Hypersensitivity Phenomena and the Kidney: Role of Drugs and Environmental Agents

Adler, Sharon G.; Cohen, Arthur H.; Border, Wayne A.

doi:10.1016/s0272-6386(85)80002-0

Cited by 24 publications

(8 citation statements)

References 77 publications

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“…This is considerably less than the dose usually associated with production of the typical upper-torso skin rash associated with capto pril or the dose generally reported to produce nephroticrange proteinuria [19]. The findings, therefore, meet the minimal criteria, reviewed by Adler et al [20], for sus pecting an immunologic pathogenesis: (1) observed re sponse dissimilar to the known pharmacologic actions of the drug; (2) small doses of the drug are capable of pro ducing the effect, and (3) the adverse effect is reproduc ible on rechallenge.…”

Section: Discussionmentioning

confidence: 84%

Captopril-Associated Acute Interstitial Nephritis

Smith¹,

Neill

Cushman³

et al. 1989

Am J Nephrol

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A 57-year-old male with mild impairment of renal function secondary to diabetic glomerulosclerosis developed acute renal failure (creatinine 32.4 mg/dl) associated with a generalized desquamative skin rash and peripheral eosinophilia shortly after initiation of antihypertensive therapy with captopril. An acute interstitial nephritis was demonstrated on renal biopsy, and improvement was temporally related to initiation of therapy with prednisone. A review of the literature revealed 5 similar cases in whom acute deterioration of renal function occurred following initiation of captopril and in whom there were features of a hypersensitivity reaction, including skin rash, fever, eosinophilia, azotemia, eosinophiluria, and a Coombs-positive hemolytic anemia. Renal biopsy, where available, revealed an acute interstitial nephritis. Observations from these cases suggest that, of the angiotensin-converting enzyme inhibitors, this syndrome appears to be specific for captopril, begins within the 1 st month of therapy, is not dose-dependent, and generally resolves on cessation of therapy. Steroids may hasten recovery, but sufficient data are not available to confirm their efficacy.

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Section: Discussionmentioning

confidence: 84%

Captopril-Associated Acute Interstitial Nephritis

Smith¹,

Neill

Cushman³

et al. 1989

Am J Nephrol

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“…Acute allergic drug-induced interstitial nephritis can be caused by an ever-increasing number and variety of drugs, as shown in Table 1, including certain antibiotics (e.g., β-lactam antibiotics), NSAIDs, diuretics, anticonvulsants, and many compounds of miscellaneous application (Galpin et al, 1978;Kleinknecht et al, 1978;Cotran and Galvenek, 1979;Laberke and Bohle, 1980;Ellis et al, 1981;Appel and Kunis, 1983;Antonovych, 1984;Bender et al, 1984;Churg et al, 1984;Adler et al, 1985;Bertani et al, 1986;Pirani et al, 1987;Cameron, 1988;Hawkins et al, 1989;Pommer et al, 1989;Buysen et al, 1990;Greising et al, 1990;Rashed et al, 1990;Mathew, 1992;Murray and Keane, 1992;Ivanyi et al, 1992;Colvin and Fang, 1994;Perneger et al, 1994;Kelly and Neilson, 1996;Appel, 1997;Cavallo, 1998;Kashgarian, 1998;Michel and Kelly, 1998;Rocha and Fernando-Alonso, 2001;Woywodt et al, 2001;Henao et al, 2002;Markowitz et al, 2003a). First reported after the administration of sulfonamides, drug-induced interstitial nephritis is a somewhat common cause of renal insufficiency.…”

Section: Chemical-induced Nephropathy 75mentioning

confidence: 99%

“…Etiology/Pathogenesis: The drugs thought to work by an immunologic mechanism are those of the penicillin group (chiefly methicillin and rifampicin), diphenylhydantoin (dilantin), and phenindione, an anticoagulant (Galpin et al, 1978;Kleinknecht et al, 1978;Cotran and Galvenek, 1979;Appel and Kunis, 1983;Adler et al, 1985;Brunati et al, 1986;Cameron, 1988;Brentjens et al, 1989;Cheng et al, 1989;Colvin and Fang, 1994;Kleinknecht, 1995; and Neilson, 1996;Appel, 1997;Cavallo, 1998;Michel and Kelly, 1998). Other compounds seem to be dose dependent and include amphotericin, colistin, polymyxin B, the cephalosporins, and gentamicin.…”

Section: Clinical Featuresmentioning

confidence: 99%

Chemical-Induced Nephropathy: A Review of the Renal Tubulointerstitial Lesions in Humans

Silva¹

2004

Toxicol Pathol

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It is almost ironic that one of the major organs that serves to maintain the "internal milieux" by secretion of various toxic agents, can itself become injured in the process. The pattern of morphologic renal injury is nonspecific and can involve any of the components of the kidney, although the injury and subsequent morphologic changes are most commonly noted in the tubules and/or interstitium. Of course, unless the drug/toxin is commonly or regularly noted to be associated with tubular and/or interstitial injury, the association of the drug with the renal changes may be missed and the correlation may not necessarily identify causation. For example, if a drug is associated with a renal injury in a given individual, it may be quite difficult to prove that the drug is the cause of the injury. This scenario is somewhat reminiscent of the test question-is it "true-true-related," or "true-true-unrelated"? Sometimes it is only by the accrual of a great many examples or correlations, and or dissection of the pathophysiology, can it be shown that the drug is directly related to the observed morphologic (and subsequent clinical) injury. Renal changes induced by chemicals can affect the tubules, interstitium or both. This review of chemically induced nephropathy in humans considers acute tubular necrosis, interstitial nephritis, and tubulointerstitial nephritis or nephropathy. Because the tubules and the interstitium are so intimately related, injury to 1 of these 2 components may eventually lead to injury of the other, resulting in tubulointerstitial disease.

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“…The pathogenic rela tion between drug and nephropathy matches the chrono logical criteria of imputability [24], and suspension of the therapy was followed by a progressive, although slow, improvement of the renal function. Admittedly, this last fact, besides reexposure, is one of the best arguments in favour of the drug-AIN connection [II, 15,25], To show this cause-effect relationship, techniques have been pro posed such as the lymphoblastic transformation test and cutaneous reactions, but their results are inconsistent and sometimes difficult to interpret [25][26][27], On the other hand, the presence of granulomas without necrosis in con nection with AIN, as observed in this case, is very sugges tive of a hypersensitivity reaction to drugs [l. 2. 28].…”

Section: Discussionmentioning

confidence: 99%

Granulomatous Interstitial Nephritis Associated with Hydrochlorothiazide/Amiloride

Enríquez

Cabezuelo

González³

et al. 1995

Am J Nephrol

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A 74-year-old woman developed acute renal failure and granulomatous interstitial nephritis associated with hydrochlorothiazide/amiloride. On stopping the drug the renal function improved, but not significantly. Around 20 months after prednisone administration, the renal function had stabilized, with a moderate degree of renal insufficiency. The case is discussed, and some aspects of acute interstitial nephritis induced by diuretics are briefly reviewed.

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Hypersensitivity Phenomena and the Kidney: Role of Drugs and Environmental Agents

Cited by 24 publications

References 77 publications

Captopril-Associated Acute Interstitial Nephritis

Captopril-Associated Acute Interstitial Nephritis

Chemical-Induced Nephropathy: A Review of the Renal Tubulointerstitial Lesions in Humans

Granulomatous Interstitial Nephritis Associated with Hydrochlorothiazide/Amiloride

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