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NDT Advance Access originally published online on June 22, 2004
Nephrology Dialysis Transplantation 2005 20(2):261-266; doi:10.1093/ndt/gfh182
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Nephrol Dial Transplant Vol. 20 No. 2 © ERA–EDTA 2004; all rights reserved


Editorial Comment

Whispers and shouts in the pathogenesis of acute renal ischaemia

Michael S. Goligorsky

Departments of Medicine and Pharmacology, Renal Research Institute and Division of Nephrology, New York Medical College, Valhalla, New York, USA

Correspondence and offprint requests to: Michael S. Goligorsky, Departments of Medicine and Pharmacology, Renal Research Institute and Division of Nephrology, New York Medical College, Valhalla, NY 10595, USA. Email: michael_goligorsky@nymc.edu

The first 150 words of the full text of this article appear below.



   Introduction
 
More than half a century of investigations on the pathogenesis of acute renal failure (ARF) have brought about two major concepts, which could be roughly dubbed as vasculocentric and tubulocentric. In the 1950s–1970s the focus of these studies was on the haemodynamic component—vasomotor nephropathy due to the no-reflow, tubuloglomerular feedback and vasoconstriction. In parallel with these studies, but more so in the 1980s–1990s there was a shift of the attention toward the tubular component—necrosis and apoptosis of tubular epithelial cells, tubular obstruction and back-leak. The goal of this review is to unveil the intrinsic coupling between the two components and to develop a unifying view, integrating the contribution of each component to the clinical manifestations of this syndrome. In this vein, the incipient phase of ARF will be putatively linked to the endothelial dysfunction (whispers), whereas the overt oliguric phase of ARF will be largely dependent on the tubular damage . . . [Full Text of this Article]



   Significant tissue injury is caused by oxidative and nitrosative stress
 


   Regenerative medicine as it may apply to the post-ischaemic kidney
 


   In vivo injection of HUVEC improves renal function after renal artery cross-clamping
 

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