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      Renal Dopamine and Salt Sensitivity of Blood Pressure in IgA Nephropathy

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          Abstract

          Background: Patients with chronic glomerulonephritis exhibit salt-sensitive (SS) hypertension. In the early stage, however, the exact characteristics are still unclear. A decrease in renal dopamine production under basal conditions or after a sodium load has been reported in a subset of patients with SS primary hypertension. Aims: The present study examined 17 untreated IgA-N patients with near-normal renal function, to determine whether salt sensitivity appears before hypertension and whether this sensitivity is related to renal dopamine production. Methods: Daily urinary excretion of dopamine, the amine precursor – L-DOPA, and metabolites was monitored in conditions of basal sodium ingestion, followed by three consecutive 5-day periods of 100, 20 and 350 mmol/day sodium intake. The sodium sensitivity index (SSI) was evaluated in each patient. In addition, the patients were considered SS when showing an increase ≧5 mm Hg in 24-hour mean BP when they changed from a 20- to a 350-mmol/day sodium diet. Results: Urinary dopamine output was lower in SS than in salt-resistant patients throughout the study (p < 0.001). This was accompanied by lower creatinine clearance values and higher urinary protein excretion in SS IgA-N patients. A strong negative relationship was observed in these 17 IgA-N patients between the SSI and the daily urinary excretion of dopamine in conditions of both 20 mmol/day sodium intake (r<sup>2</sup> = 0.592; p = 0.0003) and 350 mmol/day sodium diet (r<sup>2</sup> = 0.352; p = 0.01). However, urinary dopamine output varied appropriately throughout the study in SS patients, in agreement with changes in sodium intake. Conclusion: We conclude that in IgA-N patients, a rightward shift in the ‘pressure natriuresis’ can appear before hypertension and is related with a reduced renal production of dopamine. It is suggested that decreased renal dopamine synthesis in SS IgA-N patients results from acquired tubulointerstitial injury. In contrast to what has been found in SS primary hypertension, renal dopamine may behave appropriately in SS IgA-N patients, as a compensatory hormone.

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          Subtle acquired renal injury as a mechanism of salt-sensitive hypertension.

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            Reduced Urinary Excretion of Dopamine and Metabolites in Chronic Renal Parenchymal Disease

            Background: Chronic renal parenchymal diseases are accompanied by a progressive loss of tubular units endowed with the ability to synthesise dopamine from L -3,4-dihydroxyphenylalanine ( L -DOPA), and preliminary evidence has suggested that the urinary excretion of free dopamine may be reduced in these disorders. However, it is well recognised now that under in vitro conditions, dopamine newly synthesised in tubular epithelial cells undergoes extensive deamination to 3,4-dihydroxyphenylacetic acid (DOPAC) by monoamine oxidase (MAO); a small amount of the amine is converted to homovanillic acid by both MAO and catechol-O-methyltransferase (COMT) and a minor amount is methylated to 3-methoxytyramine. Aims: The present study aimed at examining the relationship between renal function and daily urinary levels of L -DOPA, free dopamine and its main metabolites, DOPAC and homovanillic acid (HVA) in patients (n = 28) with chronic renal parenchymal disease, in conditions of controlled sodium, potassium and phosphate intake. The levels of 5-hydroxyindolacetic acid (5-HIAA) were also evaluated in the same cohort of patients. Results: The patients were divided in two groups according to creatinine clearance (group 1, 39±6 ml/min/1.73 m 2 , n = 14; group 2, 139±6 ml/min/1.73 m 2 , n = 14). In patients of group 1, the urinary levels of L -DOPA, dopamine and DOPAC (in nmol/24 h) were significantly lower (60% reduction) than in patients of group 2 ( L -DOPA, 134±36 vs. 308±51; dopamine, 759± 175 vs. 1,936± 117; DOPAC 2,595±340 vs. 7,938±833). Also, the urinary excretion of HVA in patients group 1 was significantly lower (40% reduction) than in patients of group 2 (17,434±2,455 vs. 27,179±2,271 nmol/24 h). By contrast, no significant difference was observed in daily urinary excretion of 5-HIAA between the two groups of patients (group 1, 27,280±3,721 nmol/day; group 2, 28,851±2,854 nmol/day). A positive linear relationship was found in these 28 patients between the creatinine clearance and the daily urinary excretion of L -DOPA (r = 0.64, p dopamine/ L -DOPA and U DOPAC/dopamine ratios were found to be similar in both groups of patients, whereas the U HVA/DOPAC ratios in patients of group 1 were found greater than in group 2 (p < 0.05). Conclusion: Patients suffering from chronic parenchymal disease with a compromised renal function present with a reduced activity of their renal dopaminergic system which correlates well with the degree of deterioration of renal function. The reduced urinary dopamine output in renal insufficiency is not attributable to enhanced metabolism of renal dopamine. We suggest that the urinary levels of DOPAC may represent a useful parameter for the assessment of renal dopamine synthesis.
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              Author and article information

              Journal
              KBR
              Kidney Blood Press Res
              10.1159/issn.1420-4096
              Kidney and Blood Pressure Research
              S. Karger AG
              1420-4096
              1423-0143
              2004
              July 2004
              03 May 2004
              : 27
              : 2
              : 78-87
              Affiliations
              aDepartment of Nephrology, Faculty of Medicine, Porto, bFaculty of Nutrition Sciences, University of Porto, cInstitute of Pharmacology and Therapeutics, and dDepartment of Pathology, Faculty of Medicine, Porto, Portugal
              Article
              76022 Kidney Blood Press Res 2004;27:78–87
              10.1159/000076022
              14718752
              © 2004 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
              Figures: 4, Tables: 4, References: 38, Pages: 10
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/76022
              Categories
              Original Paper

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