What causes acute kidney injury in a previously healthy Southeast Asian individual after consuming Ketum drink?

Acute Kidney Injury from Kratom (Ketum) Consumption

This patient has developed acute kidney injury (AKI) from consuming Ketum (kratom), evidenced by severely elevated creatinine (760 µmol/L or ~8.6 mg/dL) and urea (23.1 mmol/L), requiring immediate discontinuation of kratom, supportive care with intravenous fluids, and likely urgent hemodialysis given the severity of renal dysfunction. 1, 2, 3

Understanding Kratom-Induced Kidney Injury

Kratom (Mitragyna speciosa), known as "Ketum" in Southeast Asia, contains alkaloids (mitragynine and 7-hydroxymitragynine) that cause both stimulant and opioid-like effects. 2, 3 The mechanism of kidney injury involves:

• Direct tubular toxicity: Regular kratom consumption induces proteinuria (primarily albuminuria), indicating early-stage kidney injury from direct nephrotoxic effects 1
• Rhabdomyolysis: Kratom overdose can cause muscle breakdown with elevated creatine phosphokinase, leading to acute tubular necrosis and compartment syndrome 3
• Adulteration risk: Unregulated kratom products may contain hydrocodone, morphine, or other nephrotoxic substances that compound kidney injury 2
• Hemodynamic effects: The sudden fall suggests possible syncope from cardiovascular effects (tachycardia, hypertension) or seizures, both reported with kratom toxicity 3

Immediate Management Algorithm

Step 1: Assess AKI Severity and Complications

• Creatinine 760 µmol/L (8.6 mg/dL) represents Stage 3 AKI (>3 times baseline, assuming normal baseline in previously healthy individual) 4
• Check for life-threatening complications: hyperkalemia, metabolic acidosis (bicarbonate <15 mmol/L), volume overload, uremic symptoms (pericarditis, encephalopathy, bleeding) 5, 6
• Obtain urgent ECG to assess for hyperkalemic changes (peaked T-waves, widened QRS) 4
• Measure creatine phosphokinase (CPK) to rule out rhabdomyolysis, which is a documented complication of kratom overdose 3

Step 2: Initiate Supportive Care

• Discontinue kratom immediately - this is the single most important intervention for drug-induced AKI 4, 2
• Assess volume status clinically: check peripheral perfusion, capillary refill, pulse rate, blood pressure, jugular venous pressure 4
• Administer intravenous fluids if hypovolemic (normal saline or balanced crystalloids), but monitor carefully for fluid overload given severe renal dysfunction 4, 6
• Hold all nephrotoxic medications: NSAIDs, ACE inhibitors, ARBs, diuretics (if on any) 4

Step 3: Determine Need for Urgent Dialysis

Initiate renal replacement therapy if any of the following are present: 5, 6

• Severe hyperkalemia (K+ >6.5 mmol/L) refractory to medical management
• Metabolic acidosis (pH <7.1 or bicarbonate <10 mmol/L)
• Volume overload with pulmonary edema unresponsive to diuretics
• Uremic symptoms (pericarditis, encephalopathy, bleeding)
• Creatinine >700-800 µmol/L with oliguria/anuria

Given this patient's creatinine of 760 µmol/L, urgent nephrology consultation for likely hemodialysis is warranted. 3

Step 4: Monitor and Investigate

• Serial creatinine and electrolytes: measure at least every 12-24 hours initially, then every 48 hours as clinically indicated 4
• Urine output monitoring: oliguria (<0.5 mL/kg/hr for >6 hours) indicates more severe AKI 4
• Urinalysis with microscopy: look for proteinuria, hematuria, and casts to differentiate acute tubular necrosis from acute interstitial nephritis 4, 7
• Urine drug screen: may reveal adulteration with opioids (hydrocodone, morphine) or other substances 2
• Renal ultrasound: to exclude obstructive uropathy, though unlikely given bilateral kidney involvement 4

Prognosis and Recovery

• Kratom-induced AKI can be reversible with supportive care and kratom discontinuation, with renal function normalizing over 1-2 months 1, 2
• Drug-induced AKI generally has better outcomes than septic or ischemic AKI, with lower mortality but similar need for acute kidney support therapy (31.8% vs 36.8%) 7
• Complete recovery is possible if kratom is permanently discontinued and no irreversible tubular damage has occurred 2, 3

Critical Pitfalls to Avoid

• Do not delay dialysis in severe AKI with life-threatening complications - waiting for "uremic symptoms" in the setting of creatinine >700 µmol/L risks cardiac arrest from hyperkalemia 5, 6
• Do not assume kratom is "natural and safe" - it causes documented nephrotoxicity, rhabdomyolysis, and multiorgan dysfunction 1, 2, 3
• Do not miss rhabdomyolysis - check CPK levels as this requires aggressive fluid resuscitation and may necessitate fasciotomy if compartment syndrome develops 3
• Screen for adulteration - unregulated kratom products may contain opioids or other nephrotoxins that require specific management 2

Follow-Up After Recovery

• Monitor renal function at 1 week, 1 month, and 3 months post-discharge to ensure complete recovery and detect chronic kidney disease 4, 5
• Counsel on permanent kratom avoidance - regular consumption over years causes progressive proteinuria and chronic kidney injury 1
• Screen for substance use disorder - kratom is often used for opioid withdrawal or chronic pain, requiring addiction medicine referral 2, 3