Medications are a common cause of AKI, especially for patients admitted to hospital wards and the intensive care unit. Although drug-related kidney injury occurs through different mechanisms, this review will focus on three specific types of tubulointerstitial injury. Direct acute tubular injury develops from several medications, which are toxic to various cellular functions. Their excretory pathways through the proximal tubules contribute further to AKI. Drug-induced AKI may also develop through induction of inflammation within the tubulointerstitium. Medications can elicit a T cell–mediated immune response that promotes the development of acute interstitial nephritis leading to AKI. Although less common, a third pathway to kidney injury results from the insolubility of drugs in the urine leading to their precipitation as crystals within distal tubular lumens, causing a crystalline-related AKI. Intratubular obstruction, direct tubular injury, and localized inflammation lead to AKI. Clinicians should be familiar with the pathogenesis and clinical-pathologic manifestations of these forms of kidney injury. Prevention and treatment of AKI relies on understanding the pathogenesis and judiciously using these agents in settings where AKI risk is high.

药物是 AKI 的常见原因，特别是对于入住医院病房和重症监护室的患者而言。尽管药物相关的肾损伤通过不同的机制发生，但本综述将重点关注三种特定类型的肾小管间质损伤。直接急性肾小管损伤是由多种药物引起的，这些药物对多种细胞功能具有毒性。它们通过近曲小管的排泄途径进一步导致 AKI。药物诱发的 AKI 也可能通过诱导肾小管间质内的炎症而发生。药物可以引发 T 细胞介导的免疫反应，促进急性间质性肾炎的发展，从而导致 AKI。虽然不太常见，但导致肾损伤的第三种途径是由于药物在尿液中不溶，导致其在远端肾小管腔内以晶体形式沉淀，从而引起晶体相关的 AKI。肾小管内梗阻、直接肾小管损伤和局部炎症可导致 AKI。临床医生应熟悉这些形式的肾损伤的发病机制和临床病理表现。AKI 的预防和治疗依赖于了解发病机制并在 AKI 风险高的环境中明智地使用这些药物。