SAA1 and renal fibrosis: Accordingly, transient increases in the acute-phase protein SAA stimulates multiple molecular responses that include bolstering antioxidant elements via the master regulator Nrf-2 (a direct response to oxidative stress) and the induction of pro-inflammatory and pro-fibrotic pathways that manifest as both renal and vascular dysfunction in the short term (at 4 weeks) and renal fibrosis and potentiated atherosclerosis in the longer term (at 16 weeks).