Interstitial nephritis: Difference between revisions
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==[[Interstitial nephritis classification|Classification]]== | ==[[Interstitial nephritis 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 and chronic categories. | |||
==[[Interstitial nephritis pathophysiology|Pathophysiology]]== | ==[[Interstitial nephritis pathophysiology|Pathophysiology]]== |
Revision as of 17:51, 19 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 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 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 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 introduction of percutaneous renal biopsy led to the discovery of similar findings in association with drug-related renal failure, in particular related to the use of penicillins and sulphonamides. Histological examination in ATIN reveals an infiltrate, which is largely composed of T cells, together with some macrophages and plasma cells. As there is some evidence for cutaneous delayed-type hypersensitivity and positive in vitrolymphocyte stimulation tests in response to suspected drugs, the etiology is presumed to be immune-mediated [2]. This is illustrated by the rapid recrudescence of disease upon inadvertent rechallenge in drug-related ATIN, a clear manifestation of an immunological memory response [3–5].
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
Causes
Differentiating Interstitial nephritis from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and 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