How should I evaluate and manage a patient with suspected acute kidney injury?

Evaluation and Management of Acute Kidney Injury

Immediately discontinue all nephrotoxic medications (ACE inhibitors, ARBs, NSAIDs, diuretics), assess volume status clinically, and begin isotonic crystalloid resuscitation if hypovolemic while simultaneously investigating the underlying cause through urinalysis with microscopy and renal ultrasound. 1, 2, 3, 4

Diagnostic Criteria and Staging

AKI is diagnosed when any one of the following occurs: 1, 2, 3

• Serum creatinine rise ≥0.3 mg/dL within any 48-hour window
• Serum creatinine increase to ≥1.5× baseline (≥50% rise) within 7 days
• Urine output <0.5 mL/kg/hour for ≥6 consecutive hours

Stage the severity immediately using KDIGO criteria: 1, 2

• Stage 1: Creatinine 1.5–1.9× baseline OR absolute rise ≥0.3 mg/dL OR urine output <0.5 mL/kg/h for 6–12 hours
• Stage 2: Creatinine 2.0–2.9× baseline OR urine output <0.5 mL/kg/h for ≥12 hours
• Stage 3: Creatinine ≥3.0× baseline OR creatinine ≥4.0 mg/dL with acute rise ≥0.3 mg/dL OR initiation of dialysis OR urine output <0.3 mL/kg/h for ≥24 hours OR anuria ≥12 hours

Even a modest 0.3 mg/dL creatinine rise carries approximately four-fold higher in-hospital mortality, so never dismiss small absolute increases as clinically insignificant. 2

Immediate Medication Management

Stop these medications immediately upon AKI recognition: 2, 3, 4

• All NSAIDs (including over-the-counter ibuprofen, naproxen)
• ACE inhibitors and ARBs
• Diuretics (hold or reduce in volume depletion)
• Aminoglycosides, vancomycin
• Any other identified nephrotoxic agents

The "triple whammy" combination (NSAID + diuretic + ACE-I/ARB) more than doubles AKI risk and must be avoided. 2, 4

Adjust all renally-excreted medication doses based on current estimated GFR. 3, 4

Volume Status Assessment and Fluid Management

Assess volume status through these specific clinical signs: 3, 4

• Orthostatic hypotension (systolic drop ≥20 mmHg or diastolic drop ≥10 mmHg upon standing)
• Dry mucous membranes
• Decreased skin turgor
• Tachycardia
• Jugular venous distention (suggests hypervolemia)
• Peripheral edema, pulmonary congestion (suggests volume overload)

For hypovolemic patients, administer isotonic crystalloids (balanced crystalloid solutions preferred over normal saline) for volume repletion; avoid colloids entirely and never use hydroxyethyl starch solutions. 2, 3, 5

For euvolemic or hypervolemic patients, implement strict fluid restriction and consider diuretics to prevent volume overload, which is independently associated with worse outcomes. 3, 5

Monitor strict input/output measurements and daily weights to track fluid balance. 3, 4

Etiologic Classification and Diagnostic Workup

Categorize AKI as prerenal, intrinsic renal, or postrenal: 2, 6, 7

Prerenal causes:

• Volume depletion (vomiting, diarrhea, poor oral intake, diuretic overuse)
• Low cardiac output (heart failure, cardiogenic shock)
• Medications altering glomerular hemodynamics (ACE-I, ARBs, NSAIDs)
• Sepsis with systemic vasodilation

Intrinsic renal causes:

• Acute tubular necrosis (ischemic or nephrotoxic)
• Glomerulonephritis
• Acute interstitial nephritis
• Atheroembolic disease

Postrenal causes:

• Urinary tract obstruction (prostatic hypertrophy, nephrolithiasis, malignancy)

Perform urinalysis with microscopy immediately to identify characteristic findings: 2, 3, 6

• Muddy-brown granular casts → acute tubular necrosis
• Red blood cell casts → glomerulonephritis
• White blood cell casts → acute interstitial nephritis or pyelonephritis
• Eosinophils → allergic interstitial nephritis

Calculate fractional excretion of sodium (FENa) to differentiate prerenal from intrinsic AKI: 6

• FENa <1% (or urine sodium <20 mEq/L) → prerenal azotemia
• FENa >2% (or urine sodium >40 mEq/L) → intrinsic renal injury (acute tubular necrosis)

