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Vol. 113, No. 2, 2009
Issue release date: September 2009
Section title: Original Paper
Nephron Clin Pract 2009;113:c71–c75
(DOI:10.1159/000228537)

Cutaneous Microcirculation Is Impaired in Early Autosomal Dominant Polycystic Kidney Disease

Ramunni A.a · Brescia P.a · Quaranta D.b · Bianco M.S.b · Ranieri P.c · Dolce E.d · Coratelli P.a
aDivision of Nephrology, Department of Internal and Public Medicine, bDivision of Dermatology, cCoagulation Laboratory and dDivision of Internal Medicine and Clinical Oncology, University of Bari, Bari, Italy

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 8/14/2008
Accepted: 1/14/2009
Published online: 7/14/2009
Issue release date: September 2009

Number of Print Pages: 1
Number of Figures: 0
Number of Tables: 3

ISSN: (Print)
eISSN: 1660-2110 (Online)

For additional information: http://www.karger.com/NEC

Abstract

Background/Aims: An endothelial dysfunction has been described in autosomal dominant polycystic kidney disease (ADPKD) before the development of hypertension and renal impairment. The aim of this work was to verify the existence of a microvascular reactivity in the early stages of ADPKD. Methods: Fifteen ADPKD normotensive patients with normal renal function underwent laser Doppler examination of the cutaneous microcirculation in basal conditions and after the warm test, as well as evaluation of plasma concentrations of some endothelial activation parameters [total cholesterol and fractions, fibrinogen, von Willebrand factor, Lp(a)]. The results were compared with those in 15 healthy subjects, 15 essential hypertensive patients and 15 hypertensive ADPKD patients with normal renal function. Results: Both basal and post-warm-test values were significantly lower in normotensive ADPKD subjects than controls (3.2 ± 1 vs. 5.8 ± 1.3 AU, p = 0.0001; 35.2 ± 10.9 vs. 50.5 ± 10.8 AU, p = 0.005, respectively). All evaluated parameters were within normal limits and comparable between normotensive ADPKD subjects and controls, except for LDL cholesterol (125 ± 18 vs. 101 ± 22 mg/dl, p = 0.01) and Lp(a), which was significantly higher in the ADPKD subjects (52.2 ± 36 vs. 6.0 ±4 mg/dl, p = 0.0006). Conclusion: Our study confirms the existence of a systemic microcirculation defect in ADPKD. The presence of high levels of Lp(a) could contribute to causing the high incidence of cardiovascular events in ADPKD.

© 2009 S. Karger AG, Basel


  

Author Contacts

Alfonso Ramunni, MD
Division of Nephrology, Department of Internal and Public Medicine
University of Bari, Piazza Giulio Cesare, 11
IT–70124 Bari (Italy)
Tel. +39 08 0547 8383, Fax +39 08 0547 8675, E-Mail a.ramunni@nephro.uniba.it

  

Article Information

Received: August 14, 2008
Accepted: January 14, 2009
Published online: July 14, 2009
Number of Print Pages : 5
Number of Figures : 0, Number of Tables : 3, Number of References : 37

  

Publication Details

Nephron Clinical Practice

Vol. 113, No. 2, Year 2009 (Cover Date: September 2009)

Journal Editor: El Nahas M. (Sheffield)
ISSN: 1660-2110 (Print), eISSN: 1660-2110 (Online)

For additional information: http://www.karger.com/NEC


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 8/14/2008
Accepted: 1/14/2009
Published online: 7/14/2009
Issue release date: September 2009

Number of Print Pages: 1
Number of Figures: 0
Number of Tables: 3

ISSN: (Print)
eISSN: 1660-2110 (Online)

For additional information: http://www.karger.com/NEC


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