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Nephrol Dial Transplant (2003) 18: 2211-2215
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comment

Autosomal dominant polycystic kidney disease: modifier genes and endothelial dysfunction

Olivier Devuyst, Alexandre Persu and Minh-Truc Vo-Cong

Department of Nephrology, Université catholique de Louvain Medical School, Brussels, Belgium

Correspondence and offprint requests to: Olivier Devuyst, Division of Nephrology, UCL Medical School, 10 Avenue Hippocrate, B-1200 Brussels, Belgium. Email: devuyst@nefr.ucl.ac.be

Keywords: endothelium; modifying genes; nitric oxide; polycystic kidney disease; polycystins

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

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the development of multiple cysts in both kidneys, causing progressive renal failure. By the age of 60 years, about half the patients with ADPKD have end-stage renal disease (ESRD). In Europe and North America, ADPKD is responsible for 5–10% of the patients requiring renal replacement therapy [1]. ADPKD is also characterized by extrarenal manifestations (e.g. intracranial aneurysms or liver cysts) and hypertension. The latter occurs in 50–70% of patients, even before any reduction in renal function [1]. Mutations in two genes, PKD1 and PKD2, are responsible for ~85% and 15% of ADPKD cases, respectively. The proteins encoded by PKD1 (polycystin-1) and PKD2 (polycystin-2) interact in the plasma membrane to participate in signalling pathways that regulate renal tubular cell maturation [2]. In this comment, we will discuss the role and potential implications of disease-modifying genes . . . [Full Text of this Article]

ADPKD is characterized by variable renal disease progression

Evidence supporting the role of modifier genes in ADPKD

Candidate modifier genes in ADPKD

Endothelial dysfunction in ADPKD

NO and endothelial NO synthase

Modifier effect of ENOS in ADPKD

Conclusions and perspectives


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