstruction: stones, malignancy, retroperitoneal fibrosis 5, 6
Bladder outlet obstruction: BPH, prostate cancer, neurogenic bladder 5, 6
Note: Obstruction accounts for <3% of AKI cases 4

Initial Diagnostic Workup

Immediate Laboratory Tests

Order simultaneously upon AKI suspicion: 4, 3

Serum creatinine and BUN to confirm diagnosis and stage severity 4, 6
Complete blood count to identify infection, hemolysis, or thrombotic microangiopathy 4, 3
Serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) to detect hyperkalemia and metabolic acidosis 4, 6
Urinalysis with microscopy to differentiate structural from functional causes 4, 3
Fractional excretion of sodium (FENa) to distinguish prerenal from intrinsic AKI 4, 6

Urinalysis Interpretation

Muddy-brown granular casts → acute tubular necrosis 2, 3
Red blood cell casts → glomerulonephritis 2, 3
White blood cell casts → acute interstitial nephritis 2, 3
Eosinophiluria → allergic interstitial nephritis 6

Urine Chemistry Differentiation

Parameter	Prerenal AKI	Intrinsic AKI (ATN)
Urine Na⁺	<20 mEq/L	>40 mEq/L
FENa	<1%	>2%
Urine osmolality	>500 mOsm/kg	<350 mOsm/kg
BUN:Cr ratio	>20:1	10–15:1

2, 4, 6

Caveat: FENa is unreliable if diuretics have been administered; use fractional excretion of urea (FEUrea) instead. 3

Imaging Studies

Renal ultrasonography when postrenal obstruction suspected (hydronephrosis, kidney size) 4, 6
Chest radiography if infection or volume overload suspected 4

Immediate Management Algorithm

Step 1: Discontinue All Nephrotoxic Agents

Stop immediately upon AKI diagnosis: 2, 4

ACE inhibitors and ARBs
NSAIDs
Diuretics (even in non-oliguric patients)
Aminoglycosides
Contrast media
Any other nephrotoxic medications

Critical pitfall: Continuing diuretics after AKI diagnosis worsens outcomes and increases mortality. 4

Step 2: Assess Volume Status and Resuscitate

If hypovolemic: administer isotonic crystalloids (normal saline or Ringer's lactate) rather than colloids 2, 4
Monitor: central venous pressure if available, clinical examination (JVP, skin turgor, mucous membranes) 2
Target mean arterial pressure ≥65 mmHg to ensure renal perfusion 2

Step 3: Identify and Treat Underlying Cause

Infection workup: blood cultures, urine cultures, chest X-ray; diagnostic paracentesis in cirrhotic patients to rule out spontaneous bacterial peritonitis 2, 4
Initiate empiric broad-spectrum antibiotics immediately if infection strongly suspected—do not wait for culture results, as sepsis is the most reversible cause of AKI with multiorgan dysfunction 2, 4

Step 4: Monitor Electrolytes and Complications

Repeat serum creatinine and electrolytes every 4–6 hours in Stage 2–3 AKI 2, 4
Correct hyperkalemia urgently if K⁺ >6.0 mEq/L or ECG changes present 2
Treat severe metabolic acidosis with intravenous sodium bicarbonate; consider dialysis if refractory 2

Special Considerations: AKI in Cirrhosis

Diagnostic Modifications

Use ICA-AKI criteria: creatinine rise ≥0.3 mg/dL within 48h OR ≥50% from baseline, without a fixed 1.5 mg/dL threshold, because baseline creatinine underestimates true GFR due to reduced muscle mass 2, 3
Ignore urine output criteria in cirrhotic patients—they are frequently oliguric with avid sodium retention despite relatively normal GFR, and diuretics confound interpretation 2, 3

