A large new prospective study using data from the UK Biobank shows that cumulative social disadvantage—measured using a score based on 15 social health factors—is associated with a higher risk of chronic kidney disease (CKD) and a poorer prognosis for those already affected. The study, published in Science China Life Sciences, also identifies plasma metabolome and proteome signatures that could partially explain these associations. DOI: 10.1007/s11427-025-3354-5
The polysocial risk score (PsRS) was calculated from 15 factors across the areas of economic stability, education, access to healthcare, housing, and social and community environment. The study included 279.548 participants without CKD at baseline and 19.761 patients with existing CKD.
Over a median follow-up of approximately 13 years, 6.628 new cases of CKD, 3.724 cardiovascular events, and 2.486 deaths were documented. Each one-point increase in the PsRS was associated with a 12 percent higher risk of developing CKD (adjusted HR 1,12; 95 percent CI 1,11–1,14). In CKD patients, the cardiovascular risk increased by 8 percent (HR 1,08; 95 percent CI 1,07–1,10), and the risk of all-cause mortality increased by 12 percent (HR 1,12; 95 percent CI 1,10–1,14). Compared to individuals with low socioeconomic disadvantage, participants with moderate and high socioeconomic disadvantage had a 27 percent and 78 percent higher risk of CKD, respectively. It is estimated that approximately 24,7 percent of new cases of CKD, 17,0 percent of cardiovascular events and 24,7 percent of deaths could be attributed to moderate or high social disadvantage.
The study also identified a metabolomic signature with 94 metabolites—primarily from amino acid and fatty acid metabolism as well as lipoproteins—and a proteomic signature with 428 proteins mainly involved in immune and inflammatory responses, cell signaling, and fibrosis. Mediation analyses indicate that the proteomic signature mediates the association much more strongly than the metabolomic signature. An unhealthy lifestyle explained only a small portion of the associations.
The authors emphasize that the PsRS is not a diagnostic tool and cannot replace clinical diagnosis. The study is observational and cannot prove causality. The UK Biobank cohort consists predominantly of people of European descent and may be subject to healthy volunteer bias.
