Pathophysiology of acute renal failure on a cellular level

Citation
C. Schwarz et al., Pathophysiology of acute renal failure on a cellular level, WIEN KLIN W, 112(1), 2000, pp. 5-15
Citations number
77
Categorie Soggetti
General & Internal Medicine
Journal title
WIENER KLINISCHE WOCHENSCHRIFT
ISSN journal
00435325 → ACNP
Volume
112
Issue
1
Year of publication
2000
Pages
5 - 15
Database
ISI
SICI code
0043-5325(20000114)112:1<5:POARFO>2.0.ZU;2-G
Abstract
The influence of inflammation on postischemic acute renal failure (ARF) has only recently be appreciated. In this review we therefore discuss the cell ular events occuring in ARF with special emphasis on the impact of inflamma tory processes on the pathogenesis of ARF. Furthermore, the spectrum of inj ury leading to sublethal or lethal cell damage and the time course, occurre nce and regulation of the two distinct forms of cell death, necrosis and ap optosis will be described extensively. Especially apoptosis and its regulat ion has been studied only marginally in the setting of ischemic ARF. This o verview is mainly focused on tubular cell injury since tubular epithelial c ells 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 epit helial cells to experimental ischemic renal failure in rats, and to clinica l settings of human ischemic ARF. The cellular events highlighted in this r eview are the influence of the expression of cellular adhesion molecules on the pathophysiology of ARF, and the regulation and time course of apoptosi s. Examples of these processes are being illustrated by figures exhibiting morphology and immunohistochemistry of cell proliferation and cell death re gulatory proteins.