How should I manage a patient with acute kidney disease who is worsening, evidenced by rising serum creatinine, declining eGFR, oliguria, electrolyte abnormalities, or new uremic symptoms?

Management of Worsening Acute Kidney Disease

When AKD worsens, immediately reassess for reversible causes, discontinue all nephrotoxins, optimize hemodynamics and volume status, and escalate to nephrology consultation for Stage 2 or higher AKI or if deterioration persists beyond 48-72 hours despite initial interventions. 1

Immediate Diagnostic Re-evaluation

Restage the Severity

• Determine current KDIGO AKI stage to guide management intensity: Stage 1 (creatinine 1.5-1.9× baseline or ≥0.3 mg/dL increase within 48h, or urine output <0.5 mL/kg/h for 6-12h), Stage 2 (creatinine 2.0-2.9× baseline or urine output <0.5 mL/kg/h for ≥12h), or Stage 3 (creatinine ≥3.0× baseline or ≥4.0 mg/dL or dialysis initiated or urine output <0.3 mL/kg/h for ≥24h). 2, 1

Identify New Insults

• Search aggressively for new nephrotoxic exposures including NSAIDs, aminoglycosides, contrast agents, or other medications introduced since initial presentation. 3, 1, 4
• Reassess for new hemodynamic compromise such as hypotension, sepsis, or volume depletion that may have developed. 3, 5
• Obtain urgent renal ultrasound if not already done to exclude post-renal obstruction, which accounts for <3% of AKI cases but requires urgent intervention. 3

Laboratory Monitoring

• Obtain serial creatinine measurements every 24-48 hours to determine trajectory and rate of deterioration. 3
• Check comprehensive metabolic panel for severe metabolic acidosis (pH <7.2 or bicarbonate <12 mEq/L) and refractory hyperkalemia, both of which require urgent nephrology consultation. 1
• Perform urinalysis with microscopy looking for muddy-brown granular casts (suggesting acute tubular necrosis) or red-blood-cell casts (suggesting glomerulonephritis). 3

Immediate Therapeutic Interventions

Medication Management

• Discontinue ALL nephrotoxic medications immediately including NSAIDs, ACE inhibitors, ARBs (in volume-depleted patients), and aminoglycosides. 3, 1, 4
• Hold diuretics temporarily until volume status is clarified and optimized. 1
• Adjust all medication dosages based on current renal function, not baseline values. 1

Hemodynamic Optimization

• Administer isotonic crystalloids, preferably balanced crystalloids (lactated Ringer's) for volume expansion if hypovolemia is present, as they are superior to colloids and may reduce adverse outcomes compared to normal saline. 1
• Assess volume status using clinical examination complemented by central venous pressure monitoring or inferior vena cava echocardiography to guide fluid management. 5
• Provide blood pressure support to maintain adequate renal perfusion pressure. 5

Nephrology Consultation Triggers

Mandatory Immediate Consultation

• Stage 2 or 3 AKI (creatinine ≥2.0× baseline) requires immediate nephrology consultation. 1
• Persistent AKI despite initial management after 48-72 hours warrants nephrology involvement. 1
• Severe metabolic acidosis (pH <7.2 or bicarbonate <12 mEq/L) requires urgent consultation. 1
• Refractory hyperkalemia despite medical management necessitates immediate nephrology evaluation. 1

Renal Replacement Therapy Indications

Emergent RRT Initiation

• Initiate renal replacement therapy emergently for life-threatening complications including severe metabolic acidosis (pH <7.1), refractory hyperkalemia, or refractory volume overload causing pulmonary edema. 1
• Consider RRT for uremic complications such as uremic encephalopathy, pericarditis, or pleuritis. 4

Critical Pitfalls to Avoid

Diagnostic Errors

• Do not rely on standard eGFR equations (MDRD, CKD-EPI) during worsening AKD, as they are inaccurate when serum creatinine is rapidly changing. 3
• Do not assume urine output alone reflects kidney function, as serum creatinine remains the more reliable marker in acute settings. 3
• Recognize that critical illness causes significant falls in serum creatinine due to muscle loss, potentially masking persistent renal dysfunction—a 30% decrease in creatinine can occur from prolonged hospitalization alone. 6

Management Errors

• Do not continue nephrotoxic agents while attempting other interventions—immediate discontinuation is paramount. 3, 1
• Do not delay nephrology consultation when Stage 2 or higher AKI develops or when initial management fails. 1
• Do not discharge without intensive follow-up planning, as the 7-90 day AKD window is critical for preventing progression to CKD. 2, 3

Follow-up Strategy for Worsening AKD

Short-term Monitoring

• Arrange nephrology follow-up within 1-2 weeks for patients with Stage 3 AKI due to high CKD progression risk. 1
• Monitor kidney function for at least 90 days to differentiate AKD from progression to CKD, as AKD is defined as dysfunction persisting 7-90 days after an AKI-initiating event. 2, 3, 7

Long-term Surveillance

• Evaluate all AKD patients at 3 months to assess for CKD development, with more intensive monitoring needed if pre-existing CKD, heart failure, or other comorbidities exist. 1
• Recognize that even partial recovery carries mortality risk—patients whose creatinine remains above 115% of baseline after AKI still have elevated mortality risk and require continued follow-up. 2