Abstract
Dear Editor,
The recent article by Can et al 1 addresses a question of genuine clinical relevance: whether a composite inflammatory marker can reliably identify ST-segment elevation myocardial infarction (STEMI) patients at heightened risk for contrast-induced nephropathy (CIN) before primary percutaneous coronary intervention (pPCI). The finding that the Inflammatory Prognostic Index (IPI) independently predicted CIN with an area under the curve (AUC) of 0.826—outperforming the neutrophil-to-lymphocyte ratio (NLR), C-reactive protein-to-albumin ratio (CAR), and systemic immune-inflammation index (SII)is noteworthy, particularly given that NLR and CAR lost significance in multivariate analysis despite being significant in univariate models. This is probably the first study specifically evaluating IPI in STEMI patients undergoing pPCI. The composite structure of IPI, integrating both cellular and biochemical inflammatory pathways, provides a plausible mechanistic explanation for its superior discriminative performance.
Reviewing the data, the relationship between smoking and CIN warrants closer attention. Active smokers were substantially less likely to develop CIN in this cohort (44.7% vs 69.2%, P < .001), a finding that runs counter to the prevailing assumption that smoking worsens renal outcomes. 2 This pattern likely reflects the well-described “smoker’s paradox” in acute coronary syndromes: smokers in this setting tend to present at a younger age with fewer comorbidities, conferring an apparent protective effect that is largely explained by differences in baseline risk profile rather than a true biological benefit of smoking.3,4 Since smoking was not entered into the multivariate model, despite its strong univariate association with CIN, residual confounding cannot be excluded. Whether the independent effect of IPI is maintained after formal adjustment for smoking status is a point worth addressing in future analyses.
A separate observation concerns contrast volume. Despite CIN patients exhibiting more complex coronary anatomy—higher rates of multivessel disease, greater stent numbers, and higher SYNTAX scores (P = .032)—contrast volumes did not differ significantly between groups (160 vs 150 mL, P = .545). One would reasonably expect greater contrast exposure in procedurally complex cases. Whether operators selectively limited contrast in perceived high-risk patients, or whether the urgency of pPCI constrained procedural variability, cannot be determined from the current data. Reporting the contrast volume-to-estimated glomerular filtration rate (eGFR) ratio as a continuous covariate in future models would allow a more individualized assessment of contrast-related renal risk and would complement the predictive value of IPI, as this ratio has been validated as an independent predictor of CIN in patients undergoing PCI. 5
Finally, while the comparative analysis across inflammatory indices is well executed, the study does not assess whether IPI provides incremental predictive value beyond the Mehran Risk Score (MRS), the most widely validated pre-procedural tool for CIN risk stratification after PCI.6,7 This comparison could show that IPI adds predictive value over an established composite score through net reclassification improvement or integrated discrimination improvement analyses. This would provide a much stronger rationale for its integration into routine practice.
The above points are raised in the spirit of scientific dialogue. The study makes a solid contribution to the growing literature on inflammation-based risk markers in STEMI, and the practical accessibility of IPI from routine admission bloods makes it a promising candidate for early risk assessment. Prospective validation addressing these points would considerably strengthen its clinical case.
