How should I diagnose and manage acute kidney injury?

Diagnosis and Management of Acute Kidney Injury

Diagnose AKI when serum creatinine rises ≥0.3 mg/dL within 48 hours or increases ≥50% from baseline within 7 days, then immediately discontinue all nephrotoxic medications and determine whether the cause is prerenal, intrinsic renal, or postrenal. 1, 2

Diagnostic Criteria and Staging

• AKI is confirmed by any one of three criteria: serum creatinine increase ≥0.3 mg/dL within 48 hours, creatinine rise ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/hour for ≥6 consecutive hours. 1, 2

• Stage severity using KDIGO criteria to guide monitoring intensity and treatment escalation: 1, 2

  • Stage 1: Creatinine 1.5–1.9× baseline or ≥0.3 mg/dL rise, or urine output <0.5 mL/kg/hour for >6 hours
  • Stage 2: Creatinine 2.0–2.9× baseline, or urine output <0.5 mL/kg/hour for >12 hours
  • Stage 3: Creatinine ≥3.0× baseline or ≥4.0 mg/dL with acute rise ≥0.3 mg/dL, or urine output <0.3 mL/kg/hour for ≥24 hours, or anuria ≥12 hours, or need for renal replacement therapy

• Even a modest creatinine rise of ≥0.3 mg/dL independently increases hospital mortality approximately four-fold, so early detection matters. 1

Initial Diagnostic Workup

• Obtain serum creatinine, BUN, complete blood count, urinalysis with microscopy, and fractional excretion of sodium (FENa) immediately upon suspecting AKI. 2, 3

• Perform urinalysis with microscopy to identify the pattern of injury: 1, 2

  • Muddy-brown granular casts indicate acute tubular necrosis
  • Red blood cell casts point to glomerulonephritis
  • White blood cell casts suggest acute interstitial nephritis

• Calculate FENa to distinguish prerenal from intrinsic causes: 1

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

• Obtain renal ultrasonography when postrenal obstruction is suspected (particularly in older men with prostatic hypertrophy), though obstruction accounts for <3% of AKI cases. 2, 3

• Obtain chest radiography if infection is suspected or to assess volume status and pulmonary edema. 2

Immediate Management Actions

Medication Review and Discontinuation

• Stop all nephrotoxic medications immediately upon AKI diagnosis: NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, and contrast agents. 1, 2, 4

• Review all medications including over-the-counter drugs to identify nephrotoxic exposures, as each additional nephrotoxin increases AKI odds by 53%. 4

• The "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs substantially increases AKI risk and must be avoided. 4

Infection Evaluation and Treatment

• Perform rigorous search for infection in all AKI patients: obtain blood cultures, urine cultures, and chest radiograph. 1, 4

• In cirrhotic patients, perform diagnostic paracentesis immediately to rule out spontaneous bacterial peritonitis. 1, 4

• Initiate empiric broad-spectrum antibiotics promptly when infection is strongly suspected, without awaiting culture results, as sepsis is the most reversible cause of AKI with multiorgan dysfunction. 1, 2

Volume Assessment and Fluid Management

• Assess volume status through clinical examination and potentially central venous pressure monitoring. 1

• For hypovolemic patients, provide fluid resuscitation with isotonic crystalloids rather than colloids. 1, 4

• Avoid starch-containing fluids as they are associated with harm. 4

• Maintain mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion, using vasopressors in conjunction with fluids for vasomotor shock. 1, 4

• Prefer norepinephrine over dopamine as first-line vasopressor; do not use dopamine to prevent or treat AKI. 4

Special Considerations for Cirrhotic Patients

• In cirrhotic patients with AKI, immediately discontinue diuretics and beta-blockers. 5, 4

• Administer albumin 1 g/kg/day (maximum 100 g/day) for two consecutive days when serum creatinine has doubled from baseline. 5, 1, 4

• Baseline serum creatinine underestimates true GFR in cirrhosis due to reduced muscle mass, so use the ICA-AKI criteria (creatinine rise ≥0.3 mg/dL within 48 hours or ≥50% from baseline) without requiring a fixed 1.5 mg/dL threshold. 5, 1

• Urine output alone is unreliable for AKI assessment in cirrhotic patients due to frequent diuretic use and altered sodium handling. 1

• If creatinine remains elevated after albumin therapy, add vasoactive agents: terlipressin (preferred), or norepinephrine, or the combination of midodrine plus octreotide. 1, 4

Management Algorithm by Stage

Stage 1 AKI

• Implement close monitoring with removal of risk factors: withdraw nephrotoxic drugs, vasodilators, and NSAIDs; reduce or withdraw diuretics; treat infections when diagnosed. 5

• Provide plasma volume expansion with crystalloids or albumin if clinically hypovolemic. 5

• If the patient responds (creatinine improves), continue monitoring and maintain supportive care. 5

• If AKI progresses to Stage 2 or 3, escalate management as below. 5

Stage 2–3 AKI

• Withdraw diuretics if not already done and expand plasma volume with intravenous albumin 1 g/kg/day for two consecutive days to treat prerenal AKI and allow differential diagnosis. 5

• Monitor for fluid overload using urine output, vital signs, and when indicated, echocardiography or CVP. 4

• If criteria for hepatorenal syndrome are met (in cirrhotic patients), add vasoactive agents as described above. 5, 1

Indications for Renal Replacement Therapy

• Initiate RRT urgently for any of the following absolute indications: 1, 4

  • Refractory hyperkalemia unresponsive to medical therapy
  • Severe volume overload causing pulmonary edema or respiratory compromise
  • Intractable metabolic acidosis (e.g., pH <7.1)
  • Uremic complications (encephalopathy, pericarditis, bleeding)
  • Need for toxin removal

• Do not delay RRT when clear indications exist, as postponement increases mortality. 1

• Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds alone. 4

• Reassess the need for continued RRT daily rather than adhering to a fixed schedule. 1, 4

Monitoring and Complications Management

• Monitor serum electrolytes, BUN, and creatinine every 4–6 hours initially. 1

• Correct electrolyte abnormalities, particularly hyperkalemia, which may require urgent intervention. 1

• Persistent oliguria (urine output <0.5 mL/kg/hour for >6 hours) is associated with higher mortality and should trigger intensified monitoring and therapeutic escalation. 2

• Manage metabolic acidosis with sodium bicarbonate in selected cases. 4

Follow-Up After AKI

• Schedule close post-discharge clinical evaluation for patients with moderate to severe AKI (Stage 2–3), pre-existing chronic kidney disease, or incomplete renal recovery at discharge. 1, 2

• Re-evaluate kidney function within 3 months after the AKI episode to detect early chronic kidney disease development or progression. 2

• Continue nephrotoxin avoidance during the recovery phase to prevent re-injury. 4

• Educate patients to avoid taking NSAIDs or new medications without consulting their healthcare provider. 4

Common Pitfalls to Avoid

• Never continue diuretics after AKI diagnosis, even in non-oliguric patients, as they worsen outcomes and must be stopped immediately. 2, 4

• Do not delay infection treatment; initiate empirical antibiotics before culture results if infection is suspected. 1, 2

• Avoid iodinated contrast in AKI unless there is an overriding clinical question that cannot be answered with alternative imaging, as contrast-induced nephropathy risk is substantially elevated. 2

• Do not rely on creatinine or BUN thresholds alone to decide on RRT; base decisions on the overall clinical picture including volume status, electrolytes, and uremic symptoms. 4

• In cirrhotic patients, failure to promptly recognize and treat underlying infection markedly increases the risk of AKI progression. 1