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Higher C-reactive protein-to-lymphocyte ratio linked to proteinuric CKD in hypertensive patientsBlood marker ratio linked to kidney disease risk in people with high blood pressure

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Key Takeaway
Consider CLR as a potential marker for proteinuric CKD risk in hypertension, but recognize evidence is observational.

This retrospective cohort study analyzed 5,904 hypertensive patients with preserved baseline kidney function over a median follow-up of 34.1 months. The exposure was the C-reactive protein-to-lymphocyte ratio (CLR), and the primary outcomes were incident proteinuric CKD, isolated eGFR decline, and any incident CKD.

Higher CLR was independently associated with proteinuric CKD, with a hazard ratio of 1.14 per 1-SD increase and 1.46 for the highest versus lowest quartile. Of the cohort, 598 participants developed proteinuric CKD. For any incident CKD (728 participants), the HR was 1.13 per 1-SD increase. No significant association was found for isolated eGFR decline (89 participants, HR 1.05). A significant additive interaction (RERI 0.30) was observed between high CLR and uncontrolled blood pressure, suggesting synergistic amplification of renal risk. Adding CLR to traditional risk models improved risk reclassification (NRI 0.083, P = 0.008).

Safety and tolerability data were not reported. Key limitations include the retrospective, observational design, which precludes causal inference. The findings suggest CLR may help identify hypertensive patients at higher risk for proteinuric CKD, particularly those with uncontrolled blood pressure, who might benefit from more vigilant proteinuria surveillance. However, this marker requires prospective validation before clinical implementation.

Researchers looked at whether a simple ratio from a standard blood test could help predict kidney disease in people with high blood pressure. They studied 5,904 patients who started with normal kidney function, tracking them for about three years. The ratio combined C-reactive protein (a marker of inflammation) and lymphocyte count (a type of white blood cell).

They found that patients with a higher ratio were more likely to develop a specific type of chronic kidney disease where protein leaks into the urine. This link remained even after accounting for other risk factors. However, the ratio was not linked to a different type of kidney decline based only on a filtering rate measurement.

The study also found that having both a high ratio and uncontrolled blood pressure appeared to combine for an even greater risk. Adding this ratio to traditional risk models slightly improved their ability to classify patients' risk. No safety issues were reported because this was an observational study looking at data, not testing a treatment.

It's important to remember this was a retrospective study, meaning it looked back at existing medical records. This type of research can find associations but cannot prove that the blood marker causes kidney disease. The results suggest this simple ratio might one day help doctors identify which patients with high blood pressure need closer monitoring for kidney health.

What this means for you:
A blood marker ratio was linked to kidney disease risk in an observational study, but more research is needed.

Study Details

Study typeCohort
EvidenceLevel 3
PublishedApr 2026
View Original Abstract ↓
BackgroundResidual kidney risk persists in hypertensive patients despite guideline-directed blood pressure (BP) management. Whether systemic inflammation is preferentially associated with the development of distinct early chronic kidney disease (CKD) phenotypes remains uncertain.MethodsThis retrospective cohort study included 5,904 hypertensive patients with preserved baseline kidney function. The primary exposure was the C-reactive protein-to-lymphocyte ratio (CLR). Outcomes assessed were incident proteinuric CKD, isolated estimated glomerular filtration rate (eGFR) decline, and any incident CKD. Phenotype-specific associations were evaluated using multivariable cause-specific Cox models. We additionally assessed the additive interaction between CLR and BP control, and evaluated the incremental predictive value of CLR beyond traditional risk factors.ResultsDuring a median follow-up of 34.1 months, 598 participants developed proteinuric CKD, 89 developed isolated eGFR decline, and 728 developed any incident CKD. Higher CLR was independently associated with proteinuric CKD (per 1-SD: HR 1.14, 95% CI 1.05–1.24; highest vs lowest quartile: HR 1.46, 95% CI 1.15–1.85) and any incident CKD (per 1-SD: HR 1.13, 95% CI 1.05–1.22), but not with isolated eGFR decline (per 1-SD: HR 1.05, 95% CI 0.85–1.29). A significant additive interaction emerged between high CLR and uncontrolled BP (RERI 0.30), synergistically amplifying renal risk. Adding CLR to traditional risk models significantly improved risk reclassification (NRI 0.083, P = 0.008).ConclusionsIn hypertensive patients, elevated CLR preferentially predicts new-onset proteinuria over isolated eGFR decline. As an accessible biomarker for renal risk stratification, CLR can identify patients requiring vigilant proteinuria surveillance and comprehensive management, particularly those with uncontrolled BP.
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