What are the diagnostic criteria and management steps for acute kidney injury?

Acute Kidney Injury: Diagnostic Criteria and Management

Diagnostic Criteria

Diagnose AKI when any one of the following KDIGO criteria is met: serum creatinine rise ≥0.3 mg/dL within 48 hours, OR creatinine increase ≥50% from baseline within 7 days, OR urine output <0.5 mL/kg/hour for ≥6 consecutive hours. 1, 2

Key Diagnostic Points

• Do not wait for creatinine to reach 1.5 mg/dL before diagnosing AKI—this outdated threshold indicates GFR has already fallen to approximately 30 mL/min and represents severe kidney injury. 1

• Even a modest 0.3 mg/dL creatinine rise is clinically significant, independently associated with approximately four-fold increased in-hospital mortality. 2

• Establish baseline creatinine using the most recent value from the prior 3 months; if unavailable, use admission creatinine as baseline. 2, 3

• In cirrhotic patients, rely exclusively on creatinine changes—ignore urine output criteria because these patients are frequently oliguric with avid sodium retention despite relatively normal GFR, and diuretics further confound interpretation. 1

AKI Staging (KDIGO)

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 1, 2

Stage 2: Creatinine 2.0–2.9× baseline, OR urine output <0.5 mL/kg/h for ≥12 hours 1, 2

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/h for ≥24 hours, OR anuria ≥12 hours, OR initiation of renal replacement therapy 1, 2

• Progressive staging correlates with incrementally higher mortality, with Stage 3 requiring dialysis carrying approximately four-fold higher mortality than lower stages. 2

Initial Diagnostic Workup

Immediate Laboratory Tests

• Order serum creatinine, BUN, complete blood count, comprehensive metabolic panel (sodium, potassium, calcium, magnesium, chloride, bicarbonate), and urinalysis with microscopy immediately. 2, 3

• Measure fractional excretion of sodium (FENa) to differentiate prerenal from intrinsic AKI: FENa <1% suggests prerenal azotemia; FENa >2% indicates acute tubular necrosis. 3, 4

• Monitor creatinine and electrolytes every 4–6 hours initially in Stage 2–3 AKI to track progression and detect life-threatening complications like hyperkalemia. 2

Urinalysis Interpretation

• Muddy-brown granular casts indicate acute tubular necrosis. 2

• Red blood cell casts suggest glomerulonephritis. 2

• White blood cell casts indicate acute interstitial nephritis. 2

• Proteinuria >500 mg/day or microhematuria >50 RBCs per high-power field suggests structural kidney injury and argues against hepatorenal syndrome in cirrhotic patients. 1

Imaging

• Obtain renal ultrasonography when postrenal obstruction is suspected, though obstruction accounts for <3% of AKI cases. 3, 4

• Perform chest radiography if infection or volume overload is suspected. 3

Immediate Management Steps

Medication Review and Discontinuation

Immediately discontinue all nephrotoxic medications including NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, and contrast agents upon AKI diagnosis. 2, 3

• Diuretics must be stopped even in non-oliguric patients—continuing diuretics after AKI diagnosis worsens outcomes. 3

• Review all medications for nephrotoxic potential including chemotherapeutics and herbal supplements. 2, 4

Fluid Management

• Assess volume status through clinical examination (jugular venous pressure, orthostatic vital signs, mucous membranes, skin turgor, edema). 2, 4

• For hypovolemic patients, provide fluid resuscitation with isotonic crystalloids (normal saline or lactated Ringer's) rather than colloids. 2, 3

• In cirrhotic patients with creatinine doubling, administer albumin 1 g/kg/day (maximum 100 g) for two consecutive days to expand plasma volume and improve renal perfusion. 1, 2

Infection Evaluation and Treatment

• Perform rigorous infection search in all AKI patients: obtain blood cultures, urine cultures, chest radiograph; in cirrhotic patients, perform diagnostic paracentesis to rule out spontaneous bacterial peritonitis. 2, 3

• Initiate empiric broad-spectrum antibiotics immediately when infection is strongly suspected—do not wait for culture results, as sepsis is the most reversible cause of AKI with multiorgan dysfunction. 2, 3

• In cirrhotic patients with spontaneous bacterial peritonitis, administer IV albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 along with antibiotics to reduce HRS-AKI incidence and improve survival. 1

Cirrhosis-Specific Management

Hepatorenal Syndrome-AKI Diagnosis

Diagnose HRS-AKI in cirrhotic patients with ascites when all of the following are present: 1

• AKI according to ICA-AKI criteria (creatinine rise ≥0.3 mg/dL within 48 hours or ≥50% within 7 days)
• No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin 1 g/kg/day
• Absence of shock
• No current or recent nephrotoxic drugs (NSAIDs, aminoglycosides, contrast media)
• No structural kidney injury (proteinuria <500 mg/day, microhematuria <50 RBCs/HPF, normal renal ultrasound)

HRS-AKI Treatment

Treat HRS-AKI with albumin 1 g/kg IV on day 1 followed by 20–40 g daily, plus vasoactive agents: terlipressin (preferred), or if unavailable, norepinephrine, or octreotide plus midodrine. 2

Prevention in Cirrhosis

• Administer IV albumin with antibiotics in spontaneous bacterial peritonitis to prevent HRS-AKI and improve survival. 1

• Avoid large-volume paracentesis without albumin administration—give albumin 6–8 g per liter of ascites removed. 1

• Hold diuretics and non-selective beta-blockers immediately when AKI develops. 2

Indications for Nephrology Consultation

• Emergent consultation for Stage 2 or Stage 3 AKI 2, 3, 5

• Urgent consultation for Stage 1 AKI with concomitant decompensated condition (heart failure, liver failure, sepsis) 5

• Urgent consultation when AKI etiology is unclear or glomerulonephritis is suspected 5

Renal Replacement Therapy Indications

Initiate urgent RRT for: 2

• Severe refractory hyperkalemia

• Volume overload unresponsive to diuretics

• Severe metabolic acidosis (pH <7.1)

• Uremic complications (encephalopathy, pericarditis, pleuritis)

• Certain toxin ingestions

• Reassess need for continued RRT daily—do not delay discontinuation when kidney function recovers. 2

Common Pitfalls to Avoid

• Never continue diuretics after AKI diagnosis—this is a critical error that worsens outcomes. 3

• Do not delay antibiotic therapy when infection is suspected—empiric treatment saves lives in sepsis-associated AKI. 2, 3

• Do not use urine output criteria in cirrhotic patients with ascites—focus exclusively on creatinine changes. 1

• Do not delay RRT when clear indications exist—delayed initiation increases mortality. 2

• Do not administer iodinated contrast in AKI unless absolutely necessary—contrast-induced nephropathy risk is substantially elevated. 3

• Do not assume small creatinine rises are insignificant—even 0.3 mg/dL increases quadruple mortality risk. 2

Follow-Up After AKI

• Schedule close post-discharge evaluation within 3 months for patients with Stage 2–3 AKI, pre-existing CKD, or incomplete renal recovery to detect progression to chronic kidney disease. 2, 3

• Monitor for long-term complications including cardiovascular events, CKD progression, and increased mortality risk. 6, 7