Colchicine causes both muscle and peripheral nerve toxicity of subacute onset in patients with renal insufficiency. We report three cardiac transplant recipients, treated with colchicine for cyclosporin A (CyA)-induced gout, who developed acute weakness due to colchicine myoneuropathy. The onset of disabling weakness occurred over a 1-2 week period. All three patients had concomitant renal insufficiency and an elevated serum creatine kinase and two elevated CyA levels at the time of presentation. Electromyography revealed features of myopathy and motor axonal neuropathy in all three patients. Two underwent muscle biopsy which confirmed the presence of sarcoplasmic vacuoles characteristic of colchicine-induced myopathy. All patients rapidly improved with either colchicine dose reduction or drug discontinuation. In conclusion, cardiac transplant recipients treated with CyA and colchicine may be at increased risk of developing colchicine-induced myoneuropathy especially in the setting of concurrent renal insufficiency. In patients with post-transplantation gouty arthritis, other treatment modalities are suggested; and if colchicine is administered, the dose should be reduced, CyA levels should be monitored closely and patients should be assessed for signs of neuromuscular toxicity.