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Nephrol Dial Transplant (2003) 18: 1959-1962
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comment

Kidney remodelling and scarring: the plasticity of cells

Meguid El Nahas

Sheffield Kidney Institute, University of Sheffield, Sheffield, UK

Correspondence and offprint requests to: Professor AM El Nahas, PhD, FRCP, Sheffield Kidney Institute, Sheffield Teaching Hospital Trust (Northern General Hospital Campus), Herries Road, Sheffield S5 7AU, UK. Email: M.El-Nahas@sheffield.ac.uk

Keywords: chronic kidney failure; scarring; stem cells; transdifferentiation

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

Introduction

The progression of chronic kidney failure remains one of the main challenges in nephrology in view of the ever-increasing number of patients presenting every year with end-stage renal failure. It is predicted that the increased trend will continue unabated for at least another 10 years [1]. It is therefore imperative to improve our understanding of the underlying kidney scarring process in order to design imaginative therapeutic preventive approaches.

Mechanisms of kidney scarring

Glomerular sclerosis
It is assumed currently that progressive kidney scarring is due to the interactions between resident renal cells and infiltrating, mainly inflammatory, cells [2]. Within the glomeruli, injury is followed by potential damage to resident cell lines with, as a consequence, the release by endothelial cells of pro-inflammatory cytokines, chemokines and growth factors attracting inflammatory cells to the glomerular capillaries and initiating a microinflammatory process [2]. The infiltration of the glomerular capillaries by monocytes/macrophages leads to their . . . [Full Text of this Article]

Tubulo-interstitial scarring
Therapeutic implications


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