A high prevalence of vascular calcification (VC) and a high incidence of cardiovascular events are two key complications of chronic kidney disease. Since most observational studies found a positive association between these two complications, a causal relationship has been assumed. If so, this would render VC a target of therapy. Recent studies, however, suggested this assumption might be an oversimplification. The fundamental aspects of these recent studies are two-fold. The first novel insight is that VC is not a single entity. VC can be the consequence of a wide range of different biological processes, but also of pharmacological interventions. Sometimes it is the underlying process that carries the additional risk, and sometimes it is tissue calcification itself. Both calcium-containing phosphate binders and statin therapy are associated with an increase in VC, but with divergent effects on cardiovascular risk. Moreover, VC can have different anatomical and histological locations. The second novel insight is that the assumption of a straightforward linear association between the amount of VC and risk for clinical events can be challenged. In this review we summarize recent literature that should lead to reconsidering the implications of VC in CKD. This includes an overview of the many different pathways underlying the ultimate occurrence of VC. Finally, we present a nuanced view concerning the pathophysiologic and therapeutic implications of the different types of calcification in patients with chronic kidney disease.