Case Presentation: The prevalence of cocaine use is growing worldwide. Damaging effects of cocaine on the cardiovascular, neurologic, and pulmonary systems are well-established. In recent years, evidence has emerged for cocaine-induced damage to other organs, such as the liver and kidney. This is a case of end-organ damage from regular cocaine use.
A 65-year-old man with coronary artery disease and chronic cocaine was hospitalized from a clinic appointment for acute kidney injury. Outpatient laboratory investigation revealed an elevated creatinine to 3.8 mg/dL from a normal baseline. Vital signs were within normal limits. Examination was overall normal, without rashes, synovitis, or hypervolemia. Laboratories revealed a fractional excretion of sodium of 2% and muddy brown casts on urinalysis. He was presumed to have acute tubular necrosis without a clear trigger and was observed. His urinary output remained steady and creatinine slightly improved, so he was discharged with outpatient follow-up.
Within a few weeks, his creatinine was again elevated to 3.8 mg/dL, and chest x-ray showed bilateral pleural effusions. He was admitted and repeat urinalysis now showed many dysmorphic red blood cells, and spot urine protein/creatinine ratio was 1.7 mg/g. Secondary workup for renal failure was remarkable for elevated erythrocyte sedimentation rate, elevated perinuclear anti-neutrophil cytoplasmic antibody titer, and positive myeloperoxidase antibody. Renal biopsy was performed and showed pauci-immune necrotizing crescentic glomerulonephritis.
Given these results in the setting of his cocaine use and no other clear etiology, the patient was diagnosed with cocaine-induced vasculitis. He was treated with rituximab and prednisone. Creatinine decreased to 2.8 mg/dL at a six-month follow-up appointment with resolution of symptoms.
Discussion: Cocaine-induced ANCA vasculitis has become increasingly recognized in recent decades. The pathophysiology has been attributed to levamisole, a contaminant present in the majority of cocaine products. Cutaneous lesions in the form of skin necrosis or purpura, constitutional symptoms, and arthralgias are most common clinical manifestations. Elevated perinuclear and cytoplasmic anti-neutrophil cytoplasmic antibodies have been seen in approximately 80% and 50% of patients, respectively.
Conclusions: This patient’s disease process is atypical as he did not present with any cutaneous abnormalities or constitutional symptoms. His only manifestation of levamisole-induced vasculitis was renal failure from glomerulonephritis. This case provides a unique clinical presentation of levamisole-induced vasculitis and also serves as a reminder to consider substance use as a cause of systemic disease and end-organ damage.