**5. Conclusions**

In conclusion, this study is the first demonstration in a CKD model in vivo that hyperphosphatemia (or a Pi-dependent hormonal response derived from it) drives accumulation of pro-coagulant MVs, and hence identifies Pi as a clearly defined biochemical target for future measures to reduce thrombotic disease in CKD.

**Author Contributions:** Conceptualization, N.A., A.B., J.O.B., A.H.G., and N.J.B.; Data curation, N.A. and A.B.; Formal analysis, N.A. and A.B.; Funding acquisition, N.A., A.B., J.O.B., A.H.G., and N.J.B.; Investigation, N.A. and D.B.; Methodology, N.A. and A.B.; Project administration, N.A. and A.B.; Resources, N.A. and A.B.; Software, N.A. and A.B.; Supervision, A.B.; Validation, N.A. and A.B.; Visualization, N.A. and A.B.; Writing–original draft, N.A. and A.B.; Writing–review and editing, N.A., A.B., J.O.B., D.B., A.H.G., and N.J.B. All authors have read and agreed to the published version of the manuscript.

**Funding:** This study was supported by grant ref. RP30/July 2014 from Kidney Research UK.

**Acknowledgments:** The authors wish to thank the staff of the Division of Biomedical Services, University of Leicester for their valuable support in the animal work.

**Conflicts of Interest:** The authors declare no conflict of interest.