Immediate Therapeutic Actions

Discontinue diuretics and β-blockers immediately to avoid further renal hypoperfusion 2
Administer albumin 1 g/kg/day (maximum 100 g) for 2 consecutive days when creatinine has doubled from baseline to expand plasma volume and improve renal perfusion 2
Perform diagnostic paracentesis in all cirrhotic AKI patients to rule out spontaneous bacterial peritonitis 2

Hepatorenal Syndrome (HRS-AKI) Treatment

When HRS criteria are met (Stage 2–3 AKI unresponsive to volume expansion): 2

Albumin 1 g/kg IV on day 1, then 20–40 g daily, PLUS
Vasoactive therapy: terlipressin (preferred), OR norepinephrine, OR midodrine + octreotide

Indications for Renal Replacement Therapy (Dialysis)

Urgent RRT is indicated for: 2, 4

Severe oliguria unresponsive to fluid resuscitation
Refractory hyperkalemia (K⁺ >6.5 mEq/L or ECG changes despite medical therapy)
Severe metabolic acidosis (pH <7.1) unresponsive to bicarbonate
Volume overload with pulmonary edema refractory to diuretics
Uremic complications: encephalopathy, pericarditis, pleuritis
Toxin removal (e.g., methanol, ethylene glycol, lithium)

Reassess need for continued RRT daily. 2

Critical pitfall: Delaying RRT when clear indications exist increases mortality. 2

Prevention Strategies

Identify High-Risk Patients

Risk factors for AKI: 2, 6

Older age (>65 years)
Pre-existing chronic kidney disease
Diabetes mellitus
Heart failure or cirrhosis
Sepsis or shock
Cardiac surgery
Exposure to contrast agents or nephrotoxic drugs

Preventive Measures

Ensure adequate hydration before contrast procedures 2
Avoid iodinated contrast in AKI unless absolutely necessary; use lowest possible volume 4
Implement drug stewardship programs with pharmacist involvement to identify and discontinue nephrotoxic agents 2

Follow-Up and Prognosis

Post-Discharge Monitoring

Schedule close clinical evaluation within 3 months for patients with Stage 2–3 AKI, pre-existing CKD, or incomplete renal recovery at discharge 2, 4
Reassess kidney function (serum creatinine, eGFR) to detect early CKD development or progression 2, 4

Nephrology Referral Indications

Obtain nephrology consultation when: 2, 7

Stage 2 or Stage 3 AKI (emergent referral)
Underlying cause cannot be identified after initial workup
AKI persists >48 hours despite appropriate management
Pre-existing CKD Stage 4–5 (eGFR <30 mL/min/1.73 m²)
Glomerulonephritis suspected (urgent referral)

