**7. Outlook**

Pharmaceutical treatments currently applied in clinical routine o ffer no adequate solution to treating or preventing CV calcification in CKD. Currently, we have no clear evidence that direct targeting CV calcification leads to an improvement in CV outcomes in CKD and ESRD patients. Still, vitamin K supplementation diminished the progression of aortic valve calcification and subsequently affected the cardiac and clinical outcomes in CVD patients without CKD [119], giving hope that future developments will yield the must needed treatment option to reduce CV risk in CKD patients. In experimenal CKD rodent models, new promising therapeutic interventions and potential drug targets to decrease CKD-induced calcification and prevent or reverse pathophysiological CV complications have recently been shown. However, no single animal model thoroughly reproduces the complexity of CV calcification in CKD and all attendant comorbidities. For this reason, it is essential to agree on a consistent animal model within this research area to maintain comparability.

**Author Contributions:** Designed the review, performed literature search, carried out interpretation, and drafted the manuscript, A.H. and C.C.; contributed to the review concept, participated in interpretation, and aided in overall manuscript development, C.G. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was funded by grants from the German Research Foundation (GO1801/5-1 SFB/TRR219 C02 to CG) and the START-Program of the Faculty of Medicine, RWTH Aachen (to CG).

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