In the article "Transfused Macrophages Ameliorate Pancreatic and Renal Injury in Murine Diabetes Mellitus" [Nephron Exp Nephrol. 2011;118(4):e87-99; https://doi.org/10.1159/000321034] by Zheng et al., the authors noted there was an error in Figure 6a.Fig. 6.Deactivation of endogenous kidney macrophages (EM) by M2 macrophages. a EM (CD11b+DiI-) were separated from STZ mice transfused with M2 macrophages by FACS sorting at day 70. b EM were isolated from kidney from each group at day 70, mRNA expression of cytokines was examined by real-time PCR. *p < 0.01 vs. diabetic control and diabetic-M0. Data represent mean ± SD, n = 7 per group.An error occurred during the figure assembly that resulted in the incorrect image being selected for Figure 6a. The authors have cross-referenced the replacement image against the original raw flow cytometry (FCS) files and laboratory notebooks and have confirmed there is no impact on the conclusions.The corrected Figure 6 is shown here.

This narrative review examines the intricate relationship between chronic kidney disease-mineral and bone disorder (CKD-MBD) and vascular calcification (VC), with particular emphasis on hyperphosphatemia-driven pathological mechanisms and the recognized limitations of existing therapeutic approaches. We further explore emerging strategies designed to address the "phosphate storm" phenomenon in chronic kidney disease (CKD), offering a comprehensive analysis derived from recent clinical studies and mechanistic research. Our evaluation specifically focuses on three central aspects: dysregulated phosphate metabolism in VC progression, the clinical and physiological constraints of conventional phosphate binders, and novel interventions such as Tenapanor, vitamin K2, and magnesium supplementation. Data were synthesized from a wide array of sources including epidemiological studies, animal models, and clinical trials, leading to four principal findings: 1.From the perspective of expert opinion, early intervention is proposed as a hypothesis-generating strategy. Phosphate-lowering therapy could be initiated when serum phosphate exceeds 3.9 mg/dL or FGF-23 is elevated. This threshold is an exploratory reference and is not endorsed by high-quality clinical evidence or international guidelines. 2.Tenapanor, either as monotherapy or in combination with phosphate binders, vitamin K2 and magnesium, effectively decreases intestinal phosphate absorption and may overcome the drawbacks of conventional treatments. Large and long-term clinical trials are required to confirm its safety and efficacy for routine clinical use. 3. Multimodal monitoring could include not only serum phosphate but also FGF-23, dp-ucMGP, and annual VC assessment. 4. Based on expert opinions, we developed a triad balance strategy and put forward exploratory reference ranges for serum phosphate, serum magnesium and corrected calcium. These values are not formal guideline targets and require further clinical validation. In conclusion, while phosphate-centric management fails to halt VC, multitargeted strategies-integrating controlled phosphate absorption, anti-calcification agents, and personalized monitoring-show strong potential to improve CKD-MBD outcomes. This review proposes paradigm-shifting strategies to bridge the gap between biochemical control and actual prevention of VC.