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However, among patients who do not improve after the first five to seven days of empiric glucocorticoid therapy, those without contraindications should have a biopsy in order to exclude other diagnoses or severe interstitial fibrosis.
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ong selected patients (such as those at high risk of complications of a biopsy or who do not wish to undergo a biopsy), glucocorticoids may be initiated without first obtaining a kidney biopsy. <span>However, among patients who do not improve after the first five to seven days of empiric glucocorticoid therapy, those without contraindications should have a biopsy in order to exclude other diagnoses or severe interstitial fibrosis. (See "The kidney biopsy", section on 'Contraindications' and "Treatment of acute interstitial nephritis".) ●Patients with putative drug-related AIN who are not treated with glucocortico




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Patients with putative drug-related AIN who are not treated with glucocorticoids initially and do not have a recovery following cessation of drug therapy [2,73]. We typically perform a kidney biopsy approximately two weeks after cessation of the offending drug if there has been no improvement in the kidney function over that time. However, clinicians wait a variable amount of time to allow for recovery before performing a biopsy. Some wait for three to four days, whereas others wait until the patient is approaching the need for kidney replacement therapy.
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ld have a biopsy in order to exclude other diagnoses or severe interstitial fibrosis. (See "The kidney biopsy", section on 'Contraindications' and "Treatment of acute interstitial nephritis".) ●<span>Patients with putative drug-related AIN who are not treated with glucocorticoids initially and do not have a recovery following cessation of drug therapy [2,73]. We typically perform a kidney biopsy approximately two weeks after cessation of the offending drug if there has been no improvement in the kidney function over that time. However, clinicians wait a variable amount of time to allow for recovery before performing a biopsy. Some wait for three to four days, whereas others wait until the patient is approaching the need for kidney replacement therapy. ●Patients who present with advanced kidney failure, providing the onset of kidney failure is known to be relatively recent (ie, within three months). ●Patients with any features (such a




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The major histologic changes are interstitial edema and a marked interstitial infiltrate consisting primarily of T lymphocytes and monocytes (picture 2A-E) [2,9]. Eosinophils, plasma cells, and neutrophils also may be found. The classic lesion of "tubulitis" is found when inflammatory cells invade the tubular basement membrane (TBM).
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presented separately. ●(See "Treatment of acute interstitial nephritis".) ●(See "Kidney disease in sarcoidosis".) ●(See "Tubulointerstitial nephritis and uveitis (TINU syndrome)".) Histology — <span>The major histologic changes are interstitial edema and a marked interstitial infiltrate consisting primarily of T lymphocytes and monocytes (picture 2A-E) [2,9]. Eosinophils, plasma cells, and neutrophils also may be found. The classic lesion of "tubulitis" is found when inflammatory cells invade the tubular basement membrane (TBM). Some histologic features may suggest particular variants of AIN. As an example, granuloma formation is particularly characteristic of sarcoidosis, although it may be seen in any form of




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In some series, granuloma formation also suggests a greater likelihood of infection-induced AIN compared with AIN without granulomas
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me histologic features may suggest particular variants of AIN. As an example, granuloma formation is particularly characteristic of sarcoidosis, although it may be seen in any form of AIN [86]. <span>In some series, granuloma formation also suggests a greater likelihood of infection-induced AIN compared with AIN without granulomas. In a review of 40 biopsies of patients with granulomatous kidney disease (including 37 patients with interstitial nephritis, two with associated pauci-immune crescentic glomerulonephri




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However, in a number of other series, medication-induced interstitial nephritis was the leading cause of granulomatous interstitial nephritis, equaling or exceeding sarcoidosis in all.
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nd one with vasculitis), sarcoidosis was present in 20 patients (50 percent) and drug-induced and Mycobacterium infection present in seven (18 percent) and five (13 percent), respectively [87]. <span>However, in a number of other series, medication-induced interstitial nephritis was the leading cause of granulomatous interstitial nephritis, equaling or exceeding sarcoidosis in all. Infection is a more likely etiology in areas where infections associated with granulomatous disease are more common than in westernized countries [44]. As described above, other infecti




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Infection is a more likely etiology in areas where infections associated with granulomatous disease are more common than in westernized countries [44]. As described above, other infections that have been associated with granulomatous AIN include fungi (histoplasmosis, coccidioidomycosis), bacteria (Brucella, Chlamydia, Francisella), spirochetes (Treponema), and parasites (Leishmania, Toxoplasma) [43]
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ly [87]. However, in a number of other series, medication-induced interstitial nephritis was the leading cause of granulomatous interstitial nephritis, equaling or exceeding sarcoidosis in all. <span>Infection is a more likely etiology in areas where infections associated with granulomatous disease are more common than in westernized countries [44]. As described above, other infections that have been associated with granulomatous AIN include fungi (histoplasmosis, coccidioidomycosis), bacteria (Brucella, Chlamydia, Francisella), spirochetes (Treponema), and parasites (Leishmania, Toxoplasma) [43]. (See 'Infections' above.) Characteristic histologic features that suggest immunoglobulin G4 (IgG4)-related disease include the presence of TBM immune complex deposits and an increase i




