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PATHOLOGY OF RENAL INTERSTITIUM: ‐ESPECIALLY IN VARIOUS INFLAMMATORY DISEASES‐
Author(s) -
TAKAMIYA Haruo
Publication year - 1970
Publication title -
acta patholigica japonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
ISSN - 0001-6632
DOI - 10.1111/j.1440-1827.1970.tb03072.x
Subject(s) - pathology , renal pathology , medicine , kidney tubules , kidney
Studies were made with main emphasis on changes in the renal interstitium, using 301 cases including various forms of metabolic disease, drug‐induced nephritis, viral disease, scarlet fever, delayed sepsis, obsolete pulmonary abscess, various cases in the state of prolonged sensitization, various types of collagen disease and glomerulonephritis. Pyelonephritis was excluded from this study, because it was caused directly by bacterial infection. The results induced from the study are that there are two types of interstitial nephritis: the primary type which originates in the interstitium by way of the vascular system and the secondary type which first develops degeneration or necrosis in the tubular epithelium, being followed by an interstitial inflammation. In the former the changes of the interstitium are a simultaneous affair with those of the glomeruli. When diseases are in an allergic hyperergic condition, changes of the glomeruli are more conspicuous than those of the interstitium, though the lesions are diffuse and intense in both. With the state of prolonged sensitization of the diseases or in collagen disease, inflammatory processes become localized within a part of each glomerulus and focalized also in the interstitium, forming such lesions as collected lymphocytic infiltration, occasional lymph follicles or focal fibrosis with proliferation of capillaries and small vessels. When these focalized lesions are seen markedly in the interstitium, an introduction of the morphological expression “Primary interstitial nephritis” is necessary. In typical chronic primary interstitial nephritis, though small in number, the focal interstitial lesions stand out prominent, the glomerular changes being minimal and hyperazotemia is clinically manifest or may become a cause of death. ACTA PATH. JAP. 20: 279–309, 1970.

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