Published online Sep 6, 2016. doi: 10.5527/wjn.v5.i5.398
Peer-review started: March 19, 2016
First decision: April 19, 2016
Revised: April 20, 2016
Accepted: June 27, 2016
Article in press: June 29, 2016
Published online: September 6, 2016
Processing time: 168 Days and 12.4 Hours
Chronic kidney disease (CKD) patients are endangered with the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the fatalities. Cardiovascular calcifications affect most of the CKD patients. Most of this calcification is related to disturbed renal phosphate handling. Fibroblast growth factor 23 and klotho deficiency were incriminated in the pathogenesis of vascular calcification through different mechanisms including their effects on endothelium and arterial wall smooth muscle cells. In addition, deficient klotho gene expression, a constant feature of CKD, promotes vascular pathology and shares in progression of the CKD. The role of gut in the etio-pathogenesis of systemic inflammation and vascular calcification is a newly discovered mechanism. This review will cover the medical history, prevalence, pathogenesis, clinical relevance, different tools used to diagnose, the ideal timing to prevent or to withhold the progression of vascular calcification and the different medications and medical procedures that can help to prolong the survival of CKD patients.
Core tip: The last 2 decades witnessed the failure of all intervention studies targeting different risk factors of vascular calcification in chronic kidney disease (CKD) patients on regular hemodialysis. The main aim of all these studies was to decrease cardiovascular morbidity and mortality among such patients. These disappointing results criticized the value of such interventions in clinical practice. On the other hand, when similar trials were run on patients at an earlier stage of CKD, most of these trials showed a significant impact on patient survival and/or cardiovascular morbidity. Such discrepancy indicates the value of timing of interference. We are trying in this review to develop the ideal strategy that would optimize the management of CKD patients to avoid the devastating vascular calcification, highlighting the value of different medicines used in this plan. Meanwhile we are showing the update in guidelines concerned with this issue.