Interstitial nephritis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief:

Overview

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.

Pathophysiology

Physiology

drugs have emerged as an important cause of renal injury.

Acute drug-induced tubulointerstitial nephritis (TIN) occurs as an adverse reaction to any of an increasing number of drugs such as: penicillins, rifampin, diuretics (thiazides), nonsteroidal anti-inflammatory agents, and numerous other drugs like phenindione, cimetidine.

Pathogenesis

Many features of the disease suggest an immune mechanism. Clinical evidence of hypersensitivity includes latent period, eosinophilia and rash, the idiosyncratic nature of the drug reaction (i.e., the lack of dose dependency), and the recurrence of hypersensitivity after reexposure to the same drug

or others that are similar in structure. Serum IgE levels are increased in some persons, suggesting type I hypersensitivity.

In other cases the nature of the inflammatory infiltrate (discussed below) and the presence of positive skin tests to

drugs suggest a T cell–mediated (type IV) hypersensitivity reaction.

The most likely sequence of pathogenic events is as follows: The drugs act as haptens that, during secretion by tubules, covalently bind to some cytoplasmic or extracellular component of tubular cells and become immunogenic. The resultant tubulointerstitial injury is then caused by IgE- and cell mediated immune reactions to tubular cells or their basement membranes.

The development of drug-induced AIN is not dose dependent, and recurrence or

exacerbation can occur with a second exposure to the same or a related drug

[26].UTD

since The majority  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.

bacterial infection in accompanied with obstruction or reflux such as Legionella, Leptospira, can primarily invade organs remote from the kidney and exerted an inflammatory response in the kidney without invading the kidney [28,29].

However, more recent reports describe the identification of organism-specific antigens or DNA in kidney proximal tubule cells of patients with AIN [27,31-33].

A histologic variant of AIN that is characterized by granuloma formation has been associated with Mycobacterium, fungi (histoplasmosis, coccidiomycosis), bacteria (Brucella, Chlamydia), spirochetes (Francisella, Treponema), and parasites

(Leishmania, Toxoplasma) [30]. (See 'Histology' below.)

Associated Conditions

Common conditions associated with interstitial nephritis include:

Gross Pathology

On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

The abnormalities in acute drug-induced nephritis are in the interstitium, which shows pronounced edema and infiltration

by mononuclear cells, principally lymphocytes and macrophages . Eosinophils and neutrophils may be

present, often in large numbers. With some drugs (e.g.,methicillin, thiazides, rifampin), interstitial non-necrotizing

granulomas with giant cells may be seen. The glomeruli are normal except in some cases caused by nonsteroidal antiinflammatory

agents, in which the hypersensitivity reaction also leads to podocyte foot process effacement and the nephrotic syndrome.

References

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