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The urinalysis, for example, typically shows granular and epithelial cell casts and free epithelial cells in acute tubular necrosis; red cell casts, as well as red and white cells in acute glomerulonephritis; and few, if any, abnormalities in prekidney disease and obstruction.
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ed elsewhere. (See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".) In general, the urinary findings will distinguish AIN from other causes of AKI. <span>The urinalysis, for example, typically shows granular and epithelial cell casts and free epithelial cells in acute tubular necrosis; red cell casts, as well as red and white cells in acute glomerulonephritis; and few, if any, abnormalities in prekidney disease and obstruction. Among patients with a predominance of white blood cells and white blood cell casts, renal atheroemboli should be considered, particularly among older patients [88]. Similarly to AIN, re




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Among patients with a predominance of white blood cells and white blood cell casts, renal atheroemboli should be considered, particularly among older patients [88]. Similarly to AIN, renal atheroemboli may present with eosinophiluria, eosinophilia, and skin lesions. However, atheroemboli are more commonly associated with a reticular pattern (livedo reticularis) and digital infarcts, whereas AIN is associated with a characteristic rash that is diffuse and maculopapular
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free epithelial cells in acute tubular necrosis; red cell casts, as well as red and white cells in acute glomerulonephritis; and few, if any, abnormalities in prekidney disease and obstruction. <span>Among patients with a predominance of white blood cells and white blood cell casts, renal atheroemboli should be considered, particularly among older patients [88]. Similarly to AIN, renal atheroemboli may present with eosinophiluria, eosinophilia, and skin lesions. However, atheroemboli are more commonly associated with a reticular pattern (livedo reticularis) and digital infarcts, whereas AIN is associated with a characteristic rash that is diffuse and maculopapular. The history may also distinguish between AIN and renal atheroemboli. Many atheroemboli occur in the setting of atherosclerotic cardiovascular disease and are preceded by an endovascula




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Among patients who have a completely negative sediment, as in all patients with AKI of obscure origin, obstruction should be considered as part of the differential diagnosis. Imaging studies (usually an ultrasound) generally exclude the presence of obstruction, except in rare cases when the diagnosis of AKI is made within the first two to three days
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rocedure. (See "Clinical presentation, evaluation, and treatment of renal atheroemboli" and "Clinical presentation, evaluation, and treatment of renal atheroemboli", section on 'Risk factors'.) <span>Among patients who have a completely negative sediment, as in all patients with AKI of obscure origin, obstruction should be considered as part of the differential diagnosis. Imaging studies (usually an ultrasound) generally exclude the presence of obstruction, except in rare cases when the diagnosis of AKI is made within the first two to three days (see "Clinical manifestations and diagnosis of urinary tract obstruction and hydronephrosis", section on 'Diagnosis'). In all patients, imaging should be done prior to kidney biopsy. ES




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Less commonly, a drug is not identified or suspected. Among such patients, a histologic diagnosis of AIN should provoke a search for underlying infection and systemic disorders including systemic lupus erythematosus (SLE), sarcoidosis, Sjögren's syndrome, tubulointerstitial nephritis and uveitis (TINU) syndrome, and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis
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ases of AIN are caused by a drug. A careful review of medications, including the timing of initiation in relation to the onset of acute kidney injury (AKI), may reveal the likely culprit agent. <span>Less commonly, a drug is not identified or suspected. Among such patients, a histologic diagnosis of AIN should provoke a search for underlying infection and systemic disorders including systemic lupus erythematosus (SLE), sarcoidosis, Sjögren's syndrome, tubulointerstitial nephritis and uveitis (TINU) syndrome, and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. In some cases, histologic features may suggest the underlying disease that is associated with AIN. As an example, granulomas are more likely to be seen in patients with sarcoidosis tha




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Among patients who have AIN that is not believed to be related to a drug, we perform the following tests:

● Chest radiograph to evaluate for sarcoidosis, tuberculosis, and other infections. Among patients in whom the chest radiograph is nondiagnostic, a high-resolution chest computed tomography (CT) should be obtained to evaluate for sarcoidosis.

● Serum levels of angiotensin-converting enzyme (ACE) and measurement of serum calcium and urinary calcium excretion to evaluate for sarcoidosis.

● A purified protein derivative (PPD) to exclude tuberculosis, particularly in granulomatous AIN.

● Serologic tests, in select cases, to exclude histoplasmosis, coccidioidomycosis, toxoplasmosis, and Epstein-Barr virus (EBV). Urinary antigen test to exclude Legionella infection and urine culture to exclude leptospirosis.

● ANCA to exclude ANCA-associated vasculitides.

● Antinuclear antibody (ANA) and double-stranded DNA (dsDNA) to exclude SLE.

● C3 and C4 to evaluate for SLE and IgG4-related disease and hypocomplementemic AIN. These tests, however, neither diagnose nor exclude these disorders.

● Anti-Ro/SSA, anti-La/SSb antibodies, C-reactive protein, and rheumatoid factor to exclude Sjögren's syndrome.

