# Associations of leucocyte subtypes and platelet parameters with kidney cancer risk in the UK Biobank cohort

## TL;DR

This study finds that higher neutrophil and platelet counts, along with obesity, are linked to increased kidney cancer risk, suggesting immune and inflammatory pathways are involved.

## Contribution

The study identifies specific immune and platelet biomarkers prospectively associated with kidney cancer risk using a large cohort.

## Key findings

- Neutrophil count, C-reactive protein, platelet count, and BMI are positively associated with kidney cancer risk.
- Lymphocyte count and hip index are inversely associated with kidney cancer risk.
- C-reactive protein's association is stronger in the first six years of follow-up.

## Abstract

Kidney cancer is related to obesity and inflammation and platelets are involved in thrombo-inflammation, but the prospective associations of individual leucocyte subtypes and platelet parameters with kidney cancer risk are unclear.

Using data from the UK Biobank cohort and multivariable Cox proportional hazards models, we obtained hazard ratios (HR per one standard deviation increase) with 95% confidence intervals (95%CI) for the mutually adjusted associations of inflammatory markers and platelet parameters (log-transformed), and allometric obesity indices (body mass index (BMI), a body shape index (ABSI), hip index) with kidney cancer risk (overall, by sex, and by follow-up time with a cut-off at 6 years).

During a mean follow-up of 10.4 years, 1086 kidney cancers were ascertained in 396,482 participants. Conditional on each other and covariates, neutrophil count (HR = 1.12; 95%CI = 1.04 − 1.20), C-reactive protein (HR = 1.11; 95%CI = 1.04 − 1.19), platelet count (HR = 1.18; 95%CI = 1.10 − 1.27), platelet distribution width (HR = 1.16; 95%CI = 1.09 − 1.24), and BMI (HR = 1.22; 95%CI = 1.14 − 1.30) were positively associated, while lymphocyte count (HR = 0.90; 95%CI = 0.84 − 0.96) and hip index (HR = 0.88; 95%CI = 0.83 − 0.93) were inversely associated with kidney cancer risk in participants overall, but there was little evidence for an association with ABSI (HR = 1.05; 95%CI = 0.99 − 1.12). There were no major sex differences, but the positive association with C-reactive protein was observed only for shorter follow-up time (HR = 1.26; 95%CI = 1.14 − 1.38; p-follow-up = 0.0006).

Our findings support two separate longer-acting pathways in kidney cancer development– a pathway related to general rather than abdominal obesity and an immune-cell-related pathway involving neutrophils assisted by activated platelets, as well as a cancer-induced thrombo-inflammation closer to kidney cancer diagnosis.

The online version contains supplementary material available at 10.1186/s12950-025-00458-6.