Lupus nephritis (LN) is an autoimmune disease that occurs when autoantibodies complex with self-antigen and form immune complexes that accumulate in the glomeruli. These immune complexes initiate an inflammatory response resulting in glomerular injury. LN often concomitantly affects the tubulointerstitial compartment of the kidney, leading first to interstitial inflammation and subsequently to interstitial fibrosis and atrophy of the renal tubules if not appropriately treated. Presently the only way to assess interstitial inflammation and fibrosis is through kidney biopsy, which is invasive and cannot be repeated frequently. Hence, monitoring of disease progression and response to therapy is suboptimal. In this paper we describe a mathematical model of the progress from tubulointerstitial inflammation to fibrosis.We demonstrate how the model can be used to monitor treatments for interstitial fibrosis in LN with drugs currently being developed or used for nonrenal fibrosis.
|Original language||English (US)|
|Number of pages||6|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|State||Published - Sep 30 2014|
All Science Journal Classification (ASJC) codes