Format

Send to

Choose Destination
Am J Nephrol. 2006;26(4):335-9. Epub 2006 Jul 5.

Flow-associated dilatory capacity of the brachial artery is intact in early autosomal dominant polycystic kidney disease.

Author information

1
Department of Nephrology, Rigshospitalet, University of Copenhagen, Blegdamsvej, Copenhagen, Denmark. pclaus@rh.dk

Abstract

BACKGROUND/AIMS:

Autosomal dominant polycystic kidney disease is associated with endothelial dysfunction of resistance arteries. This study tested whether endothelial dysfunction is also present in the conduit arteries in patients with preserved renal function.

METHODS:

Twenty-seven patients (9 females and 18 males, age 36 +/- 10 years) with polycystic kidney disease and normal renal function were compared to 27 healthy controls. The dilatory responses of the brachial artery to postischemic increased blood flow [endothelium-dependent flow-associated dilatation (FAD)] and to nitroglycerin [endothelium-independent nitroglycerin-induced dilatation (NID)] were measured by external ultrasound. Plasma concentrations of the stable end products of nitric oxide nitrate/nitrite (NOx) and of the endothelial markers vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1, E-selectin and von Willebrand factor antigen were also measured.

RESULTS:

No differences in FAD or NID were found between patients and controls (104.6 +/- 4.2 vs. 105.3 +/- 3.9%, mean +/- SD, p = 0.55, and 117.0 +/- 8.4 vs. 117.5 +/- 7.6%, p = 0.75). However, the plasma concentration of VCAM-1 was elevated and the plasma concentration of NOx was reduced in patients with polycystic kidney disease.

CONCLUSION:

Biochemical markers confirm an association between polycystic kidney disease and endothelial dysfunction. However, a normal FAD of the brachial artery suggests that the endothelial dysfunction does not involve the conduit arteries.

PMID:
16825759
DOI:
10.1159/000094402
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for S. Karger AG, Basel, Switzerland
Loading ...
Support Center