Association between pro- and anti-inflammatory cytokines (IL-6, IL-10), hypothyroidism, and glomerular filtration rate in chronic kidney disease

Abstract

Objective: Hypothyroidism and chronic kidney disease (CKD) frequently coexist and may potentiate systemic inflammation, but the cytokine dynamics underlying this interaction remain poorly understood. This study assessed the relationship between pro‑inflammatory (IL‑6) and anti‑inflammatory (IL‑10) cytokines, hypothyroidism, and estimated glomerular filtration rate (eGFR) in patients with chronic kidney failure.

Methods: A case‑control study was conducted at two tertiary hospitals in Thi‑Qar, Iraq, involving 100 male participants divided into four equal groups (n=25 each): isolated hypothyroidism, isolated CKD, combined hypothyroidism+CKD, and healthy controls. Serum IL‑6, IL‑10, anti‑thyroid peroxidase (anti‑TPO), thyroid‑stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), urea, creatinine, and eGFR were measured using electrochemiluminescence immunoassay.

Results: Compared with controls, all patient groups exhibited a pro‑inflammatory shift characterised by elevated IL‑6 (highest in combined group: 41.42±18.44 vs 14.51±3.66 pg/mL, p<0.001) and reduced IL‑10 (lowest in CKD: 4.91±3.23 vs 8.02±2.23 pg/mL, p<0.001). The combined group showed the most severe thyroid dysfunction (TSH: 17.14±13.19 mIU/L; FT3: 1.37±0.23 pmol/L) and the strongest inverse correlation between IL‑6 and eGFR (r=‑0.68, p=0.0001).

Conclusion: Co‑existing hypothyroidism and CKD produce a synergistic pro‑inflammatory state with marked cytokine imbalance and aggravated renal‑thyroid crosstalk. Integrated management targeting inflammatory pathways may improve outcomes in this high‑risk population.