Abstract

Interstitial kidney disease covers a group of disorders which cause interstitial inflammation associated with tubular damage. Traditionally, interstitial nephritis has been classified morphologically and clinically as either acute or chronic. Acute interstitial nephritis (AIN) usually induces rapid deterioration of kidney function, with a marked inflammatory interstitial response that is characterized by the infiltration of mononuclear cells with or without eosinophils, interstitial oedema and tubular involvement. On the other hand, chronic interstitial nephritis (CIN) follows a more indolent course, and it is characterized by interstitial fibrosis, tubular atrophy and, almost always, interstitial infiltrate of mononuclear cells. The tubulointerstitial lesion is clinically important because it is a predictor of present and future kidney function.

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