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Acute or allergic interstitial nephritis (AIN) is characterized by an acute rise in serum creatinine with fever, rash, eosinophilia, eosinouria, and by interstitial edema and cellular infiltration.
a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.
Acute interstitial nephritis is often caused by hypersensitivity to medications, especially B-lactam antibiotics, NSAIDs, sulfonamides, diuretics, anticonvulsants, proton pump inhibitors, and allopurinol.
Certain infections such as Legionnaire's disease, leptospirosis, and mononucleosis are also associated with AIN.
Inflammatory inflitrate within the interstitium onclude T cells, monocytes, and eosinophils. Interstitial edema follows.
Granulomas and interstitial fibrosis can occur over time.
Acute interstitial nephritis is characterized by sudden onset of clinical signs of renal dysfunction. Many people develop a systemic hypersensitivity reaction with fever, rash, peripheral eosinophilia and eosinophiluria. However, not all these characteristics are always present.
Physical findings include:
Urinalysis can demonstrate WBCs +/- RBCs and leukocyte casts. Wright's stain or Hansel's stain can be used to demonstrate the presence of eosinophils.
Mild to moderate proteinuria (usually <1g/day) is usually present.
Hyperkalemia, renal tubular acidosis, and renal sodium wasting may be present.
Rise in sCr over 2-3 weeks after exposure to offending agent; more rapid if re-exposure
eosinophilia and increased IgE
Hypertension and edema are uncommon in AIN, instead suggesting acute glomerulonephritis.
Discontinuing or substituting the offending drug is the primary treatment.
A short course of high-dose corticosteroids can help spped recovery, but must be weighed in balance of the added risk in patients with infections.
In most cases, renal function is restored within several weeks.
AIN is an important cause (10-20%) of acute renal failure.
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