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Nephrol Dial Transplant (2003) 18: 814-818
© 2003 European Renal Association-European Dialysis and Transplant Association

Brief Report

Detection of cell-cycle regulators in failed arteriovenous fistulas for haemodialysis

Rick de Graaf1, Ruben Dammers1, Tryfon Vainas1, Arnold P. G. Hoeks2 and Jan H. M. Tordoir1,

1 Department of Surgery, University Hospital Maastricht and 2 Department of Biophysics, University Maastricht, Maastricht, The Netherlands

Background. Chronic renal failure (CRF) patients rely on arteriovenous fistulas (AVFs) for haemodialysis vascular access. Intimal hyperplastic stenoses result in failure of AVFs and frequent intervention is required to maintain vascular access. The extent of intimal hyperplasia depends on the interplay between cyclins and cyclin-dependent kinases (e.g. cdk2), positively regulating cell-cycle progression. cdk activity is negatively modulated by the interaction with cdk inhibitory proteins, such as p21Waf1 and p27Kip1. Little is known about the expression of these proteins in the development of intimal hyperplasia in AVFs.

Methods. p21Waf1, p27Kip1, cdk2 and Proliferating Cell Nuclear Antigen immunoreactivity was determined in 18 failed AVFs from 16 CRF patients and 10 non-diseased vessels (five arteries and five veins).

Results. The percentage of p21Waf1-positive cells was significantly lower in AVFs (3±1%), compared with normal veins and arteries (62±4 and 63±4%, respectively; P<0.001). cdk2-positive cells were significantly higher in AVFs (40.7±3.7%) than in normal veins and arteries (2±1 and 0±0%, respectively; P<0.001). Although no difference in p27Kip1 immunoreactivity was found between AVFs (37±17%) and veins (23±8%; P=0.208), it was lower in healthy arteries (17±11%; P=0.037).

Conclusions. The data suggest that in failed AVFs, p21Waf1, but not p27Kip1, is related to intimal hyperplasia. This is the first report to show involvement of cell-cycle regulators in AVF-related human intimal hyperplasia.

Keywords: cell-cycle; fistula; hyperplasia; intimal; stenosis

Correspondence and offprint requests to: Jan H. M. Tordoir, MD, PhD, Department of Surgery, University Hospital Maastricht, P. Debyelaan 25, PO Box 5800, 6202 AZ Maastricht, The Netherlands. Email: j.tordoir{at}surgery.azm.nl


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