Synthetic and systems biology of kidney fibrosis Chronic Kidney Disease (CKD) is the progressive and irreversible loss of kidney function over time. Fibrosis is the pathophysiological hallmark of progressive CKD regardless of the initial aetiology and is characterized by fibroblast activation, accumulation of extracellular matrix, vascular rarefaction and tubular atrophy. It often coexists with, or is preceded by, inflammation however, what drives progressive fibrosis after resolution of inflammation is unclear. Moreover, the kidney is highly metabolically active organ and disruption of metabolic pathways has recently been associated with disease progression. In this study we aim to investigate the interplay between inflammation, fibrosis and metabolism in the progression of acute kidney injury to CKD, using an unbiased approach in both an invitro and an in vivo model.