Drug-Induced Acute Kidney Injury
Open accessAbstract
Medications are a common cause of AKI, especially for patients admitted to hospital wards and the intensive care unit. Although drug-related kidney injury occurs through different mechanisms, this review will focus on three specific types of tubulointerstitial injury. Direct acute tubular injury develops from several medications, which are toxic to various cellular functions. Their excretory pathways through the proximal tubules contribute further to AKI. Drug-induced AKI may also develop through induction of inflammation within the tubulointerstitium. Medications can elicit a T cell–mediated immune response that promotes the development of acute interstitial nephritis leading to AKI. Although less common, a third pathway to kidney injury results from the insolubility of drugs in the urine leading to their precipitation as crystals within distal tubular lumens, causing a crystalline-related AKI. Intratubular obstruction, direct tubular injury, and localized inflammation lead to AKI. Clinicians should be familiar with the pathogenesis and clinical-pathologic manifestations of these forms of kidney injury. Prevention and treatment of AKI relies on understanding the pathogenesis and judiciously using these agents in settings where AKI risk is high.
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Infection as AIN etiology requires continuation of current antibiotic therapy or even an increase in dose without immunosuppressant therapy.
“infection as AIN etiology requires the continuation of current antibiotic therapy or even an increase in dose without the need for immunosuppressant therapy [13–15]”
From The diagnosis of acute interstitial nephritis caused by infection versus antibiotic-induced interstitial nephritis: a narrative review (2024) · cites this paper as [15]
In patients with infection-induced AIN, steroids may increase the risk of immunosuppression, which could worsen the infection.
“In patients with infection-induced AIN, steroids may increase the risk of immunosuppression, which could worsen the infection.”
From The diagnosis of acute interstitial nephritis caused by infection versus antibiotic-induced interstitial nephritis: a narrative review (2024) · cites this paper as [15]
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Ultrasensitive chemiluminescent probe activated by NAG for real-time monitoring of AKI
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- Authors
- Perazella, M. A., & Rosner, M. H.
- Affiliations
- Veterans Health Administration (US)
- University of Virginia Health System (US)
- Corresponding author
- Perazella, Mark A.
- Venue
- Clinical Journal of the American Society of Nephrology
- Published
- 2022-08
- Volume
- 17
- Issue
- 8
- Pages
- 1220-1233
- ISSN
- 1555-9041 (ISSN-L)
- 1555-905X
- PMC
- PMC9435983
- OpenAlex
- W4220970233
- Cited by
- 357
- References
- 9
- Citations by year
- 2026: 94 · 2025: 100 · 2024: 87 · 2023: 65 · 2022: 10 · 2018: 1
- FWCI
- 9.85
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Journal of the American Society of Nephrology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Nephrotoxicity and Medicinal Plants
- Health Sciences › Medicine › Pathology and Forensic Medicine › Chemotherapy-induced organ toxicity mitigation
- Keywords
- drug-induced acute kidney injury, interstitial nephritis, acute tubular injury, acute interstitial nephritis, T cell immunity, drug toxicity, AKI pathogenesis, AKI prevention
- MeSH terms
- Humans, Inflammation, Kidney, Kidney Tubules, Proximal, Nephritis, Interstitial, Acute Kidney Injury
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