In chronic kidney disease, glomerular hyperperfusion and hypertension are controlled by angiotensin II, which initially enhances nephron filtration capacity and compensates for the decrease in glomerular filtration rate. However, angiotensin II is detrimental in the long term and results in further nephron loss. It also increases concentrations of transforming growth factor-beta (TGF-β), a powerful fibrogenic cytokine, which stimulates excessive production and deposition of extracellular matrix.