The pathogenic mechanisms that lead to chronic kidney disease (CKD) converge on a
common pathway that results in progressive interstitial fibrosis, peritubular capillary loss with
hypoxia, and destruction of functioning nephrons because of tubular atrophy. Interstitial
recruitment of inflammatory leukocytes and myofibroblasts occurs early in kidneys destined
to develop fibrosis. Circulating monocytes are recruited by locally secreted chemoattractant
molecules, facilitated by leukocyte adhesion molecules. Functionally heterogeneous …