Abstract
It is well established that certain therapeutic agents can cause acute interstitial nephritis (AIN),* which is characterized histologically by interstitial edema, leukocytic infiltration, and tubular cell damage (Baldwin et al., 1968; McCluskey and Colvin, 1978). The infiltrate usually consists principally of mononuclear cells, most of which have the appearance of lymphocytes, but eosinophils are usually present, often in large numbers, and plasma cells, as well as small numbers of basophils, are frequently found. Tubules are often invaded by leukocytes and severe tubular damage may be seen. The glomeruli and blood vessels appear normal. In most cases there are no characteristic immunofluorescence findings and distinctive ultrastructural features are not seen.
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McCluskey, R.T., Bhan, A.K. (1982). Immunologic Mechanisms in Drug-Induced Acute Interstitial Nephritis. In: Porter, G.A. (eds) Nephrotoxic Mechanisms of Drugs and Environmental Toxins. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4214-4_34
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DOI: https://doi.org/10.1007/978-1-4684-4214-4_34
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