Abstract
Chronic tubulointerstitial nephritis (TIN) is characterised histologically by tubular cell damage with interstitial changes consisting of infiltration with mononuclear cells in a matrix which is expanded with increased amounts of collagen, proteoglycans and fluid. Chronic TIN is a common final pathway towards chronic renal failure regardless of whether the primary insult is glomerular, as in glomerulonephritis or diabetes, or vascular, as in hypertension or renal ischaemia, or directly affects the tubulointerstitium. In this chapter, we therefore consider these conditions where TIN is the result of direct injury to the tubulointerstitium, focusing on the epidemiology, pathology and clinical presentation.
Almost universally, therapy directed at the chronic interstitial nephritides is given with the aim of preventing progressive renal injury and the development of interstitial fibrosis both directly and indirectly. Acceptable therapies exist but are as yet not fully evidence based with appropriately designed randomised clinical trials. Agents aimed at blocking other specific mediators (such as endothelin, PDGF and TGF-β[beta]1) are on the horizon but are still not available clinically.
Keywords
- Chronic Kidney Disease
- Renal Tubular Acidosis
- Aristolochic Acid
- Tubular Atrophy
- Nephrogenic Diabetes Insipidus
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Walker, R.G., Hewitson, T.D., Becker, G.J. (2014). Chronic Interstitial Nephritis. In: Fervenza, F., Lin, J., Sethi, S., Singh, A. (eds) Core Concepts in Parenchymal Kidney Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-8166-9_24
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