**Should We Consider the Cardiovascular System While Evaluating CKD-MBD?**

### **Merita Rroji 1,\*, Andreja Figurek 2 and Goce Spasovski 3**


Received: 6 January 2020; Accepted: 20 February 2020; Published: 25 February 2020

**Abstract:** Cardiovascular (CV) disease is highly prevalent in the population with chronic kidney disease (CKD), where the risk of CV death in early stages far exceeds the risk of progression to dialysis. The presence of chronic kidney disease-mineral and bone disorder (CKD-MBD) has shown a strong correlation with CV events and mortality. As a non-atheromatous process, it could be partially explained why standard CV disease-modifying drugs do not provide such an impact on CV mortality in CKD as observed in the general population. We summarize the potential association of CV comorbidities with the older (parathyroid hormone, phosphate) and newer (FGF23, Klotho, sclerostin) CKD-MBD biomarkers.

**Keywords:** chronic kidney disease; uremic cardiopathy; left ventricular hypertrophy; phosphate; PTH; FGF23; klotho; sclerostin

**Key Contribution:** Although the managemen<sup>t</sup> of CKD patients was significantly improved, CV mortality continues to be at a higher rate. Here the impact of CKD-MBD has already extended beyond the role in the skeleton, so we tried to go from the candidate mineral disorder to cardiovascular abnormalities. Focusing on such toxins and/or their relevant mediators at early CKD stages might help to interfere on time with the vicious cycle of the cardio–renal connection and improve the outcome of the patients.
