What is the urgent management approach for acute kidney injury superimposed on chronic kidney disease?

Urgent Management of Acute Kidney Injury Superimposed on Chronic Kidney Disease

Immediately discontinue all nephrotoxic medications (NSAIDs, aminoglycosides, ACE inhibitors, ARBs), stop diuretics and beta-blockers, assess volume status, and administer albumin 1 g/kg/day for 2 consecutive days (maximum 100g/day) if AKI is beyond stage 1A without an obvious cause. 1, 2

Immediate Universal Actions (First 30 Minutes)

Stop these medications immediately:

• All diuretics 1, 2
• NSAIDs 1, 2
• ACE inhibitors and ARBs 1, 2
• Aminoglycosides 1, 2
• Beta-blockers 1
• Any iodinated contrast media 1, 2

This is critical because each additional nephrotoxin increases AKI odds by 53%, and the "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs dramatically amplifies risk. 2

Review all medications including over-the-counter drugs that may contribute to kidney injury. 1, 2

Volume Assessment and Initial Resuscitation (First 2 Hours)

Assess volume status clinically by looking for:

• Orthostatic hypotension 2
• Skin turgor 2
• Edema 2
• Signs of fluid overload (pulmonary edema, respiratory compromise) 3

If hypovolemia is present:

• Administer isotonic crystalloids (normal saline or balanced crystalloids) for initial volume expansion 1, 2
• Avoid hydroxyethyl starches as they are associated with harm 1, 2
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 1, 2

If volume overload is present:

• Do NOT give additional fluids 3
• Recognize that inappropriate attempts to "reverse" established AKI with fluids result in a vicious cycle of fluid overload worsening kidney function 3

Albumin Administration Protocol (Within 24 Hours)

For AKI stage >1A with no obvious cause:

• Administer 20% albumin solution at 1 g/kg bodyweight for 2 consecutive days (maximum 100g/day) 1, 2
• This serves both diagnostic and therapeutic purposes 1

Response assessment at 48 hours:

• Pre-renal AKI (superimposed on CKD) responds with improvement in serum creatinine within 48 hours 1
• Intrinsic/ATN does not respond, with creatinine remaining elevated or worsening 1

Hemodynamic Optimization

Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion. 1, 2

If fluid resuscitation fails to restore adequate blood pressure:

• Use norepinephrine as first-line vasopressor (preferred over dopamine) 1, 2
• Do NOT use dopamine as it does not prevent or treat AKI 1, 2

Monitoring During First 48-72 Hours

Monitor closely:

• Serum creatinine and urine output to assess response 1, 2
• Hemodynamic status 3, 2
• Volume status 3, 2
• Complications: fluid overload, acidosis, hyperkalemia 3, 2

Persistent AKI is defined as continuation beyond 48 hours from onset despite initial management. 3, 1 Complete reversal within 48 hours characterizes rapid reversal and typically indicates pre-renal etiology. 3, 1

Reassessment for Non-Responders (After 48 Hours)

If no response after 48 hours of diuretic withdrawal and albumin:

• Reassess for intrinsic renal causes (ATN, acute interstitial nephritis, glomerulonephritis) 1, 2
• Re-evaluate hemodynamic status and adequacy of kidney perfusion 3, 1
• Identify complications (fluid overload, acidosis, hyperkalemia) 3, 1
• Obtain urine sediment analysis, proteinuria measurement, and biomarker assessment 4
• Perform renal ultrasound to identify obstruction or structural abnormalities 5, 6

Consider nephrology consultation if:

• Etiology unclear 3, 1, 2
• Stage 3 or higher AKI 6
• Preexisting stage 4 or higher CKD 6
• Subspecialist care needed 3, 1, 2

Indications for Urgent Renal Replacement Therapy

Initiate RRT immediately for:

• Refractory hyperkalemia not responding to medical therapy 2, 5, 6
• Severe volume overload causing pulmonary edema or respiratory compromise 2, 5, 6
• Intractable metabolic acidosis (pH <7.1) 2, 5, 6
• Uremic complications (encephalopathy, pericarditis, bleeding) 2, 5, 6

Do not delay RRT when absolute indications are present, as postponement is associated with increased mortality. 2

Critical Pitfalls to Avoid

Do NOT:

• Continue nephrotoxic medications during evaluation 1, 2
• Over-resuscitate with fluids, as volume overload worsens outcomes 1
• Delay albumin administration in stage >1A AKI without obvious cause 1
• Use hydroxyethyl starches for volume expansion 1, 2
• Attempt to "reverse" established AKI with aggressive fluids, leading to fluid overload 3
• Restart ACE inhibitors, ARBs, or NSAIDs until renal function has stabilized 2

Special Considerations for AKI on CKD

Patients with pre-existing CKD who develop AKI are at extremely high risk for:

• Kidney disease progression 3
• Development of acute kidney disease (AKD) - defined as persistence of AKI criteria for 7-90 days 3, 7, 8
• Progression to advanced CKD 9, 8
• Death 9, 8

The continuum: AKI superimposed on CKD frequently becomes AKD on a background of CKD, representing the highest-risk population for adverse outcomes. 3 Each recurrent AKI episode accelerates CKD progression. 4

Drug Stewardship During AKI on CKD

Include a clinical pharmacist for drug stewardship. 3

Assess the dynamic impact of:

• AKI/AKD on drug pharmacokinetics/pharmacodynamics 3
• Renal recovery on drug pharmacokinetics/pharmacodynamics 3
• Concurrent illness (sepsis, heart failure) on drug handling 3
• RRT on drug pharmacokinetics/pharmacodynamics 3

Perform medication reconciliation at all transitions of care. 3

Recovery Phase Management

Continue nephrotoxin avoidance during recovery to prevent re-injury. 2, 4

Do not restart ACE inhibitors, ARBs, or NSAIDs until renal function has stabilized. 2

Close post-discharge evaluation is essential, with timing based on AKI severity, as AKI survivors are at high risk for progression to advanced CKD. 4, 9