| Title
of the article |
Transplant glomerulopathy. |
| Authors |
Cosio FG, Gloor JM, Sethi S, Stegall MD. |
| Journal
|
Am J Transplant. 2008 Mar;8(3):492-6 |
| Subject
Consultant |
V. Nickeleit |
| Score
(1 to 3 stars) |
* |
| Comments |
A nice review. The reader should, however, remember that transplant glomerulopathy, i.e. the duplication of the GBM, is not specific for an underlying cause, but it is rather induced by various forms of protracted endothelial cell injury ("thrombotic-microangiopathy-lik"). Thus, identical lesions are seen in: a) remodeling stages of thrombotic microangiopathies,b) late structural calcineurin inhibitor induced toxicity, and c) remodeling stages of rejection (antibody and/or cell mediated). Occasionally, even membranoproliferative gloemrulonephritides may mimic 'transplant glomerulopathies'. |