Goel Narender, Pullman James M, Coco Maria
Division of Nephrology and Hospital Medicine , Middletown Medical PC and Orange Regional Medical Center , Middletown, NY , USA ; Division of Nephrology , Montefiore Medical Center & Albert Einstein College of Medicine , Bronx, NY , USA.
Division of Pathology , Montefiore Medical Center & Albert Einstein College of Medicine , Bronx, NY , USA.
Clin Kidney J. 2014 Dec;7(6):513-7. doi: 10.1093/ckj/sfu092. Epub 2014 Sep 12.
Cocaine is abused worldwide as a recreational drug. It is a potent activator of the sympathetic nervous system leading to intense vasoconstriction, endothelial dysfunction, oxidative stress, platelet activation and decrease in prostaglandins E2 and prostacyclin. Cocaine can lead to widespread systemic adverse effects such as stroke, myocardial infarction, arterial dissection, vascular thrombosis and rhabdomyolysis. In human and rat kidneys, cocaine has been associated with glomerular, tubular, vascular and interstitial injury. It is not uncommon to diagnose cocaine-related acute kidney injury (AKI), malignant hypertension and chronic kidney disease. Cocaine abuse can lead to AKI by rhabdomyolysis, vasculitis, infarction, thrombotic microangiopathy and malignant hypertension. It is reported that 50-60% of people who use both cocaine and heroin are at increased risk of HIV, hepatitis and additional risk factors that can cause kidney diseases. While acute interstitial nephritis (AIN) is a known cause of AKI, an association of AIN with cocaine is unusual and seldom reported. We describe a patient with diabetes mellitus, hypertension and chronic hepatitis C, who presented with AKI. Urine toxicology was positive for cocaine and a kidney biopsy was consistent with AIN. Illicit drugs such as cocaine or contaminants may have caused AIN in this case and should be considered in the differential diagnosis of causes of AKI in a patient with substance abuse. We review the many ways that cocaine adversely impacts on kidney function.
可卡因作为一种消遣性毒品在全球被滥用。它是交感神经系统的强效激活剂,会导致强烈的血管收缩、内皮功能障碍、氧化应激、血小板活化以及前列腺素E2和前列环素减少。可卡因可导致广泛的全身不良反应,如中风、心肌梗死、动脉夹层、血管血栓形成和横纹肌溶解。在人类和大鼠肾脏中,可卡因与肾小球、肾小管、血管和间质损伤有关。诊断出与可卡因相关的急性肾损伤(AKI)、恶性高血压和慢性肾病并不罕见。可卡因滥用可通过横纹肌溶解、血管炎、梗死、血栓性微血管病和恶性高血压导致AKI。据报道,同时使用可卡因和海洛因的人群中有50%-60%感染艾滋病毒、肝炎的风险增加,还有其他可导致肾脏疾病的风险因素。虽然急性间质性肾炎(AIN)是AKI的已知病因,但AIN与可卡因的关联并不常见,鲜有报道。我们描述了一名患有糖尿病、高血压和慢性丙型肝炎的患者,该患者出现了AKI。尿液毒理学检测可卡因呈阳性,肾脏活检结果与AIN一致。在这种情况下,可卡因等非法药物或污染物可能导致了AIN,在药物滥用患者AKI病因的鉴别诊断中应予以考虑。我们回顾了可卡因对肾功能产生不利影响的多种方式。