Interstitial nephritis pathophysiology: Difference between revisions
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The normal physiology of [name of process] can be understood as follows: | The normal physiology of [name of process] can be understood as follows: | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
==References== | ==References== | ||
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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: