Renal Fibrosis in Lupus Nephritis

Fibrosis can be defined as a pathological process in which deposition of connective tissue replaces normal parenchyma. The kidney, like any organ or tissue, can be impacted by this maladaptive reaction, resulting in persistent inflammation or long-lasting injury. While glomerular injury has traditionally been regarded as the primary focus for classification and prognosis of lupus nephritis (LN), increasing attention has been placed on interstitial fibrosis and tubular atrophy as markers of injury severity, predictors of therapeutic response, and prognostic factors of renal outcome in recent years. This review will discuss the fibrogenesis in LN and known mechanisms of renal fibrosis. The importance of the chronicity index, which was recently added to the histological categorization of LN, and its role in predicting treatment response and renal prognosis for patients with LN, will be explored. A better understanding of cellular and molecular pathways involved in fibrosis in LN could enable the identification of individuals at higher risk of progression to chronic kidney disease and end-stage renal disease, and the development of new therapeutic strategies for lupus patients.

Automated summary

Fibrosis is a pathological process that can affect the kidney, leading to persistent inflammation or long-term injury. Recently, there has been increasing attention on interstitial fibrosis and tubular atrophy as markers of injury severity, predictors of treatment response, and prognostic factors for renal outcome in lupus nephritis (LN). This review explores the mechanisms of fibrogenesis in LN and the importance of the chronicity index in predicting treatment response and renal prognosis. Understanding the cellular and molecular pathways involved in fibrosis in LN could help identify individuals at higher risk of chronic kidney disease and develop new therapeutic strategies for lupus patients.