Vascular calcification (VC) is the heterogeneous endpoint of multiple vascular insults, which varies by arterial bed, the layer of the arterial wall affected, and is propagated by diverse cellular and biochemical mechanisms. A variety of in vivo and ex vivo techniques have been applied to the analysis of VC in preclinical studies, but clinical examination has principally relied on a number of noninvasive and invasive imaging modalities for detection and quantitation. Most imaging methods suffer from suboptimal spatial resolution, leading to the inability to distinguish medial from intimal VC and insufficient sensitivity to detect microcalcifications that are indicative of active mineral deposition and of vulnerable plaques which may be prone to rupture. Serum biomarkers lack specificity for VC and cannot discriminate pathology. Overall, uncertainties surrounding the sensitivity and specificity of different VC testing modalities, the absence of a clear cause-effect relationship, and lack of any evidence-based diagnostic or therapeutic protocols in relation to VC testing in chronic kidney disease has yielded weak or ungraded recommendations for their use in clinical practice.