Acute or chronic infection is a major trigger of systemic inflammation, which can simultaneously elevate PLR (via neutrophilia and lymphopenia) and exacerbate renal anemia (via hepcidin upregulation, impaired EPO production, and shortened red blood cell survival).[26] This creates a potential confounder: infection could independently drive both elevated PLR and reduced Hb, mimicking a direct association between PLR and anemia. The gene discussed is EPO; the disease is lymphopenia.