Injury to the interstitium of the kidney is regarded as a common pathway leading to end-stage
renal insufficiency, regardless of etiology. Tubular
interstitial nephritis is characterized histologically by inflammatory changes in the tubulointerstitial compartment, such as interstitial
edema, leukocyte infiltration, accumulation of
extracellular matrix proteins, tubular dilation and
atrophy. Acute
interstitial nephritis is often associated with use of drugs, such as β-
lactam antibiotics and non-steroidal anti-inflammatory drugs, and is likely mediated through allergic mechanisms. On the other hand, chronic progressive tubular
interstitial nephritis has a much more diverse etiology, ranging from
infection and drugs to immune-mediated, hematologic, metabolic and hereditary disorders. Experimental studies in the past decade have focused mainly on common factors and mechanisms underlying chronic tubulointerstitial injury, such as activation of peritubular fibroblasts, leukocyte infiltration, release of inflammatory
cytokines and
growth factors at affected regions, epithelial-mesenchymal transition of tubular epithelium, and apoptosis. The execution of each is mediated by a number of local stimuli, such as filtered
albumin, chronic
hypoxia and oxidative stress, in addition to
cytokines and
growth factors. This chapter provides an overview of acute and chronic tubular
interstitial nephritis, according to clinical manifestations of the disease. It also provides insight into common pathways underlying chronic tubular
interstitial nephritis based on recent advances in translational and experimental research.