Clin J Am Soc Nephrol. Conclusions: To our knowledge, this is the first report of nephrotic syndrome induced by levamisole-adulterated 3-Indolebutyric acid cocaine, proven by cocaine sample toxicology. Lack of renal biopsy is a limitation of this report. cellular and animal studies to support the existence of cocaine-induced renal changes through multifactorial pathophysiology: vasoconstrictive effects (inhibition of catecholamine reuptake at the presynaptic nerve terminal, increase of endothelins, activation of the renin-angiotensin-aldosterone system, increase of cellular oxidative stress and platelet aggregation), and nonspecific 3-Indolebutyric acid glomerular, interstitial, and tubular cell lesions. Case reports of renal infarction, anti-glomerular basement membrane antibody-mediated glomerulonephritis, and acute interstitial nephritis have been described in cocaine users. In addition, opioids can amplify cocaine-induced expression of tissue inhibitors of metalloproteinase-2, resulting in mesangial matrix accumulation. Focal segmental glomerulosclerosis and membranoproliferative glomerulonephritis have been found in renal biopsy of heroin users. Otherwise, chronic skin suppurative infections can lead to development of renal amyloidosis, in a similar manner to those who subcutaneously inject drugs (skin popping) [10]. However, in our patient, despite the absence of renal biopsy, the typical skin lesions and serologic spectrum, in addition to detection of levamisole in a cocaine sample, suggest cocaine-levamisoleCinduced vasculitis causing renal injury revealed as nephrotic syndrome. Jenkins et al. reported the first case of vasculitis after levamisole 3-Indolebutyric acid snorting that was proven by urine toxicology [11]. The short half-life of levamisole (5.6 hours) and small amount of the parent drug ( 5%) detected in urine, limits the utility of detection of this substance in determining the cause of this syndrome; therefore, in a patient known to have used cocaine and with a high index of medical suspicion, detection of levamisole should not be regarded as essential for analysis [2]. The natural course of LIV may be self-limited [3]. There is a lack of evidence that systemic corticosteroids improve the clinical course of LIV. Discontinuation of levamisole is definitely a critical part of the treatment. Nonetheless, in individual individuals with striking indications of inflammation, corticosteroids might be regarded as [2]. Conclusions End-organ involvement is an uncommon demonstration of ANCA-positive vasculitis induced by levamisole-adulterated cocaine. To our knowledge, this is the 1st statement of nephrotic syndrome induced by levamisole-adulterated cocaine, verified by cocaine sample toxicology. Lack of renal biopsy is definitely a limitation of Mmp13 this report. It is important to perform a differential analysis with additional infectious or idiopathic vasculitis, considering that discontinuation of levamisole-adulterated cocaine can improve the clinical course of the condition without immunosuppressive therapy. Referrals: 1. Graf J, Lynch K, Yeh C, et al. 3-Indolebutyric acid Purpura, cutaneous necrosis and antineutrophil cytoplasmic antibodies associated with levamisole-adulterated cocaine. Arthritis Rheum. 2011;63(12):3998C4001. [PubMed] [Google Scholar] 2. Pearson T, Bremmer M, Cohen J, et al. Vaculopathy related to cocaine adultered with levamisole: A review of the literature. Dermatol Online J. 2012;18(7):1. [PubMed] [Google Scholar] 3. Arora N. Cutaneous vasculopathy and neutropenia associated with levamisole-adulterated cocaine. Am J Med Sci. 2013;345(1):45C51. [PubMed] [Google Scholar] 4. Ventura M, Caudevilla F, Vidal C. Grupo Investigadores SELECTO. Cocana adulterada con levamisol: posibles implicaciones clnicas. [Levamisole-adulterated cocaine: potential medical implications] Med Clin (Barc) 2011;136(8):365C68. [PubMed] [Google Scholar] 5. Arora N, Jain T, Bhanot R, et al. Levamisole-induced leukocytoclastic vasculitis and neutropenia in a patient with cocaine use: an extensive case with necrosis of pores and 3-Indolebutyric acid skin, soft cells, and cartilage. Addict Sci Clin Pract. 2012;7(1):19. [PMC free article] [PubMed] [Google Scholar] 6. Geller.
