Comment on “The time-averaged serum uric acid can better predict the prognosis of IgA nephropathy”

Dear Editor, We read with great interest the article by Qi et al. published in Nutrition, Metabolism & Cardiovascular Diseases on the role of timeaveraged serum uric acid (TA-SUA) in predicting the prognosis of IgA nephropathy (IgAN) [1]. This study aligns with previous findings that support the role of SUA as a biomarker for kidney damage, but it emphasizes TA-SUA as a more precise and reliable prognostic predictor in IgAN. As demonstrated by several prior studies on primary glomerulonephritis, a significant linear correlation has been established between SUA levels and the progression of renal injury [2]. This relationship is mechanistically linked to renin-angiotensin-aldosterone system hyperactivation, endothelial dysfunction, oxidative stress, sustained chronic inflammation, and hypoxia-driven pathways, all of which contribute to renal hemodynamic alterations and fibrotic remodeling [3]. These pathophysiological mechanisms are in agreement with the findings of the Authors [1], who demonstrated that persistently elevated SUA levels are associated with histopathological alterations, particularly increased interstitial fibrosis and significant tubular atrophy. This observation is consistent with the results of our recent study, ‘Serum Uric Acid/Serum Creatinine Ratio and Chronic Vascular Lesions on Renal Biopsy: A Retrospective Observational Study’, conducted on a cohort of patients with primary glomerulonephritis, which demonstrated the harmful effect of SUA not only on the glomerular disease progression but also in interstitial fibrous, tubular atrophy and vascular lesions [4]. A substantial contribution to the current knowledge concerning the cardiovascular implications of SUA has been made and contributed by the Italian URic acid Right for heArt Health (URRAH) project. The URRAH study has confirmed, over the years, the link between high SUA levels and cardiorenal complications, and also supports evidence suggesting a role in the development of arteriolar damage [5]. In the analysis of TA-SUA underscores the critical importance of longitudinal monitoring of SUA levels rather than relying on isolated measurements. Over the past decades, the prognostic role of SUA has been the subject of ongoing debate. However, several studies have demonstrated that indexing SUA values against additional parameters, such as the Serum Uric Acid/Serum Creatinine Ratio, significantly enhances the robustness and discriminative power of this measurement in predicting disease progression, affecting both renal and clinical outcomes in patients with cardiorenal multimorbidity [4,6]. Qi et al. demonstrates that the integration of TA-SUA assessment is a more precise approach for data standardization, enhancing its usefulness in clinical risk stratification and prognosis [1]. In conclusion, we acknowledge the authors for their valuable contribution. These findings further validate the use of uric acid as a clinical biomarker for kidney disease and underscore the necessity of accounting for its dynamic variations. The methodological approach and analysis presented provide significant insights for both research and clinical practice, laying the groundwork for further exploration in this field.