Obtain renal ultrasound in most patients, particularly older men, to exclude urinary obstruction. 3, 6, 7

Retrieve all prior serum creatinine values from the previous 3–12 months to establish baseline and confirm acute change. 2

Hemodynamic Support

Use norepinephrine as the first-line vasopressor when hypotension persists after adequate fluid resuscitation; maintain mean arterial pressure >65 mmHg to ensure renal perfusion. 2, 3

Do not use dopamine to prevent or treat AKI—it provides no benefit. 2

Electrolyte and Metabolic Monitoring

Monitor serum creatinine, electrolytes (especially potassium), BUN every 4–6 hours initially in severe AKI (Stage 2–3). 2, 3

For Stage 1 AKI, monitor serum creatinine every 2–4 days during the initial treatment phase. 4

Administer intravenous sodium bicarbonate for severe metabolic acidosis; consider dialysis if acidosis is refractory to medical therapy. 2

Correct hyperkalemia urgently when present, as it is a life-threatening complication. 2

Indications for Renal Replacement Therapy

Initiate urgent dialysis for any of the following absolute indications: 2, 3, 6

• Refractory hyperkalemia unresponsive to medical management
• Severe volume overload unresponsive to diuretics
• Intractable metabolic acidosis
• Uremic complications (encephalopathy, pericarditis, pleuritis)
• Severe oliguria (<0.3 mL/kg/h for ≥24 hours) unresponsive to fluid resuscitation
• Certain toxin ingestions requiring removal

Reassess the need for continued RRT daily. 2, 3

Delaying RRT when clear indications exist increases mortality—do not hesitate. 2, 3

Nephrology Consultation Criteria

Obtain urgent nephrology consultation for: 2, 4, 7

• Stage 2 or Stage 3 AKI (creatinine ≥2.0× baseline)
• AKI persisting >48 hours despite appropriate initial management
• Unclear etiology after initial workup
• Suspected glomerulonephritis, vasculitis, or rapidly progressive AKI
• Pre-existing chronic kidney disease Stage 4 or higher (eGFR <30 mL/min/1.73 m²)
• Need for renal replacement therapy

Special Considerations for Cirrhotic Patients

In cirrhosis patients with AKI, perform diagnostic paracentesis immediately to rule out spontaneous bacterial peritonitis. 2, 3

Hold diuretics, beta-blockers, and all nephrotoxic drugs immediately. 3

Administer albumin 1 g/kg/day (maximum 100 g/day) for two consecutive days if serum creatinine has doubled from baseline. 2, 3

Start broad-spectrum antibiotics whenever infection is strongly suspected, without awaiting culture results. 2

Use the ICA-AKI criteria (creatinine rise ≥0.3 mg/dL within 48 hours or ≥50% from baseline) without a fixed 1.5 mg/dL threshold, because baseline creatinine underestimates true GFR in cirrhosis due to reduced muscle mass. 2

Follow-Up and Long-Term Management

Evaluate renal function at 3 months after AKI to assess for resolution, new-onset CKD, or worsening of pre-existing CKD. 1, 3, 4

Patients with Stage 3 AKI require earlier follow-up within 1–2 weeks due to higher risk of CKD progression. 2

Document the AKI episode clearly in the medical record and educate patients to avoid NSAIDs, maintain adequate hydration, and seek prompt medical attention for intercurrent illnesses. 2, 4

Even when creatinine appears to recover, AKI is associated with sustained increased risk of CKD, cardiovascular disease, and mortality—long-term monitoring is mandatory. 2, 5

Common Pitfalls to Avoid

Do not apply eGFR equations (MDRD or CKD-EPI) during acute changes in kidney function—they require steady-state creatinine and were validated only in stable CKD patients. 1, 2

Do not dismiss a modest absolute creatinine rise in CKD patients as "insignificant" merely because the percentage change is small—the KDIGO absolute 0.3 mg/dL criterion captures clinically relevant AKI across all baseline renal functions. 2

Do not use loop diuretics to prevent or treat AKI—they provide no benefit and may cause harm. 2

Do not continue nephrotoxic medications during AKI recovery. 2, 3

Do not administer albumin in patients with traumatic brain injury, as it increases the risk of adverse outcomes. 2

Do not perform overly aggressive fluid administration in non-hypovolemic patients, as volume overload worsens outcomes. 3, 5