ArticleCritical care (London, England)2022
Serum IL-17 levels are higher in critically ill patients with AKI and associated with worse outcomes.
Article in Critical care (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- CRAC channels as targets for immunotherapy.Current opinion in immunology · 2026Review
- Interferon-γ and interleukin-17A associations with vascular dysfunction following paediatric cardiac surgery with cardiopulmonary bypass.Cardiology in the young · 2026Article
- Inhibition of Calcium Release-Activated Calcium Channels to Treat Acute Kidney Injury: Design and Rationale of the KOURAGE Study a Randomized Trial.American journal of nephrology · 2026Article
- Review
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Protective effect and mechanism of Xiaoyu Xiezhuo decoction on ischemia-reperfusion induced acute kidney injury based on gut-kidney crosstalk.Renal failure · 2024Article
- The immune regulatory role of lymphangiogenesis in kidney disease.Journal of translational medicine · 2024Review
- The renoprotective activity of amikacin-gamma-amino butyric acid-chitosan nanoparticles: a comparative study.Inflammopharmacology · 2024Article
- Heterogeneity in the definition of major adverse kidney events: a scoping review.Intensive care medicine · 2024Article
- Molecular mechanisms underlying the renal protective effects of coenzyme Q10 in acute kidney injury.Cellular & molecular biology letters · 2022Review
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8 authors.
Funding
Abstract
backgroundInterleukin-17 (IL-17) antagonism in rats reduces the severity and progression of AKI. IL-17-producing circulating T helper-17 (TH17) cells is increased in critically ill patients with AKI indicating that this pathway is also activated in humans. We aim to compare serum IL-17A levels in critically ill patients with versus without AKI and to examine their relationship with mortality and major adverse kidney events (MAKE).
methodsMulticenter, prospective study of ICU patients with AKI stage 2 or 3 and without AKI. Samples were collected at 24-48 h after AKI diagnosis or ICU admission (in those without AKI) [timepoint 1, T1] and 5-7 days later [timepoint 2, T2]. MAKE was defined as the composite of death, dependence on kidney replacement therapy or a reduction in eGFR of ≥ 30% from baseline up to 90 days following hospital discharge.
resultsA total of 299 patients were evaluated. Patients in the highest IL-17A tertile (versus lower tertiles) at T1 had higher acuity of illness and comorbidity scores. Patients with AKI had higher levels of IL-17A than those without AKI: T1 1918.6 fg/ml (692.0-5860.9) versus 623.1 fg/ml (331.7-1503.4), p < 0.001; T2 2167.7 fg/ml (839.9-4618.9) versus 1193.5 fg/ml (523.8-2198.7), p = 0.006. Every onefold higher serum IL-17A at T1 was independently associated with increased risk of hospital mortality (aOR 1.35, 95% CI: 1.06-1.73) and MAKE (aOR 1.26, 95% CI: 1.02-1.55). The highest tertile of IL-17A (vs. the lowest tertile) was also independently associated with higher risk of MAKE (aOR 3.03, 95% CI: 1.34-6.87). There was no effect modification of these associations by AKI status. IL-17A levels remained significantly elevated at T2 in patients that died or developed MAKE.
conclusionsSerum IL-17A levels measured by the time of AKI diagnosis or ICU admission were differentially elevated in critically ill patients with AKI when compared to those without AKI and were independently associated with hospital mortality and MAKE.
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