Chronic Kidney Disease (CKD) is an emerging public health priority that affects 10-12% of the population, and >50% of the elderly have signs of CKD. The predominant early vascular ageing process mediated by medial vascular calcification (arteriosclerosis) and plaque formation (atherosclerosis) results in a marked discrepancy between chronological and biological vascular age in CKD. Our aim is to characterize different cell types based on gene expression data and/or cell clonal architecture from data on somatic mutations among CKD patients. For this purpose, we will analyze arteries from patients with atherosclerosis, including atherosclerotic plaques in addition to neighboring non-plaque regions and CKD patients with arteries that have various degree of media calcification, and healthy control arteries. To begin with, the somatic mutations are called, we will analyse the relationship between somatic mutation load (mutation burden) and the expression patterns of signature genes at single-cell resolution. Different clinical parameters of the patients (e.g., Age) will be compared with the obtained correlative patterns to determine the clonal complexity of CKD.