Alcohol and acute kidney injury—prospective evidence from the UK Biobank in 250,791 alcohol consumers
Abstract
The relationship between alcohol consumption and acute kidney injury (AKI) is controversial. Current understanding is AKI develops secondary to alcohol-induced liver disease. However, in vitro and in vivo evidence suggests alcohol could cause renal damage directly. We investigated associations between incident AKI and consumption of spirits, beer, red wine and white wine, independent of liver disease. We also investigated associations between these drink types and neutrophils and C-reactive protein (CRP), as well as their interactions in association with AKI. UK Biobank involved baseline data collection from 22 assessment centres across the United Kingdom. The cohort consisted of 250,791 current alcohol consumers. Participants were followed for a median 14.0 years capturing incident AKI events. Alcohol intake (units/week), C-reactive protein (mg/L) level and neutrophil count (cells/µL) were captured at baseline. Alcohol intake was reported as units per week. After adjustment for covariables and/or potential confounders in Cox proportional hazard regression analyses, spirits (HR, 1.40; 95% CI, 1.30 to 1.50) and beer (HR, 1.24; 95% CI, 1.17 to 1.32) consumption were associated with AKI, while associations were absent for red wine (HR, 0.96; 95% CI, 0.90 to 1.02) and white wine (HR, 1.06; 95% CI, 0.98 to 1.14). Neutrophils and CRP increased by tertiles of spirits (both P -trend ≤ 0.001) and beer (both P -trend < 0.001) consumption, while decreases were observed by tertiles of red wine (both P -trend < 0.001) and white wine (both P -trend < 0.001) consumption. CRP (HR, 1.41; 95% CI, 1.34 to 1.47) and neutrophils (HR, 2.60; 95% CI, 2.25 to 3.01) associated with AKI and interactions existed with spirits (both P < 0.001) and beer (both P < 0.001) in association with AKI. Alcohol captured from spirits and beer consumption was associated with AKI, independent of liver disease. The significant interactions between inflammatory markers and spirits and beer consumption in association with AKI supports current in vitro and in vivo evidence proposing a direct mechanistic link.
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BibTeX
@article{schutte2026alcohol,
title = {{Alcohol and acute kidney injury—prospective evidence from the UK Biobank in 250,791 alcohol consumers}},
author = {Rudolph Schutte and Jufen Zhang and Barbara Pierscionek},
journal = {Scientific Reports},
year = {2026},
month = oct,
doi = {10.1038/s41598-026-76255-9},
url = {https://www.nature.com/articles/s41598-026-76255-9},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Alcohol and acute kidney injury—prospective evidence from the UK Biobank in 250,791 alcohol consumers
AU - Rudolph Schutte
AU - Jufen Zhang
AU - Barbara Pierscionek
PY - 2026
DA - 2026/10/20
JO - Scientific Reports
DO - 10.1038/s41598-026-76255-9
UR - https://www.nature.com/articles/s41598-026-76255-9
AB - The relationship between alcohol consumption and acute kidney injury (AKI) is controversial. Current understanding is AKI develops secondary to alcohol-induced liver disease. However, in vitro and in vivo evidence suggests alcohol could cause renal damage directly. We investigated associations between incident AKI and consumption of spirits, beer, red wine and white wine, independent of liver disease. We also investigated associations between these drink types and neutrophils and C-reactive protein (CRP), as well as their interactions in association with AKI. UK Biobank involved baseline data collection from 22 assessment centres across the United Kingdom. The cohort consisted of 250,791 current alcohol consumers. Participants were followed for a median 14.0 years capturing incident AKI events. Alcohol intake (units/week), C-reactive protein (mg/L) level and neutrophil count (cells/µL) were captured at baseline. Alcohol intake was reported as units per week. After adjustment for covariables and/or potential confounders in Cox proportional hazard regression analyses, spirits (HR, 1.40; 95% CI, 1.30 to 1.50) and beer (HR, 1.24; 95% CI, 1.17 to 1.32) consumption were associated with AKI, while associations were absent for red wine (HR, 0.96; 95% CI, 0.90 to 1.02) and white wine (HR, 1.06; 95% CI, 0.98 to 1.14). Neutrophils and CRP increased by tertiles of spirits (both P -trend ≤ 0.001) and beer (both P -trend < 0.001) consumption, while decreases were observed by tertiles of red wine (both P -trend < 0.001) and white wine (both P -trend < 0.001) consumption. CRP (HR, 1.41; 95% CI, 1.34 to 1.47) and neutrophils (HR, 2.60; 95% CI, 2.25 to 3.01) associated with AKI and interactions existed with spirits (both P < 0.001) and beer (both P < 0.001) in association with AKI. Alcohol captured from spirits and beer consumption was associated with AKI, independent of liver disease. The significant interactions between inflammatory markers and spirits and beer consumption in association with AKI supports current in vitro and in vivo evidence proposing a direct mechanistic link.
SN - 2045-2322
ER -