These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Pathophysiology of acute renal failure at the cellular level].
    Author: Schwarz C, Gruber U, Oberbauer R.
    Journal: Wien Klin Wochenschr; 2000 Jan 14; 112(1):5-15. PubMed ID: 10689734.
    Abstract:
    The influence of inflammation on post-ischemic acute renal failure (ARF) has only recently be appreciated. In this review we therefore discuss the cellular events occurring in ARF with special emphasis on the impact of inflammatory processes on the pathogenesis of ARF. Furthermore, the spectrum of injury leading to sublethal or lethal cell damage and the time course, occurrence and regulation of the two distinct forms of cell death, necrosis and apoptosis will be described extensively. Especially apoptosis and its regulation has been studied only marginally in the setting of ischemic ARF. This overview is mainly focused on tubular cell injury since tubular epithelial cells are the major victims of ischemia whereas cells inside the glomerular tuft show only little pathology. The models of tubular injury described in this paper are ranging from primary cultures of isolated human tubular epithelial cells to experimental ischemic renal failure in rats, and to clinical settings of human ischemic ARF. The cellular events highlighted in this review are the influence of the expression of cellular adhesion molecules on the pathophysiology of ARF, and the regulation and time course of apoptosis. Examples of these processes are being illustrated by figures exhibiting morphology and immunohistochemistry of cell proliferation and cell death regulatory proteins.
    [Abstract] [Full Text] [Related] [New Search]