The Interplay between Inflammation and Fibrosis in Kidney Transplantation

Figure 2

Progression of fibrosis after kidney transplantation. Fibrosis is already present in a proportion of grafts, especially in renal allograft obtained from expanded criteria donors. Ischemia/reperfusion (I/R) injury and alloimmune response trigger inflammation and its severity is modulated by immunosuppressive treatment. Subclinical inflammation can be ameliorated by treatment with steroid boluses or by increasing exposure to immunosuppressive drugs. Quiescent interstitial fibrosis/tubular atrophy (IF/TA) may represent the healing of the inflammatory insult while inflammation in areas of fibrosis (i-F/TA) and antibody-mediated rejection (ABMR) due to the appearance of de novo donor specific antibodies (DSA) may represent an ongoing inflammatory response that is associated with decreased allograft survival.