Acute interstitial nephritis
Open accessAbstract
Acute interstitial nephritis (AIN) represents a frequent cause of acute kidney injury, accounting for 15-27% of renal biopsies performed because of this condition. By and large, drug-induced AIN is currently the commonest etiology of AIN, with antimicrobials and nonsteroidal anti-inflammatory drugs being the most frequent offending agents. Pathogenesis is based on an immunologic reaction against endogenous nephritogenic antigens or exogenous antigens processed by tubular cells, with cell-mediated immunity having a major pathogenic role. The characteristic interstitial infiltrates, mostly composed of lymphocytes, macrophages, eosinophils, and plasma cells, experience a rapid transformation into areas of interstitial fibrosis. A significant proportion of AIN has nowadays an oligosymptomatic presentation, although the presence of specific extrarenal symptoms such as fever, skin rash, arthralgias, and peripheral eosinophilia has an important role to orientate clinical diagnosis. Identification and removal of the offending drug are the mainstay of the treatment, but recent studies strongly suggest that early steroid administration (within 7 days after diagnosis) improves the recovery of renal function, decreasing the risk of chronic renal impairment. Delayed steroid treatment, when interstitial fibrosis has taken place, would have a less pronounced or nule therapeutic benefit.
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Direct cytopathic effects of microbial antigens or cytokine-mediated inflammation may explain renal injury in infection-associated AIN.
“the direct cytopathic effects of microbial antigens or cytokine-mediated inflammation may be the explanation for the renal injury [14, 51]”
From The diagnosis of acute interstitial nephritis caused by infection versus antibiotic-induced interstitial nephritis: a narrative review (2024) · cites this paper as [14]
The Definition and Etiology section says microbial antigens may elicit an immune reaction and that inflammatory infiltrates produce cytokines that amplify inflammation and promote fibrosis. It does not describe direct cytopathic effects of microbial antigens as an explanation for renal injury. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe amoxicillin-clavulanate case demonstrates an idiosyncratic immune response, with no correlation between the dose or duration of therapy.
“This case demonstrates an idiosyncratic immune response, with no correlation between the dose or the duration of amoxicillin–clavulanate therapy [6, 14, 77].”
From The diagnosis of acute interstitial nephritis caused by infection versus antibiotic-induced interstitial nephritis: a narrative review (2024) · cites this paper as [14]
The Definition and Etiology section describes drug-induced acute interstitial nephritis as an immune reaction with a dose-independent character, supporting the idiosyncratic-response point. The Conservative Treatment section says treatment duration has not shown a clear correlation with serum creatinine at follow-up—not that the occurrence of the reaction is unrelated to treatment duration. Neither passage addresses the specific amoxicillin–clavulanate case (page numbers unavailable in our copy). (LLM, conf=0.87)
Experimental — accuracy not yet measuredInfection 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 [14]
The Definition and Etiology section identifies infection-related AIN, but the Treatment of Other Types of AIN section gives no treatment recommendation for it. Searches for infection-related AIN treatment and antibiotic dosing found no passage advising continuation or an increased dose of antibiotics without immunosuppressant therapy. The recommendation to withdraw an offending drug concerns drug-induced AIN, a different etiology. (LLM, conf=0.74)
Experimental — accuracy not yet measuredIn 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 [14]
The Clinical Features section discusses AIN secondary to infectious diseases, but not steroid treatment in those patients. The Steroid Treatment and Treatment of Other Types of AIN sections discuss steroids for other forms of AIN; searches for infection-induced AIN, immunosuppression, and worsening infection found no passage addressing the claimed risk. (LLM, conf=0.73)
Experimental — accuracy not yet measured
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- Authors
- Praga, M., & González, E.
- Affiliations
- Hospital Universitario 12 De Octubre (ES)
- Corresponding author
- Praga, Manuel
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 77
- Issue
- 11
- Pages
- 956-961
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2091234866
- Cited by
- 507
- References
- 36
- Citations by year
- 2026: 31 · 2025: 32 · 2024: 43 · 2023: 46 · 2022: 39 · 2021: 32 · 2020: 26 · 2019: 42 · 2018: 32 · 2017: 25 · 2016: 24 · 2015: 35 · 2014: 32 · 2013: 23 · 2012: 23
- FWCI
- 2.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Kidney International (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Nephrotoxicity and Medicinal Plants
- Keywords
- acute interstitial nephritis, acute kidney injury, drug-induced nephrotoxicity, nonsteroidal anti-inflammatory drugs, antimicrobial agents, cell-mediated immunity, interstitial fibrosis, corticosteroid therapy, renal biopsy, pathogenesis
- MeSH terms
- Acute Disease, Animals, Humans, Kidney Tubules, Nephritis, Interstitial, Predictive Value of Tests, Risk Factors, Steroids, Time Factors, Treatment Outcome, Disease Progression, Recovery of Function
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