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      Renal Resistive Index Early Detects Chronic Tubulointerstitial Nephropathy in Normo- and Hypertensive Patients

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          Abstract

          Background: We studied whether the measurement of intrarenal vascular resistance by Doppler ultrasonography, capable of investigating renal interstitial compartment, allows the early detection of chronic tubulointerstitial nephropathy (TIN). Methods: 30 normotensive and 28 hypertensive (I-II OMS) patients with a clinical history suggestive of chronic TIN and normal renal function were enrolled. 40 healthy volunteers served as controls. Patients were considered TIN-negative or TIN-positive after investigating tubular function by urine concentrating and acidification tests. Renal sonographic parameters and renal resistive index (RRI) were obtained by duplex scanner. Glomerular filtration rate/effective renal plasmatic flow ratio was investigated by sequential renal scintigraphy in TIN-negative and TIN-positive patients; <sup>99m</sup>Tc-DMSA scintigraphy was also performed in TIN-positive patients. Results: RRI values of TIN-positive normotensive and hypertensive patients were significantly higher (p < 0.01 for both) than those of TIN-negative patients and of controls. RRI values resulted to be linearly related to uricemia (r = 0.88, p < 0.0001) only in normotensive patients. RRI values also resulted to be linearly related to filtration ratio values (r = 0.60, p < 0.0001). <sup>99m</sup>Tc-DMSA scintigraphy confirmed interstitial renal damage (grade 1 and 2). Conclusion: RRI measurement allows the early identification of both normotensive and hypertensive patients with chronic TIN and signs of tubular dysfunction, when renal function is still preserved.

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          Most cited references 12

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          Mild hyperuricemia induces vasoconstriction and maintains glomerular hypertension in normal and remnant kidney rats.

          Hyperuricemia has been associated with renal disease. Because glomerular hemodynamic alterations critically contribute to initiation and progression of renal disease, we evaluated the effect of mild hyperuricemia in glomerular microcirculatory changes in rats under normal conditions and with renal injury induced by subtotal renal ablation (RK). Hyperuricemia was induced in normal and remnant kidney (RK) rats on a normal sodium diet by administration of oxonic acid (OA). To prevent hyperuricemia, allopurinol (AP) was administered concomitantly. Glomerular hemodynamics were evaluated by micropuncture techniques. Systolic blood pressure (SBP), proteinuria, arterial morphology, and serum uric acid were measured. In RK rats, glomerulosclerosis, fibrosis, and inflammatory cell infiltration (CD5+) were also assessed. In normal rats, hyperuricemia resulted in afferent arteriole thickening associated with renal cortical vasoconstriction [single nephron glomerular filtration rate (SNGFR) -35%, P < 0.05) and glomerular hypertension (P < 0.05). Allopurinol treatment prevented structural and functional alterations. In RK rats, hyperuricemia produced more renal vascular damage than control animals coupled with severe cortical vasoconstriction (SNGFR -40%, P < 0.05) and persistent glomerular hypertension. Allopurinol partially prevented cortical vasoconstriction, and fully prevented arteriolopathy and glomerular hypertension associated with significantly less infiltration of CD5+ cells. Hyperuricemia induces arteriolopathy of preglomerular vessels, which impairs the autoregulatory response of afferent arterioles, resulting in glomerular hypertension. Lumen obliteration induced by vascular wall thickening produces severe renal hypoperfusion. The resulting ischemia is a potent stimulus that induces tubulointerstitial inflammation and fibrosis, as well as arterial hypertension. These studies provide a potential mechanism by which hyperuricemia can mediate hypertension and renal disease.
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            Subtle acquired renal injury as a mechanism of salt-sensitive hypertension.

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              Renal resistance index and progression of renal disease.

              The progression of renal disease depends on various clinical parameters such as hypertension and proteinuria. We recently showed that an increased renal resistance index measured by duplex ultrasound is associated with a poor prognosis in patients with renal artery stenosis. We now prospectively tested the hypothesis that a high renal resistance index (greater-than-or-equal 80) predicts progression of renal disease in patients without renal artery stenosis. In 162 patients newly diagnosed with renal disease, the resistance index (1-[end diastolic velocity/maximum systolic velocity]*100) was measured in segmental arteries of both kidneys. Creatinine clearance was measured at baseline, at 3, 6, and 12 months, and then at yearly intervals thereafter (mean follow-up 3 +/- 1.4 years). The combined endpoint was a decrease of creatinine clearance by greater-than-or-equal 50%, end-stage renal disease with replacement therapy, or death. Twenty-five patients (15%) had a renal resistance index value greater-than-or-equal 80 at baseline. Nineteen (76%) had a decline in renal function; 16 (64%) progressed to dialysis, and 6 (24%) died. In comparison, in patients with renal resistance index values <80, 13 (9%) had a decline in renal function, only 7 (5%) became dialysis-dependent, and 2 (1%) died (P<0.001). In a multivariate regression analysis, only proteinuria and resistance index were independent predictors of declining renal function. A renal resistance index value of greater-than-or-equal to 80 reliably identifies patients at risk for progressive renal disease.
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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
                2006
                April 2006
                05 April 2006
                : 26
                : 1
                : 16-21
                Affiliations
                Clinica Medica Generale e Cardiologia, Dipartimento di Area Critica Medico-Chirurgica, University of Florence, Florence, Italy
                Article
                90786 Am J Nephrol 2006;26:16–21
                10.1159/000090786
                16401882
                © 2006 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: 3, Tables: 2, References: 21, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/90786
                Categories
                Original Report: Laboratory Investigation

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