What is the initial assessment and management of suspected acute kidney injury?

Initial Assessment and Management of Acute Kidney Injury

Immediately discontinue all nephrotoxic medications including ACE inhibitors, ARBs, NSAIDs, and diuretics upon suspecting AKI, as this is the single most critical intervention to prevent further kidney damage. 1, 2

Diagnostic Criteria and Classification

AKI is defined by any of the following criteria 1, 2, 3:

• Serum creatinine increase ≥0.3 mg/dL within 48 hours
• Serum creatinine increase ≥50% from baseline within 7 days
• Urine output <0.5 mL/kg/hour for 6 hours

Stage the severity using KDIGO criteria (stages 1-3) based on degree of creatinine elevation and urine output reduction, as this guides management intensity and need for nephrology consultation. 2, 3

History and Physical Examination

Critical History Elements

Obtain the following specific information 1, 4, 5:

• Medication exposure: nephrotoxic drugs (NSAIDs, aminoglycosides, contrast agents), the "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) 1, 6
• Volume status indicators: vomiting, diarrhea, decreased oral intake, bleeding, third-spacing 4, 7
• Systemic illness: sepsis, heart failure, liver disease, recent surgery 4, 5
• Urinary symptoms: oliguria, anuria, dysuria, obstruction symptoms (especially in older men with prostatic hypertrophy) 4, 5
• Pre-existing kidney disease: baseline creatinine, chronic kidney disease, previous AKI episodes 8, 3

Physical Examination Priorities

Assess the following specific findings 1, 4, 7:

• Volume status: jugular venous pressure, mucous membranes, skin turgor, peripheral edema, pulmonary crackles, weight changes 1, 7
• Hemodynamic parameters: blood pressure (including orthostatic changes), heart rate, mean arterial pressure (target >65 mmHg) 2, 7
• Signs of uremia: altered mental status, pericardial rub, asterixis 1, 6
• Skin findings: rashes suggesting systemic vasculitis or interstitial nephritis 4
• Bladder distension: palpable suprapubic mass suggesting obstruction 4

Initial Laboratory Workup

Obtain the following tests immediately 1, 2, 4:

• Serum studies: creatinine, BUN, electrolytes (particularly potassium and sodium), complete blood count 1, 4
• Urinalysis with microscopy: detect hematuria, proteinuria, casts (granular casts suggest acute tubular necrosis, RBC casts suggest glomerulonephritis, WBC casts suggest interstitial nephritis) 1, 4
• Fractional excretion of sodium (FENa): <1% suggests prerenal etiology, >2% suggests intrinsic renal disease 4
• Monitor frequency: repeat electrolytes, BUN, and creatinine every 4-6 hours initially for severe AKI 1, 6

Imaging

Perform renal ultrasound in most patients, particularly older men and those with risk factors for obstruction, to rule out postrenal causes. 1, 4, 5

Immediate Management Algorithm

Step 1: Medication Review and Adjustment

• Discontinue immediately: ACE inhibitors, ARBs, NSAIDs, diuretics, aminoglycosides, other nephrotoxins 1, 2, 6
• Adjust all medication dosages based on reduced GFR and reassess frequently as kidney function changes 1, 6
• Avoid the "triple whammy" combination which more than doubles AKI risk 6

Step 2: Volume Status Assessment and Fluid Management

For hypovolemic patients 1, 2:

• Provide fluid resuscitation with isotonic crystalloids (avoid colloids) 1
• Monitor response with urine output, vital signs, and clinical examination 7

For euvolemic or hypervolemic patients 1:

• Implement fluid restriction to prevent volume overload 1
• Monitor for peripheral edema, pulmonary congestion, weight gain 1, 6
• Avoid hypotonic fluids which worsen hyponatremia 1, 6

Step 3: Hemodynamic Support

• Maintain mean arterial pressure >65 mmHg using vasopressors if needed to ensure renal perfusion 2, 7
• Consider central venous pressure monitoring for volume status assessment in complex cases 1, 2, 7

Step 4: Identify and Treat Underlying Cause

Classify AKI as prerenal, intrinsic renal, or postrenal 2, 4, 5:

• Prerenal: volume depletion, sepsis, heart failure, liver disease—treat with volume optimization and hemodynamic support 4, 7
• Intrinsic renal: acute tubular necrosis, glomerulonephritis, interstitial nephritis—requires specific targeted therapy 4, 5
• Postrenal: obstruction from prostatic hypertrophy, stones, malignancy—requires urgent urologic intervention 4, 5

For cirrhosis patients with AKI 1, 2, 6:

• Perform diagnostic paracentesis to evaluate for spontaneous bacterial peritonitis 1, 2
• Hold diuretics, beta-blockers, and all nephrotoxic drugs 1, 6
• Administer albumin 1 g/kg/day (maximum 100 g/day) for 2 days if creatinine doubles from baseline 1, 2

Step 5: Monitor for Complications

Track the following with strict input/output measurements 1, 6:

• Electrolyte abnormalities (particularly hyperkalemia requiring urgent intervention) 2
• Metabolic acidosis 1, 2
• Uremic complications (encephalopathy, pericarditis, pleuritis) 1, 4
• Fluid overload 1, 6

Indications for Urgent Renal Replacement Therapy

Initiate RRT immediately for any of the following 1, 2, 6:

• Severe oliguria unresponsive to fluid resuscitation 1, 2, 6
• Refractory hyperkalemia 1, 4
• Severe metabolic acidosis 1, 2
• Volume overload refractory to diuretics 1, 4
• Uremic encephalopathy, pericarditis, or pleuritis 1, 4
• Certain toxin ingestions requiring removal 4

Reassess the need for continued RRT daily. 1, 2, 6

Nephrology Consultation Criteria

Refer urgently for 3, 5:

• Stage 2 or 3 AKI 3
• Stage 1 AKI with decompensated comorbid conditions 3
• Unclear etiology despite initial workup 3, 5
• Inadequate response to supportive treatment 5
• Pre-existing stage 4 or higher chronic kidney disease 5
• Suspected glomerulonephritis requiring biopsy 3, 5

Critical Pitfalls to Avoid

• Delaying RRT when clear indications exist increases mortality 2, 6
• Failing to identify and address the underlying cause leads to continued kidney damage 2, 6
• Inappropriate continuation of nephrotoxic medications during AKI recovery 1, 6
• Overly aggressive fluid administration in non-hypovolemic patients worsens outcomes 6
• Overly rapid correction of hyponatremia can cause osmotic demyelination syndrome 1, 6
• Neglecting to adjust medication dosages as kidney function changes 1, 6

Follow-up

• Evaluate renal function within 3-7 days after last RRT session 1
• Perform follow-up at 3 months after AKI to assess for progression to chronic kidney disease 1
• Schedule close post-discharge evaluation for moderate to severe AKI 2
• Even one episode of AKI increases risk of cardiovascular disease, chronic kidney disease, and death, making long-term follow-up essential 8