Flowchart: AKI Diagnostic and Management Algorithm

┌─────────────────────────────────────────────┐
│  Suspect AKI (↑Cr ≥0.3 mg/dL in 48h OR     │
│  ≥1.5× baseline in 7d OR UO <0.5 mL/kg/h)  │
└──────────────────┬──────────────────────────┘
                   ↓
┌─────────────────────────────────────────────┐
│  IMMEDIATE ACTIONS:                         │
│  1. Stop nephrotoxic drugs (ACEi, ARB,      │
│     NSAIDs, diuretics, aminoglycosides)     │
│  2. Order labs: Cr, BUN, CBC, lytes, UA     │
│  3. Calculate FENa                          │
│  4. Review medication list                  │
└──────────────────┬──────────────────────────┘
                   ↓
┌─────────────────────────────────────────────┐
│  ASSESS VOLUME STATUS                       │
│  (JVP, skin turgor, mucous membranes, CVP)  │
└──────────────────┬──────────────────────────┘
                   ↓
        ┌──────────┴──────────┐
        ↓                     ↓
┌───────────────┐    ┌────────────────┐
│  HYPOVOLEMIC  │    │  EUVOLEMIC/    │
│               │    │  HYPERVOLEMIC  │
└───────┬───────┘    └────────┬───────┘
        ↓                     ↓
┌───────────────────┐  ┌──────────────────┐
│  Give isotonic    │  │  Restrict fluids │
│  crystalloids     │  │  Consider        │
│  (NS or LR)       │  │  diuretics if    │
│                   │  │  volume overload │
└───────┬───────────┘  └──────┬───────────┘
        └────────┬─────────────┘
                 ↓
┌─────────────────────────────────────────────┐
│  URINALYSIS INTERPRETATION:                 │
│  • Muddy-brown casts → ATN                  │
│  • RBC casts → Glomerulonephritis           │
│  • WBC casts → Interstitial nephritis       │
│  • FENa <1% → Prerenal                      │
│  • FENa >2% → Intrinsic (ATN)               │
└──────────────────┬──────────────────────────┘
                   ↓
┌─────────────────────────────────────────────┐
│  IDENTIFY & TREAT UNDERLYING CAUSE:         │
│  • Infection → Blood/urine cultures, CXR,   │
│    empiric antibiotics immediately          │
│  • Obstruction → Renal ultrasound           │
│  • Cirrhosis → Paracentesis for SBP         │
└──────────────────┬──────────────────────────┘
                   ↓
┌─────────────────────────────────────────────┐
│  STAGE AKI (KDIGO):                         │
│  Stage 1: Cr 1.5–1.9× baseline OR ≥0.3 mg/dL│
│  Stage 2: Cr 2.0–2.9× baseline              │
│  Stage 3: Cr ≥3.0× baseline OR ≥4.0 mg/dL   │
│           OR dialysis initiated             │
└──────────────────┬──────────────────────────┘
                   ↓
        ┌──────────┴──────────┐
        ↓                     ↓
┌───────────────┐    ┌────────────────────┐
│  STAGE 1 AKI  │    │  STAGE 2–3 AKI     │
└───────┬───────┘    └────────┬───────────┘
        ↓                     ↓
┌───────────────────┐  ┌──────────────────────┐
│  • Monitor Cr     │  │  • Monitor Cr/lytes  │
│    every 24h      │  │    every 4–6h        │
│  • Continue       │  │  • Nephrology consult│
│    supportive care│  │  • Assess for RRT    │
└───────┬───────────┘  └──────┬───────────────┘
        └────────┬─────────────┘
                 ↓
┌─────────────────────────────────────────────┐
│  INDICATIONS FOR URGENT DIALYSIS:           │
│  • Refractory hyperkalemia (K⁺ >6.5)        │
│  • Severe acidosis (pH <7.1)                │
│  • Volume overload with pulmonary edema     │
│  • Uremic complications (encephalopathy,    │
│    pericarditis, pleuritis)                 │
│  • Severe oliguria unresponsive to fluids   │
└──────────────────┬──────────────────────────┘
                   ↓
┌─────────────────────────────────────────────┐
│  FOLLOW-UP:                                 │
│  • Repeat Cr/eGFR within 3 months for       │
│    Stage 2–3 AKI or incomplete recovery     │
│  • Monitor for CKD development              │
└─────────────────────────────────────────────┘

Key Pitfalls to Avoid

Do not dismiss a 0.3 mg/dL creatinine rise as "insignificant"—it carries 4-fold mortality risk even in advanced CKD. 2, 3
Do not continue diuretics after AKI diagnosis—they worsen outcomes and must be stopped immediately. 4
Do not delay antibiotics when infection is suspected—initiate empiric therapy before culture results. 2, 4
Do not rely on urine output alone in cirrhotic patients—use only creatinine criteria. 2, 3
Do not delay RRT when clear indications exist—this increases mortality. 2
Do not use eGFR equations during acute creatinine changes—they require steady-state and were validated only in stable CKD. 2
Do not back-calculate baseline creatinine in cirrhotic patients—use the most recent known value. 3

Provide concise, exam‑style notes on acute kidney injury (AKI) for a 10‑mark MBBS final medicine question, including classification, evaluation, management, and a flowchart/diagram, referencing the Archit Boloor and Manipal textbooks.

Help us tailor your experience