Reasons for this are not clear, but may include inflammation and CRP being more pronounced in GN thereby playing a more prominent role in the development of CVD; albuminuria reflecting local renal pathology in GN patients instead of being a marker of endothelial dysfunction and CV risk as it is in the general and all-cause CKD populations; and [5, 6, 10, 31]. This evidence concerns the gene CRP and chronic kidney disease.