Interstitial nephritis pathophysiology: Difference between revisions

Revision as of 03:57, 26 June 2018

Overview

It is thought that acute interstitial nephritis is mediated by hypersensitivity reaction to endogenous or exogenous antigens expressed by tubular cells. Numerous drugs such as antibiotics, NSAIDS, sulfa-containing drugs, etc, as well as systemic diseases, and Infections may lead injury to renal cells. the cascade activation owing to cellular injury toward inflammatory cell infiltration, and activation of cytokines causes an immunologic reaction in acute or chronic process.

In acute interstitial nephritis, this cascade activation can cause renal tubular dysfunction, whereas in chronic interstitial nephritis an insidious interstitial fibrosis,scarring, , and tubular atrophy spreads gradually and causes progressive chronic renal insufficiency.

Pathophysiology

Physiology

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

Pathogenesis

References

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 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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