● Serum protein electrophoresis.

● Slit lamp examination in patients with eye pain or redness to evaluate for tubulointerstitial nephritis and uveitis (TINU syndrome).

● The diagnostic evaluation of a particular infection-related AIN should be guided by extrarenal clinical manifestations.

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enters. Such histologic features, although often suggestive, are not diagnostic, and, in general, the etiology of non-drug-related AIN must be established by means other than the kidney biopsy. <span>Among patients who have AIN that is not believed to be related to a drug, we perform the following tests: ●Chest radiograph to evaluate for sarcoidosis, tuberculosis, and other infections. Among patients in whom the chest radiograph is nondiagnostic, a high-resolution chest computed tomography (CT) should be obtained to evaluate for sarcoidosis. ●Serum levels of angiotensin-converting enzyme (ACE) and measurement of serum calcium and urinary calcium excretion to evaluate for sarcoidosis. ●A purified protein derivative (PPD) to exclude tuberculosis, particularly in granulomatous AIN. ●Serologic tests, in select cases, to exclude histoplasmosis, coccidioidomycosis, toxoplasmosis, and Epstein-Barr virus (EBV). Urinary antigen test to exclude Legionella infection and urine culture to exclude leptospirosis. ●ANCA to exclude ANCA-associated vasculitides. ●Antinuclear antibody (ANA) and double-stranded DNA (dsDNA) to exclude SLE. ●C3 and C4 to evaluate for SLE and IgG4-related disease and hypocomplementemic AIN. These tests, however, neither diagnose nor exclude these disorders. ●Anti-Ro/SSA, anti-La/SSb antibodies, C-reactive protein, and rheumatoid factor to exclude Sjögren's syndrome. ●Serum protein electrophoresis. ●Slit lamp examination in patients with eye pain or redness to evaluate for tubulointerstitial nephritis and uveitis (TINU syndrome). ●The diagnostic evaluation of a particular infection-related AIN should be guided by extrarenal clinical manifestations. NSAID-INDUCED AIN AND NEPHROTIC SYNDROME — Nonsteroidal antiinflammatory drugs (NSAIDs) may cause AIN with an interstitial infiltrate composed primarily of T lymphocytes, with the nephr




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How NSAIDs produce AIN and nephrotic syndrome are not known; it is possible that COX inhibition by the NSAID results in the preferential conversion of arachidonic acid to leukotrienes, which can then activate helper T cells.
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n but probably can be induced by any nonselective NSAID. There have also been case reports of selective cyclooxygenase (COX)-2 inhibitors also being associated with this pattern of injury [92]. <span>How NSAIDs produce AIN and nephrotic syndrome are not known; it is possible that COX inhibition by the NSAID results in the preferential conversion of arachidonic acid to leukotrienes, which can then activate helper T cells. Affected patients typically present with hematuria, pyuria, white cell casts, proteinuria, and an acute rise in the plasma creatinine concentration. The full picture of an allergic reac




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Affected patients typically present with hematuria, pyuria, white cell casts, proteinuria, and an acute rise in the plasma creatinine concentration. The full picture of an allergic reaction (fever, rash, eosinophilia, and eosinophiluria) is typically absent, but one or more of these findings may be present. Spontaneous recovery generally occurs within weeks to a few months after therapy is discontinued [75,89]. All NSAIDs should be terminated in patients suspected of having NSAID-induced AIN. Since topically administered NSAIDs can be systemically absorbed, such therapy should also be terminated [93].
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rotic syndrome are not known; it is possible that COX inhibition by the NSAID results in the preferential conversion of arachidonic acid to leukotrienes, which can then activate helper T cells. <span>Affected patients typically present with hematuria, pyuria, white cell casts, proteinuria, and an acute rise in the plasma creatinine concentration. The full picture of an allergic reaction (fever, rash, eosinophilia, and eosinophiluria) is typically absent, but one or more of these findings may be present. Spontaneous recovery generally occurs within weeks to a few months after therapy is discontinued [75,89]. All NSAIDs should be terminated in patients suspected of having NSAID-induced AIN. Since topically administered NSAIDs can be systemically absorbed, such therapy should also be terminated [93]. There is no definitive evidence that corticosteroid therapy is beneficial in this setting. However, a course of prednisone may be considered in patients whose kidney failure persists mo




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There is no definitive evidence that corticosteroid therapy is beneficial in this setting. However, a course of prednisone may be considered in patients whose kidney failure persists more than one to two weeks after the NSAID has been discontinued [2]. (See "Treatment of acute interstitial nephritis".)
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All NSAIDs should be terminated in patients suspected of having NSAID-induced AIN. Since topically administered NSAIDs can be systemically absorbed, such therapy should also be terminated [93]. <span>There is no definitive evidence that corticosteroid therapy is beneficial in this setting. However, a course of prednisone may be considered in patients whose kidney failure persists more than one to two weeks after the NSAID has been discontinued [2]. (See "Treatment of acute interstitial nephritis".) Such patients should avoid the subsequent administration of NSAIDs. Relapse may occur with rechallenge [94]. SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelin




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