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Nephrol Dial Transplant (2003) 18: 27-32
© 2003 European Renal Association-European Dialysis and Transplant Association


Invited Comment

Inflammation modifies lipid-mediated renal injury

Xiong Z. Ruan, Zac Varghese and John F. Moorhead

Centre for Nephrology, Royal Free and University College Medical School, University College London, Royal Free Campus, London, UK

Keywords: dyslipidaemia; focal and segmental glomerulosclerosis; progressive renal disease

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

Introduction

Clinical findings in humans suggest, and experimental studies in animal models demonstrate, that dyslipidaemia can lead to disease progression and glomerulosclerosis [1,2]. Thus, it has been established that cholesterol supplementation of the diets of several animal species leads to focal and segmental glomerulosclerosis (FSGS) [3–7] and foam cells and lipid deposits are found in focal segmental sclerosis in human renal biopsies [8]. Many of the features of progressive glomerular and tubulo-interstitial diseases share biological mechanisms with those of atherosclerosis [9,10], which affects both large and medium sized arteries and the microvasculature, as well as in progressive renal disease. A consequence of this shared pathology has led to the use of lipid-lowering drugs to assess the contribution of hyperlipidaemia to the progression of renal damage [11].

Although many animal models of diet-induced hyperlipidaemia support the . . . [Full Text of this Article]

Atherosclerosis as an inflammatory disease

Inflammation modifying lipid-mediated renal injury

Lipid-mediated inflammatory signals
Inflammation may also accelerate lipid-mediated renal injury by affecting cholesterol metabolism
Inflammation accelerates lipid-mediated renal injury by affecting cholesterol homeostasis at the cellular level
Protective measures against inflammation

Conclusion


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