Introduction:
Colchicine, is a well-known treatment for gout and pericarditis, but its narrow therapeutic window poses a significant risk for toxicity, even at therapeutic doses. We present the case of a woman who suffered a severe colchicine poisoning resulting in multi-organ failure, including acute kidney injury (AKI), and her complete recovery following renal replacement therapy.
Methods:
A 44-year-old-female with a history of anxiety, depression, cirrhosis, hypertension, chronic pericarditis, on colchicine, was admitted after taking 40 colchicine tablets (0.6 mg each) in a suicide attempt. On arrival, her vital signs were blood pressure of 162/77 mmHg, heart rate of 96 beats per minute, respiratory rate of 22 breaths per minute, and oxygen saturation of 91%. Initial laboratory work revealed aspartate aminotransferase (AST) of 46 U/L, alanine aminotransferase (ALT) of 37 U/L, alkaline phosphatase (ALP) of 170 U/L, and creatinine of 0.58 mg/dL. She was started on a 96-hour activated charcoal protocol (50 g every 4 hours) to reduce enterohepatic circulation of colchicine. Despite this, she deteriorated with multi-organ failure, including respiratory failure, hypotension, transaminitis (AST 139 U/L, ALT 60 U/L, ALP 339 U/L), lactic acidosis (lactate acid 9.2 mmol/L), thrombocytopenia, leukopenia, and AKI with creatinine increasing from 0.58 to 1.3 mg/dL, progressing to anuria. Given the life-threatening nature of her condition and the ineffectiveness of dialysis in removing colchicine, continuous renal replacement therapy (CRRT) was initiated.
Results:
After starting CRRT, the patient’s urine output and hemodynamic status improved, allowing for vasopressors discontinuation. By day seven, CRRT was discontinued as her kidney function improved. She was extubated and transitioned to intermittent hemodialysis, then discharged with plans for outpatient follow-up and dialysis. Two months later, her kidney function fully recovered, and dialysis was discontinued. Colchicine was removed from her treatment regimen. It is important to note that her recovery occurred without the use of plasmapheresis, which has been applied in some cases of colchicine-induced multi-organ failure. Her successful outcome with CRRT alone is significant given the known challenges in removing colchicine, a drug that is highly protein-bound and poorly dialyzable using traditional methods. This case underscores the potential efficacy of CRRT in managing colchicine toxicity, even in severe cases with multi-organ failure, by supporting kidney recovery and stabilizing metabolic imbalances.
Conclusions:
This case highlights the serious risks of colchicine toxicity, particularly its narrow therapeutic window and the limited dialyzability. Despite these challenges, CRRT effectively stabilized the patient and supported recovery from multi-organ failure, including AKI. The success without plasmapheresis, despite colchicine’s high protein binding and tissue distribution, suggests CRRT can be a valuable supportive therapy in severe cases of colchicine toxicity. This case underscores the importance of early intervention and tailored renal support in similar toxicities, offering a potential path for full recovery even in life-threatening cases. It also emphasizes the need for careful dosing and monitoring of colchicine, especially in patients with pre-existing renal impairment, to minimize the risk of toxicity.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.