What is the best course of action for a patient presenting with Acute Kidney Injury (AKI), Transaminitis (elevated liver enzymes), and Ascending paralysis, possibly indicative of Guillain-Barré Syndrome?

Immediate Diagnostic Workup for Suspected Guillain-Barré Syndrome with Multi-Organ Involvement

This clinical triad of AKI, transaminitis, and ascending paralysis strongly suggests Guillain-Barré Syndrome (GBS) with concurrent multi-organ dysfunction, requiring immediate neurological consultation, respiratory monitoring, and supportive management of renal and hepatic complications.

Critical First Steps

Neurological Emergency Assessment

• Obtain immediate neurology consultation for suspected GBS, as respiratory failure can develop rapidly and is the leading cause of mortality
• Measure forced vital capacity (FVC) and negative inspiratory force (NIF) every 2-4 hours to detect impending respiratory failure
• Prepare for intubation if FVC <20 mL/kg, NIF >-30 cm H₂O, or inability to clear secretions
• Perform lumbar puncture for cerebrospinal fluid analysis (expect albuminocytologic dissociation: elevated protein with normal cell count)
• Order nerve conduction studies and electromyography to confirm demyelinating polyneuropathy

Simultaneous AKI Management

• Immediately discontinue all nephrotoxic medications including NSAIDs, ACE inhibitors, ARBs, and aminoglycosides 1, 2
• Hold diuretics and beta-blockers temporarily 1, 2
• Measure serum creatinine daily and stage AKI severity using KDIGO criteria 2
• Assess volume status through jugular venous pressure, orthostatic vital signs, and lung examination 1, 2
• Administer isotonic crystalloids (preferably balanced crystalloids like lactated Ringer's over 0.9% saline) for volume expansion if hypovolemic 2
• Obtain urinalysis with microscopy to exclude glomerulonephritis (look for dysmorphic RBCs, RBC casts, proteinuria) 1, 3
• Calculate fractional excretion of sodium (FENa <1% suggests prerenal causes) 1

Hepatic Function Evaluation

• Obtain comprehensive hepatic panel including AST, ALT, alkaline phosphatase, bilirubin, albumin, and INR
• Perform right upper quadrant ultrasound to exclude biliary obstruction or structural liver disease
• Assess for signs of hepatic synthetic dysfunction (coagulopathy, hypoalbuminemia, encephalopathy)
• Rule out viral hepatitis, drug-induced liver injury, and ischemic hepatitis

Infection Screening (Critical in GBS Context)

• Perform rigorous infection workup as infections commonly precipitate both GBS and AKI 1, 2
• Obtain blood cultures, urine cultures, and chest radiograph 1
• Test for recent Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and Mycoplasma pneumoniae infections (common GBS triggers)
• If ascites present, perform diagnostic paracentesis to exclude spontaneous bacterial peritonitis 1
• Start broad-spectrum antibiotics empirically only if infection is strongly suspected 1

Monitoring and Supportive Care

Respiratory Monitoring

• Admit to intensive care unit for continuous cardiorespiratory monitoring
• Measure FVC and NIF every 2-4 hours initially, then every 4-6 hours once stable
• Monitor for bulbar weakness (dysphagia, dysarthria) which increases aspiration risk
• Keep intubation equipment at bedside

Renal Monitoring

• Monitor urine output hourly 2
• Check serum creatinine, potassium, bicarbonate, and phosphate daily 2
• Assess fluid balance carefully to avoid both hypovolemia and pulmonary edema 1
• Consult nephrology immediately if Stage 2 or 3 AKI (creatinine ≥2.0× baseline) 2, 4
• Consider nephrology consultation for persistent AKI despite initial management after 48-72 hours 2

Cardiovascular Monitoring

• Monitor for autonomic dysfunction (labile blood pressure, cardiac arrhythmias, bradycardia) common in GBS
• Avoid aggressive fluid resuscitation if autonomic instability present
• Use caution with vasopressors due to potential exaggerated response

Specific GBS Treatment Considerations

Immunotherapy Timing

• Initiate intravenous immunoglobulin (IVIG) 0.4 g/kg/day for 5 days as soon as GBS diagnosis is confirmed
• Alternative: Plasma exchange (5 exchanges over 10-14 days) if IVIG contraindicated
• Do not delay immunotherapy for complete diagnostic workup if clinical suspicion is high
• Avoid corticosteroids as monotherapy (not beneficial in GBS)

Renal Dosing Adjustments

• Adjust IVIG infusion rate based on renal function to minimize risk of osmotic nephropathy
• Use sucrose-free IVIG formulations when possible to reduce AKI risk
• Ensure adequate hydration before and during IVIG administration
• Monitor for IVIG-associated complications including aseptic meningitis, thrombosis, and hemolysis

Renal Replacement Therapy Indications

• Initiate dialysis for refractory hyperkalemia, severe metabolic acidosis (pH <7.1), or uremic symptoms 2, 4
• Consider RRT for refractory volume overload that could compromise respiratory function 2
• Early nephrology involvement for RRT planning if AKI progresses 2

Common Pitfalls to Avoid

Critical Errors

• Do not attribute ascending paralysis solely to uremia or hepatic encephalopathy without excluding GBS—this delay can be fatal
• Do not wait for complete diagnostic confirmation before initiating respiratory monitoring and supportive care
• Avoid aggressive diuresis in prerenal AKI as this worsens kidney injury 4
• Do not use albumin-containing colloids for initial volume expansion (use isotonic crystalloids) 2
• Avoid nephrotoxic contrast agents for imaging studies 1

Monitoring Pitfalls

• Do not rely solely on oxygen saturation—respiratory muscle weakness causes hypercapnia before hypoxemia
• Avoid missing autonomic dysfunction signs (can cause sudden cardiac arrest)
• Do not overlook fluid overload risk when administering albumin for HRS-AKI in cirrhotic patients 1

Follow-Up and Long-Term Considerations

Post-Acute Phase

• Reassess renal function at 3 months even if AKI resolves, as patients remain at increased risk for CKD 2, 4
• Stage 3 AKI requires earlier follow-up (within 1-2 weeks) due to higher CKD progression risk 4
• Monitor for proteinuria and hematuria indicating ongoing kidney damage 3
• Permanently avoid nephrotoxic medications when possible 4

GBS Recovery

• Arrange physical and occupational therapy for rehabilitation
• Monitor for chronic inflammatory demyelinating polyneuropathy (CIDP) development
• Assess for residual neuropathic pain requiring management
• Screen for depression and post-ICU syndrome

Hepatic Follow-Up

• Repeat liver function tests weekly until normalization
• Investigate persistent transaminitis for underlying chronic liver disease
• Avoid hepatotoxic medications during recovery

The key to managing this complex presentation is recognizing GBS as a neurological emergency requiring immediate respiratory monitoring and immunotherapy, while simultaneously addressing AKI through nephrotoxin avoidance, volume optimization, and infection treatment. 1, 2