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Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin

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Drug-induced acute interstitial nephritis.

Mark A Perazella¹, Glen S Markowitz

¹Section of Nephrology, Yale University School of Medicine, FMP 107, 330 Cedar Street, New Haven, CT 06520-8029, USA.

Nature Reviews. Nephrology

|June 3, 2010

Summary

Acute interstitial nephritis (AIN), often drug-induced, is a key cause of acute kidney injury. Early recognition and discontinuing the drug can improve kidney function, though biopsy is definitive for diagnosis.

Area of Science:

Nephrology
Pathology
Pharmacology

Background:

Acute interstitial nephritis (AIN) is a frequent cause of acute kidney injury (AKI).
Drug-induced AIN accounts for the majority of cases (60-70%).
AIN involves interstitial inflammation, tubulitis, and edema, potentially leading to fibrosis.

Purpose of the Study:

To review the etiologies, diagnosis, and management of acute interstitial nephritis.
To highlight the significance of drug-induced AIN and its clinical implications.
To emphasize the importance of early recognition for favorable prognosis.

Main Methods:

Review of literature on AIN etiologies, clinical presentation, diagnosis, and treatment.
Analysis of diagnostic utility of kidney biopsy versus noninvasive tests.

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Evaluation of therapeutic strategies, including drug discontinuation and corticosteroid use.

Main Results:

Drug-induced AIN is the most common form, with varied presentations based on drug class.
Kidney biopsy remains the gold standard for definitive AIN diagnosis.
Discontinuing the offending agent is the primary treatment; corticosteroids may benefit selected patients.

Conclusions:

Early identification and withdrawal of causative agents are critical for managing drug-induced AIN.
Prompt treatment can lead to partial or complete recovery of kidney function.
Untreated or delayed diagnosis of AIN may progress to chronic kidney disease.