New Biomarkers in Acute Tubulointerstitial Nephritis: A Novel Approach to a Classic Condition
Open accessAbstract
Acute tubulointerstitial nephritis (ATIN) is an immunomediated cause of acute kidney injury. The prevalence of ATIN among the causes of acute kidney injury (AKI) is not negligible, especially those cases related to certain drugs. To date, there is a lack of reliable non-invasive diagnostic and follow-up markers. The gold standard for diagnosis is kidney biopsy, which shows a pattern of tubulointerstitial leukocyte infiltrate. The urinalysis findings can aid in the diagnosis but are no longer considered sensitive or specific. Atthe present time, there is a rising attentiveness tofinding trustworthy biomarkers of the disease, with special focus in urinary cytokines and chemokines that may reflect kidney local inflammation. Cell-based tests are of notable interest to identify the exact drug involved in hypersensitivity reactions to drugs, manifesting as ATIN. Certain single-nucleotide polymorphisms in HLA or cytokine genes may confer susceptibility to the disease according to pathophysiological basis. In this review, we aim to critically examine and summarize the available evidence on this topic.
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MCP-1 level may be elevated in infection-induced AIN due to its significant role in recruitment of monocytes, neutrophils and lymphocytes in tissue inflammation.
“it is possible that the level of monocyte chemoattractant protein-1 (MCP-1) is elevated in infection-induced AIN due to its significant role in the recruitment of monocytes, neutrophils and lymphocytes in tissue inflammation processes [63].”
From The diagnosis of acute interstitial nephritis caused by infection versus antibiotic-induced interstitial nephritis: a narrative review (2024) · cites this paper as [63]
Section 4 states that MCP-1 recruits monocytes, neutrophils, and lymphocytes and reports elevated MCP-1 in drug-induced ATIN and in a cohort with ATIN from different causes. The Introduction identifies infections as a cause of ATIN, but the paper does not report MCP-1 levels specifically in infection-induced cases. The proposed elevation in that subgroup is therefore a plausible extrapolation, not a finding the source establishes. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe absence of pyuria does not exclude the diagnosis of AIN.
“However, the absence of pyuria does not exclude the diagnosis [63].”
From The diagnosis of acute interstitial nephritis caused by infection versus antibiotic-induced interstitial nephritis: a narrative review (2024) · cites this paper as [63]
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Cites
Urine TNF-α and IL-9 for clinical diagnosis of acute interstitial nephritis
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Mechanisms of Drug-Induced Interstitial Nephritis
Raghavan, R., & Shawar, S. (2017) · Advances in Chronic Kidney Disease · doi:10.1053/j.ackd.2016.11.004 · Cited by 117 · see citing works
Clinical Approach to Diagnosing Acute and Chronic Tubulointerstitial Disease
Perazella, M. A. (2017) · Advances in Chronic Kidney Disease · doi:10.1053/j.ackd.2016.08.003 · Cited by 79 · see citing works
Urinary Sediment Findings in Acute Interstitial Nephritis
Fogazzi, G. B., Ferrari, B., Garigali, G., Simonini, P., & Consonni, D. (2012) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2012.05.002 · Cited by 71 · see citing works
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Sorted by citations
Muhammad, A., Zhang, Y., Huang, L., Yuan, Q., Wang, W., Pu, J., Lin, W., Tang, R., & Xiao, X. (2024) · Clinical Kidney Journal · doi:10.1093/ckj/sfae054 · Cited by 13 · see citing works
“There is a growing interest in finding cell-based tests that can identify the exact drug involved in hypersensitivity reactions to drugs, manifesting as AIN or ATIN [63 ].”
BackgroundInfluential
- Authors
- Martinez Valenzuela, L., Draibe, J., Fulladosa, X., & Torras, J.
- Affiliations
- Bellvitge University Hospital, Nephrology Department, Hospitalet de Llobregat, 08907 Barcelona, Spain
- Bellvitge University Hospital (ES)
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-06-30
- Volume
- 21
- Issue
- 13
- Pages
- 4690
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7369789
- OpenAlex
- W3038453963
- Cited by
- 19
- References
- 5
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 5 · 2023: 3 · 2022: 5 · 2021: 1 · 2020: 1
- FWCI
- 0.40
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- 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, biomarkers, acute kidney injury, drug-induced nephrotoxicity, urinary cytokines, renal inflammation, hypersensitivity, cytokine gene polymorphisms, non-invasive diagnosis
- MeSH terms
- Humans, Nephritis, Interstitial, T-Lymphocytes, Biomarkers, Chemokines, Genetic Predisposition to Disease
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