It is thought that acute<unk>  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<unk>  nephritis, this cascade activation can cause renal tubular dysfunction, whereas in chronic<unk>  nephritis an insidious<unk>  fibrosis,scarring, and tubular atrophy  spreads gradually and causes  progressive chronic renal insufficiency.
Interstitial nephritis pathophysiology
Renal papillary necrosis pathophysiology
Acute tubular necrosis pathophysiology
Membranous glomerulonephritis pathophysiology
Contrast induced nephropathy pathophysiology
Renal amyloidosis pathophysiology
Analgesic nephropathy pathophysiology
Post-streptococcal glomerulonephritis pathophysiology