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The glomerulo‐tubular junction: a target in renal diseases
Author(s) -
Lindop G. B. M.,
Gibson I. W.,
Downie T. T.,
Vass D.,
Cohen E. P.
Publication year - 2002
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1087
Subject(s) - glomerulus , nephron , proteinuria , renal tubule , kidney glomerulus , pathology , fibrosis , kidney , medicine , biology , anatomy , glomerulonephritis
Both global and segmental glomerulopathies may damage specific areas of the renal glomerulus. Diseases associated with glomerular hyperperfusion cause lesions at the vascular pole, while diseases associated with proteinuria often damage the tubular pole. Atubular glomeruli are now known to be plentiful in a variety of common renal diseases. These glomeruli are disconnected from their tubule at the tubular pole and therefore cannot participate in the production of urine. It is widely believed that the disconnection is a result of external compression by periglomerular fibrosis. However, the variable anatomy and cell populations within both the glomerulus and the beginning of the proximal tubule at the glomerulo‐tubular junction may also have important roles to play in the response to damage at this sensitive site of the nephron. Copyright © 2002 John Wiley & Sons, Ltd.

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