What is the initial evaluation and management approach for a young patient presenting with acute kidney injury?

Approach to Acute Kidney Injury in Young Patients

Immediately discontinue all nephrotoxic medications—including NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, and contrast agents—while simultaneously initiating diagnostic workup, as medication withdrawal is the single highest-priority intervention that takes precedence over all other management steps. 1, 2

Initial Diagnostic Workup

Obtain the following tests immediately upon suspicion of AKI 2, 3, 4:

• Serum creatinine and BUN to confirm AKI diagnosis using KDIGO criteria: increase ≥0.3 mg/dL within 48 hours OR ≥50% rise from baseline within 7 days 5
• Urinalysis with microscopy to identify hematuria, proteinuria, casts (muddy brown casts suggest acute tubular necrosis; RBC casts indicate glomerulonephritis), and epithelial cells 2, 3
• Fractional excretion of sodium (FENa): <1% suggests prerenal AKI; >2% indicates intrinsic renal disease 2, 4
• Complete blood count to assess for infection, hemolysis, or thrombocytopenia 2
• Renal ultrasonography if obstruction is suspected (though this accounts for <3% of AKI cases in young patients) 2

Medication Review and Immediate Actions

Stop these medications immediately 1, 2:

• NSAIDs (the "triple whammy" of NSAIDs + diuretics + ACE inhibitors/ARBs is particularly dangerous) 1
• All diuretics (even in non-oliguric patients—diuretics worsen outcomes and must be discontinued) 2
• ACE inhibitors and ARBs
• Aminoglycosides
• Beta-blockers and vasodilators
• Any other identified nephrotoxins

Each additional nephrotoxic agent increases AKI odds by 53%, so avoid poly-nephrotoxic regimens. 1

Volume Status Assessment and Fluid Management

Assess volume status through clinical examination (jugular venous pressure, skin turgor, mucous membranes, orthostatic vital signs) and consider dynamic indices like passive leg-raising test rather than static measurements 1:

For Hypovolemic/Prerenal AKI:

• Administer isotonic crystalloids as first-line therapy, preferentially using balanced solutions (lactated Ringer's) over 0.9% saline to prevent metabolic acidosis and hyperchloremia 1, 2
• Avoid hydroxyethyl starches—they worsen AKI outcomes 1
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 1
• Expect creatinine improvement within 48 hours if truly prerenal; lack of response suggests intrinsic renal disease (acute tubular necrosis) 1

For Euvolemic/Hypervolemic Patients:

• Avoid excessive fluid administration—volume overload >10-15% body weight is associated with adverse outcomes 1
• Consider earlier use of vasopressors (norepinephrine as first-line) rather than excessive fluids for hypotension 1

Infection Management

Initiate empirical antibiotics immediately if infection is suspected or strongly suspected—do not wait for culture results, as sepsis is the most reversible cause of AKI with multiorgan dysfunction. 2 Sepsis is a frequent trigger for both prerenal AKI and acute tubular necrosis 1.

Monitoring Protocol

During acute management 1, 2:

• Measure serum creatinine and electrolytes every 12-24 hours
• Monitor urine output continuously (oliguria <0.5 mL/kg/h for >6 hours is associated with higher mortality) 5
• Track vital signs and fluid balance closely in the first 48-72 hours
• Use echocardiography or CVP when indicated to assess volume status

Staging and Risk Stratification

Use KDIGO staging criteria 5:

Stage	Creatinine Criteria	Urine Output
Stage 1	Rise ≥0.3 mg/dL within 48h OR 1.5-1.9× baseline within 7 days	<0.5 mL/kg/h for >6h
Stage 2	2.0-2.9× baseline	<0.5 mL/kg/h for >12h
Stage 3	≥3.0× baseline OR creatinine ≥4.0 mg/dL OR need for RRT	<0.3 mL/kg/h for 24h or anuria for 12h

However, management should be based on overall clinical status—including specific AKI cause, trends in kidney function, comorbidities, volume status, and electrolyte disturbances—rather than stage alone. 5

Renal Replacement Therapy Indications

Consider RRT for 1, 2:

• Refractory hyperkalemia
• Severe, intractable metabolic acidosis
• Volume overload causing pulmonary edema unresponsive to diuretics
• Uremic complications (encephalopathy, pericarditis, pleuritis)

Individualize timing based on overall clinical condition rather than specific creatinine or BUN thresholds. 1

What Does NOT Work (Avoid These)

Based on Level 1A/B evidence 1:

• Dopamine for prevention or treatment of AKI
• Furosemide or other diuretics to treat AKI (except for managing volume overload after adequate perfusion is restored)
• N-acetylcysteine (NAC) for AKI treatment
• Recombinant human insulin-like growth factor 1

Common Pitfalls to Avoid

• Never use eGFR equations (MDRD, CKD-EPI) in AKI—they require steady-state creatinine and are inaccurate in acute settings 1
• Do not delay fluid resuscitation in truly hypovolemic patients 1
• Never continue diuretics after AKI diagnosis—they worsen outcomes even in non-oliguric patients 2
• Avoid indiscriminate fluid administration based solely on the label "prerenal" without hemodynamic assessment 1

Follow-Up After AKI

Target follow-up intensity to high-risk populations, including those with severe AKI (Stage 2-3), baseline CKD, or incomplete recovery at discharge. 5 Young patients with mild, readily reversible AKI (e.g., simple volume depletion with complete recovery) are at relatively low risk of progressive CKD and may not require intensive follow-up 5.

For higher-risk patients 5:

• Evaluate kidney function within 3 months after AKI
• Monitor for development or progression of CKD, as even patients with complete recovery remain at increased risk
• Intensity of surveillance should be proportionate to AKI severity and presence of risk factors (diabetes, proteinuria, recurrent AKI)