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Dear Editor, We read with great interest the recent article by Waseem et al investigating the protective role of nicorandil against contrast-induced nephropathy (CIN) among patients undergoing cardiac catheterization[1].CIN remains a challenging and concerning complication after angiographic and interventional procedures often leaving clinicians with less preventive options. That said, we would like to offer a few reflections that might be useful for future research on this topic. This editorial adheres to the TITAN 2025 guidelines for the transparent reporting of AI-assisted content[2]. First, the study account outcomes upto 72 hours post procedure which is insufficient to estimate the long-term renoprotective effect of nicorandil such as the prevention of chronic kidney disease progression[3]. This limits the clinical applicability of their findings and is the major limitations of the study itself. Future studies should include long follow-up period. Second, the studies included used a varying range of nicorandil doses (5–20 mg), but the authors do not discuss how this variation might influence the overall pooled effect[4]. This oversight significantly limits the transitional value of their findings and limits the applicability for clinicians whether the proposed benefit comes from the specific dosage regimen. Future studies should ensure the use of standardized and consistent drug administration protocols to enhance comparability and reliability findings. This manuscript complies with TITAN guidelines[5]. Third, changes in serum creatinine are the sole basis for diagnosis for CIN, which is questionable since this parameter is a rather late and insensitively measured indicator of renal injury. Early or subclinical sensations of renal injury would have easily evaded the conventional measure because serum creatinine levels may rise within 24–48 hours after injury and are subject to alteration by non-renal variables. This may in turn lead to the underestimation of the incidence of CIN and exaggeration of the protective effect of nicorandil. More sensitive biomarkers such as NGAL and IL-18 can measure renal injury much earlier and with greater accuracy[6]. Future studies should include early biomarkers alongside serum creatinine to better capture subclinical kidney injury. In addition, the analysis could not determine the contrast volumes or whether the media were iso-osmolar or low-osmolar because these two factors are independent it helps for the prediction of CIN. Lower volumes of contrast as well as safer contrast agents would usually predispose a patient to lower risk, making it all the more challenging to estimate the effect of nicorandil without this adjustment[5]. Future research should be adjusted for contrast dose and outcome measures by media type to avoid confounding. In conclusion, while the study by Waseem et al adds to the growing evidence on nicorandil’s potential renoprotective role, several methodological limitations restrict the strength of its conclusions. Addressing issues of follow-up duration, dosage variability, outcome measures, and confounding contrast factors would enhance reliability. Future well-designed trials are warranted to clarify the true clinical benefit of nicorandil in preventing CIN. Ethical approval Not applicable. Consent Not appliable.