Interstitial nephritis: Difference between revisions
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'''''Synonyms and keywords:''''' Tubulo-interstitial nephritis | '''''Synonyms and keywords:''''' Tubulo-interstitial nephritis | ||
==[[Interstitial nephritis overview|Overview]]== | ==[[Interstitial nephritis overview|Overview]]== | ||
Two main diseases involve the renal tubules are: [[Acute tubular necrosis]] due to [[Ischemic]] or [[Toxic|toxic injury]] .(for more about ATN click [[Acute tubular necrosis|here]]), and tubulointerstitial nephritis with [[Inflammatory]] involvement of tubules and [[interstitium]] and its consequent reactions. | Two main diseases involve the renal tubules are: [[Acute tubular necrosis]] due to [[Ischemic]] or [[Toxic|toxic injury]] .(for more about ATN click [[Acute tubular necrosis|here]]), and tubulointerstitial nephritis (TIN) with [[Inflammatory]] involvement of tubules and [[interstitium]] and its consequent reactions. | ||
Since some cases of | Since some cases of involvement of renal tubulointerstitium 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 are 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 activation of [[inflammatory responses]] not direct damage of [[Pathogens|microbial pathogens]]. | ||
==[[Interstitial nephritis historical perspective|Historical Perspective]]== | ==[[Interstitial nephritis historical perspective|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]]. | * 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. | * 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 | * 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. | ||
==[[Interstitial nephritis classification|Classification]]== | ==[[Interstitial nephritis classification|Classification]]== | ||
Revision as of 15:08, 23 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.
Synonyms and keywords: Tubulo-interstitial nephritis
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 (TIN) with Inflammatory involvement of tubules and interstitium and its consequent reactions.
Since some cases of involvement of renal tubulointerstitium 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 are 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 activation of inflammatory responses not direct damage of microbial pathogens.
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 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 Interstitial nephritis 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.
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, older patients and presence of tubular atrophy and interstitial fibrosis in the renal biopsy are associated with worse prognosis.
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | KUB X Ray | CT | MRI | Biopsy and Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies