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      Left Ventricular Hypertrophy in Hypertensive Patients with Autosomal Dominant Polycystic Kidney Disease: Influence of Blood Pressure and Humoral and Neurohormonal Factors

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          Abstract

          Left ventricular hypertrophy (LVH) is a common finding in hypertensive autosomal dominant polycystic kidney disease (ADPKD) patients. There are few studies on the influence of blood pressure (BP) and nonhemodynamic factors on LVH in these patients. The aim of this study was to evaluate the relationship between BP, humoral and neurohormonal factors and left ventricular mass (LVM) in hypertensive ADPKD patients. In 20 hypertensive ADPKD patients, ambulatory BP was monitored for 24 h, left ventricular dimensions were estimated by echocardiography, and plasma renin activity (PRA), plasma noradrenaline (NA), angiotensin II (Ang II), aldosterone, atrial natriuretic peptide (ANP) and insulin-like growth factor I (IGF-I) were also determined. Twenty age- and sex-matched essential hypertensive subjects served as controls. Ambulatory BP and LVM index were similar in the two groups, although male ADPKD patients had higher LVM indices than their matched controls. Eight ADPKD patients (40%) and 6 essential hypertensives (30%) showed LVH. PRA, Ang II, aldosterone, ANP and IGF-I levels were similar in the two groups, but plasma NA levels were higher in ADPKD patients than in controls (281 ± 158 vs. 160 ± 62 pg/ml, p = 0.004). ADPKD patients with LVH did not differ from those without LVH with regard to humoral and neurohormonal parameters, but had higher ambulatory BP levels. In ADPKD patients, correlation analysis revealed a significant association between LVM index and 24-hour systolic and diastolic BP, but not with any of the hormonal factors evaluated. On multiple regression analysis, 24-hour diastolic BP was the only independent variable linked to LVM index. In conclusion, ambulatory BP is one of the most important determinants of LVM in hypertensive ADPKD patients. Further studies are warranted to elucidate the role of nonhemodynamic factors in the pathogenesis of LVH in this population.

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          Most cited references 3

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          Sympathetic Activity and Blood Pressure Pattern in Autosomal Dominant Polycystic Kidney Disease Hypertensives

          To study the potential role of sympathetic activity in the pathogenesis of arterial hypertension associated with autosomal dominant polycystic kidney disease (ADPKD) and to analyze its relationship with 24-hour blood pressure pattern, plasma catecholamines and 24-hour ambulatory blood pressure monitoring were evaluated in 30 ADPKD hypertensive patients (of which 17 without and 13 with renal failure) and in 50 essential hypertensives. The groups were matched for sex, body mass index, known duration of hypertension, and clinic blood pressure. Plasma catecholamines, determined in resting position, were higher in ADPKD patients without renal failure than in essential hypertensives. Nighttime diastolic blood pressure was higher and the percentage day-night difference in mean blood pressure was lower in hypertensives with ADPKD compared to patients with essential hypertension. Blood pressure was significantly correlated with plasma noradrenaline in ADPKD patients, independently of renal function. No significant differences were observed between ADPKD patients with and without renal failure, with respect to plasma catecholamines, 24-hour daytime and nighttime ambulatory blood pressures and the percentage day-night difference in mean blood pressure.
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            Microalbuminuria in normotensive patients with autosomal-dominant polycystic kidney disease.

            Microalbuminuria (MA) is present in hypertensive autosomal-dominant polycystic kidney disease (ADPKD) patients, but has not been reported in normotensive ADPKD patients. We examined the prevalence of MA and the effect of different determinants on urinary albumin excretion in a group of 42 normotensive ADPKD patients. Metabolic parameters, plasma renin activity and aldosterone and serum angiotensin-converting enzyme (ACE) activity were determined. A 24-h urine sample two or three times over a 6-month period was collected to evaluate MA. Each patient underwent an echocardiography to measure left ventricular mass. Eight patients (19%) showed MA (61.6 mg/day, range 37-164), whereas 34 patients (81%) were normoalbuminuric (8.8 mg/day, range 2-29). The groups were matched for all possible confounding variables, but microalbuminuric patients showed a tendency towards greater systolic blood pressure, plasma renin activity and left ventricular mass. There was no correlation between MA and age, sex, body mass index, systolic or diastolic blood pressure, plasma renin activity, serum ACE levels or left ventricular index. The present study demonstrates a high prevalence of MA in normotensive ADPKD patients. MA may be a predictor of early renal and vascular damage in these patients.
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              Influence of humoral and neurohormonal factors on cardiovascular hypertrophy in intreated essential hypertensives

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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2000
                June 2000
                30 June 2000
                : 20
                : 3
                : 193-200
                Affiliations
                aNephrology Service, bCardiology Section and cResearch Unit, Hospital Universitari de Tarragona Joan XXIII, Department of Medicine and Surgery, University Rovira i Virgili, Tarragona, Spain
                Article
                13583 Am J Nephrol 2000;20:193–200
                10.1159/000013583
                10878400
                © 2000 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 5, References: 48, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/13583
                Categories
                Clinical Study

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