Drug-induced drug-induced kidney injury (DIKI) represents a prevalent challenge in clinical practice and novel drug development, with diverse pathological manifestations affecting multiple renal components, including glomeruli, renal vasculature, tubules, and interstitium. Among various forms of DIKI, tubulointerstitial nephritis (TIN) stands as a critical and common pathological subtype. Its pathogenesis is complex, primarily categorized into two types: direct cytotoxic damage to renal tubular epithelial cells by drugs or their metabolites, and immune-mediated hypersensitivity reactions triggered by the host response to drugs.
J Wang (Wed,) studied this question.
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