There is still considerable confusion over certain forms of renal disease where the main changes are in the interstitium and the tubular system. To this group, the name interstitial nephritis has been given, and although exception can be taken to this term because of its lack of precision, it remains a useful one to retain until such time as its constituents become unraveled. The main characteristics are the presence in the interstitium of variable numbers of inflammatory cells (usually mononuclears, lymphocytes, and plasma cells, with smaller numbers of eosinophils in some instances and polymorphonuclear leukocytes in others), accompanied by variable degrees of tubular atrophy or loss. The interstitium is edematous in some cases and fibrous in others. Acute and chronic forms are recognized, and are dealt with separately in this review. It must be admitted at the outset that this is a motley group, with numerous etiologies and doubtless many pathogenetic mechanisms. It is the failure to recognize that the kidney has a limited number of ways in which to respond to a large number of stimuli that has caused so much confusion over the diagnosis of chronic pyelonephritis (also a separate chapter) - for example, because the end result of bacterial infection of the kidney is only one of the conditions contributing to the picture of the chronic form of interstitial nephritis. It must also be added that, whereas the term interstitial nephritis is reserved for those cases in which there is no primary glomerular damage, there is frequently a conspicuous interstitial reaction in patients with glomerulonephritis. Indeed it is from such cases that many of the notions on the pathogenesis of interstitial nephritis are derived.
|Original language||English (US)|
|Number of pages||23|
|Journal||American Journal of Pathology|
|State||Published - Dec 1 1976|
ASJC Scopus subject areas
- Pathology and Forensic Medicine