Which type of hypersensitivity reaction is associated with NSAID-induced interstitial nephritis?

NSAID-induced interstitial nephritis is primarily associated with a Type IV hypersensitivity reaction, which is a delayed-type hypersensitivity mediated by T cells and the release of cytokines rather than by antibodies. In this context, nonsteroidal anti-inflammatory drugs (NSAIDs) may cause an allergic response in susceptible individuals, often resulting in inflammation of the renal interstitium.

Type IV hypersensitivity does not involve the production of antibodies. Instead, it hinges on the activation of T-lymphocytes (specifically CD4+ T helper cells) that react to the drug or its metabolites. This leads to the recruitment of additional inflammatory cells, ultimately resulting in damage to renal tubular cells and a clinical picture of interstitial nephritis.

In contrast, Type I hypersensitivity is characterized by IgE-mediated responses, often resulting in anaphylaxis or urticaria, while Type II hypersensitivity involves antibody-mediated reactions against cell surface antigens, leading to cytotoxic effects. Type III hypersensitivity involves immune complex-mediated diseases, which is not the primary mechanism in NSAID-induced renal issues.

Understanding that NSAID-induced interstitial nephritis is aligned with the mechanisms of Type IV hypersensitivity clarifies the role of the immune system in this adverse reaction