Interstitial nephritis pathophysiology

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Overview

It is thought that acute tubulointerstitial nephritis is mediated by hypersensitivity reaction to numerous drugs such as antibiotics,NSAIDS, sulfa-containing drugs, etc, as well as systemic disease, and Infections. cascade activation owing to cellular injury toward collagenases and metalloproteinases release causes an immunologic reaction against endogenous or exogenous antigens processed by tubular cells, with cell-mediated immunity having a major pathogenic role. may play parts in the pathogenesis of ATN from activation of cascade of cellular injury toward collagenases and metalloproteinases

activation and release of proinflammatory cytokines into the interstitium.

Pathophysiology

Physiology

The normal physiology of [name of process] can be understood as follows:

Pathogenesis

  • The exact pathogenesis of [disease name] is not completely understood.

OR

  • It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothdeveesis 3].
  • [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
  • Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
  • [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
  • The progression to [disease name] usually involves the [molecular pathway].
  • The pathophysiology of [disease/malignancy] depends on the histological subtype.

References

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