Regardless of its etiology, chronic kidney disease (CKD) is characterized by proteinuria, serum creatinine retention, glomerulosclerosis (GS), and tubulointerstitial damage. Notably, the last one has been correlated more closely with the evolution to kidney failure than the extent of glomerular injury. Tubulointerstitial inflammation comprises the activation of tubular epithelial cells, which release inflammatory mediators and chemokines promoting the influx of leukocytes in the renal parenchyma and the activation/proliferation of resident fibroblasts, leading to excessive production of extracellular matrix (EM), fibrosis, and renal function loss. Therefore, inflammation exerts a key role in the pathogenesis of CKD, although the mechanisms by which this process is activated and perpetuated, even when the initial insult is not immune-mediated, such as in the hypertensive nephrosclerosis, in the diabetic nephropathy, and in the crystal-induced renal disease, remain unclear. This chapter provides an overview on inflammation and CKD development not related to autoimmunity or caused by presence of foreign antigens. Cellular and molecular mechanisms involved in different pathways and its potential therapeutic targets to detain the progression of inflammation and fibrosis in CKD are also presented ahead as a contribution in this book.
Part of the book: Chronic Kidney Disease