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Nephrol Dial Transplant (2000) 15: 149-151
© 2000 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Chronic allograft nephropathy—a model of impaired repair from injury?

Leendert C. Paul

Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands

Correspondence and offprint requests to: L. C. Paul, Department of Nephrology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.

Introduction

Chronic allograft nephropathy (CAN) is characterized by excessive tissue fibrosis and sclerosis, resulting in the disruption of the tissue architecture (Figure 1Go). The common thread of transplants with CAN is that they all have undergone previous tissue injury, and recent experimental data suggest that the excessive fibrosis results from impaired repair from injury.



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  		Fig. 1. Photomicrograph of a renal transplant removed because of chronic rejection. There is extensive intimal thickening with narrowing of the vascular lumen, glomerulosclerosis with expansion of the mesangial matrix, interstitial fibrosis, and tubular atrophy. Trichrome staining. (Courtesy Dr H. Benediktsson, Calgary, Canada.)

 
Injury to renal transplants

Only one kidney is transplanted and is usually exposed to several different forms of injury that may result in further reduction in renal mass such as brain-death injury [1], ischaemia–reperfusion injury, prolonged cold storage, acute . . . [Full Text of this Article]

The normal tissue response to injury

Hypothesis to explain chronic allograft nephropathy

Chronic rejection theory
Cytokine excess theory
Interference in the tissue repair following injury
Loss of supporting extracellular matrix architecture
Premature senescence theory
Conclusion

References


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