Interstitial nephritis overview: Difference between revisions
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Since some cases of TIN are due to bacterial infection, and the renal pelvis is deeply involved, therefore [[pyelonephritis]] is term describes this condition; and In general, the term interstitial nephritis is used for TIN that is owing to nonbacterial causes of tubular injury such as drugs, viral infections,[[Autoimmune disease|autoimmune systemic diseases]], in which these condition mechanism of damage is due to [[inflammatory responses]] not direct damage. | Since some cases of TIN are due to bacterial infection, and the renal pelvis is deeply involved, therefore [[pyelonephritis]] is term describes this condition; and In general, the term interstitial nephritis is used for TIN that is owing to nonbacterial causes of tubular injury such as drugs, viral infections,[[Autoimmune disease|autoimmune systemic diseases]], in which these condition mechanism of damage is due to [[inflammatory responses]] not direct damage. | ||
== Historical Perspective == | |||
In 1938, Councilman was the first to discover the association between systemic infections and the development of TIN; in autopsy kidneys of children dying of [[diphtheria]] and [[scarlet fever]]. He described the findings as: cellular and fluid exudation in the interstitial tissue of kidneys, before the era of antibiotics. | |||
The widespread use of renal biopsy and histological examination in TIN revealed a cellular infiltration, which is dominantly composed of [[T cells]], together with some[[macrophages]] and [[plasma cells]], and led to the discovery of similar findings in association with drug-related [[Renal insufficiency and failure|renal failure]] and the same conditions. | |||
==Classification== | ==Classification== | ||
There is no established system for the classification of TIN, however according to clinical manifestations and the [[inflammatory process]], TIN, in spite of the etiologic agent, can be divided into [[Acute (medicine)|acute]] and [[Chronic (medical)|chronic]] categories. | |||
==Pathophysiology== | ==Pathophysiology== | ||
It is thought that acute interstitial nephritis is mediated by [[hypersensitivity reaction]] to endogenous or exogenous [[antigens]] expressed by [[Nephron|tubular cells]]. Numerous drugs such as [[antibiotics]], NSAIDS, [[Sulfa-containing antibiotics|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 [[Atrophy|tubular atrophy]] spreads gradually and causes progressive [[chronic renal insufficiency]]. | |||
==Causes== | ==Causes== | ||
Common causes of interstitial nephritis include drug side effects, particularly [[analgesics]] and [[antibiotics]]. Other common causes include associated nephrologic conditions, as well as [[microbial]] infections. | |||
==Differentiating Xyz from Other Diseases== | ==Differentiating Xyz from Other Diseases== | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Interstitial nephritis accounts for 10-15% of kidney disease worldwide. [[Nephritis|Analgesic-induced nephritis]] is 5-6 times more common in women. The elderly have more severe disease and increased risk of permanent damage. Children exposed to [[lead poisoning]] are more likely to develop [[nephritis]] as young adult. | |||
==Risk Factors== | ==Risk Factors== | ||
There are no established risk factors for TIN; Whereas according to etiologic causative factors, consumption of culprit drugs in causing TIN,previous history of [[hypersensitivity reactions]] to specific drug, presence of [[Autoimmune disease|autoimmune systemic disease]] or some [[neoplasia]] or genetic condition, occupational or environmental exposure to heavy metals, and infection etiologies in association with obstructive uropathy, play role in in the development of TIN. | |||
==Screening== | ==Screening== | ||
There is insufficient evidence to recommend routine screening for TIN. | |||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
In the majority of patients with TIN, recovery of [[renal function]] has been observed, and improvement immediately occurs upon stopping the offensive agent, nevertheless, about 12% of patients may progress to develop [[ESRD]] and its complications; and thus require [[dialysis]] or [[Organ transplant|transplantation]]. | |||
However there is no definite prognostic indicators for TIN, but [[Renal insufficiency|renal failure]] lasts for >3 weeks, elderly patients and presence of tubular [[atrophy]] and [[interstitial fibrosis]] in the renal biopsy are associated with worse prognosis. | |||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic Study of Choice=== | ===Diagnostic Study of Choice=== |
Revision as of 17:10, 31 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohsen Basiri M.D.
Overview
Two main diseases involve the renal tubules are: Acute tubular necrosis due to Ischemic or toxic injury .(for more about ATN click here), and tubulointerstitial nephritis with Inflammatory involvement of tubules and interstitium and its consequent reactions.
Since some cases of TIN are due to bacterial infection, and the renal pelvis is deeply involved, therefore pyelonephritis is term describes this condition; and In general, the term interstitial nephritis is used for TIN that is owing to nonbacterial causes of tubular injury such as drugs, viral infections,autoimmune systemic diseases, in which these condition mechanism of damage is due to inflammatory responses not direct damage.
Historical Perspective
In 1938, Councilman was the first to discover the association between systemic infections and the development of TIN; in autopsy kidneys of children dying of diphtheria and scarlet fever. He described the findings as: cellular and fluid exudation in the interstitial tissue of kidneys, before the era of antibiotics.
The widespread use of renal biopsy and histological examination in TIN revealed a cellular infiltration, which is dominantly composed of T cells, together with somemacrophages and plasma cells, and led to the discovery of similar findings in association with drug-related renal failure and the same conditions.
Classification
There is no established system for the classification of TIN, however according to clinical manifestations and the inflammatory process, TIN, in spite of the etiologic agent, can be divided into acute and chronic categories.
Pathophysiology
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.
Causes
Common causes of interstitial nephritis include drug side effects, particularly analgesics and antibiotics. Other common causes include associated nephrologic conditions, as well as microbial infections.
Differentiating Xyz from Other Diseases
Epidemiology and Demographics
Interstitial nephritis accounts for 10-15% of kidney disease worldwide. Analgesic-induced nephritis is 5-6 times more common in women. The elderly have more severe disease and increased risk of permanent damage. Children exposed to lead poisoning are more likely to develop nephritis as young adult.
Risk Factors
There are no established risk factors for TIN; Whereas according to etiologic causative factors, consumption of culprit drugs in causing TIN,previous history of hypersensitivity reactions to specific drug, presence of autoimmune systemic disease or some neoplasia or genetic condition, occupational or environmental exposure to heavy metals, and infection etiologies in association with obstructive uropathy, play role in in the development of TIN.
Screening
There is insufficient evidence to recommend routine screening for TIN.
Natural History, Complications, and Prognosis
In the majority of patients with TIN, recovery of renal function has been observed, and improvement immediately occurs upon stopping the offensive agent, nevertheless, about 12% of patients may progress to develop ESRD and its complications; and thus require dialysis or transplantation.
However there is no definite prognostic indicators for TIN, but renal failure lasts for >3 weeks, elderly patients and presence of tubular atrophy and interstitial fibrosis in the renal biopsy are associated with worse prognosis.