What is the recommended immediate management for a patient with acute kidney injury?

Management of Acute Kidney Injury

Immediate Actions: Stop All Nephrotoxins First

The single most critical intervention is to immediately discontinue all nephrotoxic medications—including NSAIDs, ACE inhibitors, ARBs, diuretics, beta-blockers, aminoglycosides, and contrast agents—as each additional nephrotoxin increases AKI odds by 53%. 1, 2, 3

• The "triple whammy" combination (NSAID + diuretic + ACE-I/ARB) is particularly dangerous and must be stopped immediately. 1, 2
• Review all prescription and over-the-counter medications to identify hidden nephrotoxins. 1, 3
• Continue nephrotoxin avoidance throughout the recovery phase to prevent re-injury. 4, 3

Determine the Underlying Cause

Classify AKI as prerenal, intrinsic renal, or postrenal through focused evaluation to guide specific therapy. 1, 5, 6

Key Diagnostic Steps:

• Prerenal indicators: Urine sodium <20 mEq/L (or fractional excretion of sodium <1%), history of volume depletion, hypotension, or heart failure. 1
• Intrinsic renal clues: Muddy-brown casts suggest acute tubular necrosis; red-cell casts indicate glomerulonephritis; white-cell casts point to interstitial nephritis. 1
• Postrenal obstruction: Obtain renal ultrasonography in older men with prostatic hypertrophy or any patient with risk factors for obstruction. 6, 7
• Measure serum creatinine, electrolytes, BUN, complete blood count, and urinalysis with microscopy immediately. 1, 6

Fluid Management: Restore Perfusion Without Overload

For hypovolemic (prerenal) AKI, administer isotonic crystalloids—preferably balanced solutions like lactated Ringer's over 0.9% saline—to restore renal perfusion. 1, 2, 8

• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion. 1, 2, 3
• Avoid hydroxyethyl starches entirely, as they worsen AKI outcomes. 1, 2, 8
• Use dynamic indices (passive leg-raising test, pulse-pressure variation) rather than static central venous pressure to guide fluid therapy. 2, 3
• Stop fluid administration once euvolemia is achieved; volume overload >10-15% body weight is associated with adverse outcomes and creates a vicious cycle of worsening renal function. 2, 3

Hemodynamic Support

If hypotension persists after adequate fluid resuscitation, use norepinephrine as the first-line vasopressor. 1, 2

• Do not use dopamine to prevent or treat AKI—it is ineffective (Level 1A evidence). 1, 2
• Earlier use of vasopressors may be appropriate instead of excessive fluid administration when hypotension is due to vasomotor shock. 2, 3

Special Management for Cirrhotic Patients

In cirrhosis with AKI, immediately discontinue both diuretics AND beta-blockers (not just diuretics). 1, 2, 3

Stage-Based Algorithm for Cirrhosis:

• When serum creatinine has doubled from baseline: Administer IV albumin 1 g/kg/day (maximum 100 g) for two consecutive days. 1, 2, 3
• If creatinine remains elevated after 48 hours of albumin therapy and hepatorenal syndrome criteria are met: Add vasoactive agents (terlipressin preferred; or norepinephrine; or midodrine plus octreotide) along with continued albumin. 1, 2, 3
• Perform diagnostic paracentesis to rule out spontaneous bacterial peritonitis in all cirrhotic patients with AKI. 1

Monitor for Life-Threatening Complications

Check serum creatinine and electrolytes every 4-6 hours initially in severe AKI (KDIGO Stage 2-3). 1

• Monitor for hyperkalemia, metabolic acidosis, volume overload, and uremic complications continuously. 1, 6, 7
• Assess urine output, vital signs, and fluid balance closely in the first 48-72 hours. 2, 3

Indications for Urgent Renal Replacement Therapy

Initiate RRT immediately when any of the following absolute indications are present, as delaying RRT increases mortality: 1, 3

• Refractory hyperkalemia unresponsive to medical therapy

• Severe volume overload causing pulmonary edema or respiratory compromise

• Intractable metabolic acidosis (pH <7.1)

• Uremic complications (encephalopathy, pericarditis, bleeding)

• Do not wait for arbitrary creatinine or BUN thresholds; base RRT decisions on overall clinical status. 2, 3

• Reassess the need for continued RRT daily rather than following a fixed schedule. 1, 3

Nephrology Consultation Triggers

Obtain nephrology consultation when: 1, 7

• The underlying cause of AKI remains unclear after initial evaluation
• AKI persists beyond 48 hours despite appropriate management
• Stage 3 AKI or pre-existing CKD stage 4-5 is present
• Glomerulonephritis, vasculitis, or rapidly progressive AKI is suspected

Expected Timeline and Reassessment

Prerenal AKI should show creatinine improvement within 48 hours of volume expansion and nephrotoxin removal; lack of response indicates intrinsic renal injury (ATN) or other causes. 1, 3

• If AKI persists beyond 48 hours, reassess the underlying etiology, hemodynamic status, volume status, and adequacy of renal perfusion. 1, 3
• Continue close monitoring for complications including fluid overload, acidosis, and hyperkalemia during this reassessment period. 1, 3

Common Pitfalls to Avoid

• Never use furosemide or other diuretics in hemodynamically unstable patients with prerenal AKI—they worsen volume depletion and reduce renal perfusion. 2
• Do not apply eGFR equations (MDRD, CKD-EPI) during acute changes in kidney function; they require steady-state creatinine and are inaccurate in AKI. 1, 2
• Avoid indiscriminate fluid administration based solely on the label "prerenal" without hemodynamic assessment. 2
• Do not restart ACE inhibitors, ARBs, or NSAIDs until renal function has stabilized to reduce the risk of recurrent AKI. 3

Post-AKI Follow-Up

Schedule close outpatient follow-up within 1-2 weeks for patients with Stage 3 AKI, as they face markedly increased risk of CKD progression, cardiovascular disease, and mortality. 1, 8, 7

• Educate patients to avoid NSAIDs and to consult their provider before taking any new medications. 4, 3
• Document the AKI episode clearly in the medical record to guide future care. 1