# Association of triglyceride-glucose index and high-sensitivity C-reactive protein with contrast-induced nephropathy after percutaneous coronary intervention in patients with acute coronary syndrome: a retrospective cohort study

**Authors:** Guowei Tian, Caiyuan Qian, Zhihao Liu, Ye Xu, Li Yang, Liqun He

PMC · DOI: 10.3389/fcvm.2026.1733377 · Frontiers in Cardiovascular Medicine · 2026-02-11

## TL;DR

High triglyceride-glucose index and C-reactive protein levels increase the risk of kidney damage after heart procedures in patients with acute coronary syndrome.

## Contribution

Identifies a synergistic effect of TyG index and hs-CRP on contrast-induced nephropathy risk in ACS patients after PCI.

## Key findings

- TyG index and hs-CRP independently increase CIN risk with significant additive interactions.
- Optimal cutoffs of TyG ≥8.5 and hs-CRP ≥5.0 mg/L sharply increase CIN risk.
- The predictive model achieved an AUC of 0.780 for CIN risk assessment.

## Abstract

Contrast-induced nephropathy (CIN) remains a frequent and serious complication after percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) patients. The triglyceride-glucose (TyG) index, a marker of insulin resistance, and high-sensitivity C-reactive protein (hs-CRP), an inflammatory biomarker, may contribute to CIN development.

This retrospective cohort study included 1,818 ACS patients undergoing PCI between 2017 and 2024. Logistic regression, restricted cubic splines (RCS), and interaction analyses were performed to examine the nonlinear relationships and additive effects of TyG index and hs-CRP on CIN risk.

Multivariate logistic regression analysis indicated that both the TyG index (OR = 4.08, 95% CI: 2.95–5.71) and hs-CRP levels (OR = 1.07, 95% CI: 1.05–1.10) were significant independent risk factors for CIN (all P < 0.001). The RCS analysis revealed nonlinear associations between the TyG index, hs-CRP, and CIN risk (P < 0.001). Threshold effect analysis identified optimal cutoff values of TyG index ≥8.5 and hs-CRP ≥5.0 mg/L, beyond which CIN risk sharply increased. Patients with both TyG index ≥8.5 and hs-CRP ≥5.0 mg/L showed the highest CIN risk (adjusted OR = 8.356, 95% CI: 2.13–32.8), with significant additive interactions observed (RERI = 4.914, AP = 0.588, SI = 3.012). The predictive model demonstrated a robust area under the ROC curve (AUC = 0.780, 95% CI: 0.750–0.809), with sensitivity of 77.7% and specificity of 69.3%.

Elevated TyG index and hs-CRP levels independently and synergistically increase CIN risk in ACS patients after PCI. These findings highlight the interplay between metabolic and inflammatory pathways in CIN pathogenesis and may help identify high-risk individuals for early preventive strategies.

## Linked entities

- **Diseases:** acute coronary syndrome (MONDO:0005542)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** acute kidney injury (MESH:D058186), NSTEMI (MESH:D000072657), autoimmune diseases (MESH:D001327), CIN (MESH:D005119), metabolic dysfunction (MESH:D008659), stenosis (MESH:D003251), mitochondrial dysfunction (MESH:D028361), ACS (MESH:D054058), inflammation (MESH:D007249), pulmonary infection (MESH:D012141), disordered glucose metabolism (MESH:D044882), chronic kidney dysfunction (MESH:D051436), -induced (MESH:D000092582), malignant (MESH:D009369), DM (MESH:D003920), dysfunction (MESH:D006331), coronary artery disease (MESH:D003324), Renal Disease (MESH:D007674), UA (MESH:D000789), atherosclerotic (MESH:D050197), hematologic diseases (MESH:D006402), Hypertension (MESH:D006973), hyperglycemic (MESH:D006944), thrombosis (MESH:D013927), IR (MESH:D007333), chronic kidney failure (MESH:D007676), cardiovascular disease (MESH:D002318), Thrombolysis in Myocardial Infarction (MESH:D009203)
- **Chemicals:** advanced glycation end products (MESH:D017127), aspirin (MESH:D001241), nitric oxide (MESH:D009569), cholesterol (MESH:D002784), sodium chloride (MESH:D012965), TG (MESH:D014280), iohexol (MESH:D007472), polyol (MESH:C024617), reactive oxygen species (MESH:D017382), creatinine (MESH:D003404), glucose (MESH:D005947), heparin (MESH:D006493), ticagrelor (MESH:D000077486), clopidogrel (MESH:D000077144), ACEI (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

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## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12932434/full.md

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Source: https://tomesphere.com/paper/PMC12932434