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Nephrol Dial Transplant (2000) 15: 747-750
© 2000 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Transepithelial chloride secretion and cystogenesis in autosomal dominant polycystic kidney disease

Alexandre Persu and Olivier Devuyst

Division of Nephrology, Université Catholique de Louvain, Medical School, Brussels, Belgium

Introduction

Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common monogenic hereditary diseases (prevalence 1 : 400–1 : 1000). It is characterized by the development of multiple cysts in both kidneys. These cysts grow slowly but steadily, inducing a progressive renal insufficiency which leads, in about half of the patients, to end-stage renal failure at a mean of 55 years. In Western Europe and North America, ADPKD is responsible for 4–10% of the patients requiring renal replacement therapy. Several extrarenal manifestations, including extrarenal cysts, cardiac valvular abnormalities, and arterial aneurysms, contribute to the morbidity and mortality of the disease. Treatment of ADPKD is currently restricted to the control of associated complications such as hypertension or infection [1].

Linkage to two loci named PKD1 and PKD2 was found in about 85 and 15% of the families affected with ADPKD respectively. A third locus is probably involved in . . . [Full Text of this Article]

Transepithelial fluid secretion in ADPKD cysts

Molecular identification of chloride transporters

A model of intracystic fluid secretion

Regulation of cyst fluid accumulation

Towards modifier genes

Conclusion, questions, and perspectives

Acknowledgments

Notes

References


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