Abstract
Acute interstitial nephritis (AIN) may be the result of indirect injury by drugs, reaction to systemic infections, direct renal infection (viral and selected bacteria), humoral immune responses (anti-tubular basement membrane disease), hereditary and metabolic disorders, and obstruction and reflux in the acute stages. Similar changes can also be observed in the kidney in systemic diseases such as lupus erythematosus and in transplant rejection. Acute tubulointerstitial nephritis also occurs to varying degrees in association with glomerulonephritides. This section is largely confined to the drug-induced, reactive, idiopathic, and immunologic disorders inducing AIN. Acute interstitial nephritis usually presents with acute renal failure, often oliguric; it is sometimes associated with systemic manifestations, such as arthralgia, fever, eosinophilia, and rash, typically as a consequence of drug hypersensitivity [1–3].
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Fogo, A.B., Cohen, A.H., Colvin, R.B., Jennette, J.C., Alpers, C.E. (2014). Acute Interstitial Nephritis. In: Fundamentals of Renal Pathology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-39080-7_13
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DOI: https://doi.org/10.1007/978-3-642-39080-7_13
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