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      Hyperuricemic Nephropathies

      Nephron

      S. Karger AG

      Hyperuricemia, Urate, Nephropathy, Renal failure

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          Abstract

          This review explores the relationship between uric acid or urate and the pathogenesis of renal impairment. The following points and conclusions are emphasized: (1) uric acid is an end product of purine degradation in humans and normally depends upon renal excretion for the majority of its elimination from the body; (2) massive urate overproduction – usually occurring acutely because of tumor lysis, rhabdomyolysis, or some other cause of rapid nucleic acid turnover or tissue destruction – tends to cause acute renal failure because of an increase of intratubular uric acid precipitation and obstruction; (3) chronic urate overproduction (with increased urate excretion) is more likely to be associated with stones or gout than with acute renal failure; (4) chronic asymptomatic hyperuricemia is unlikely to cause renal disease, gout, or stones, but is associated with cardiovascular impairment over the long term, and (5) asymptomatic hyperuricemia may serve as an indicator of renal vascular disease, or, to the extent that it may reflect insulin-induced acceleration of renal tubule urate reabsorption, hyperuricemia may serve as an indicator of insulin resistance. Therefore chronic asymptomatic hyperuricemia may predict the adverse cardiovascular consequences of insulin resistance.

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          Most cited references 3

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          Effect of insulin on renal sodium and uric acid handling in essential hypertension.

          In normal subjects, insulin decreases the urinary excretion of sodium, potassium, and uric acid. We tested whether these renal effects of insulin are altered in insulin resistant hypertension. In 37 patients with essential hypertension, we measured the changes in urinary excretion of sodium, potassium, and uric acid in response to physiological euglycemic hyperinsulinemia (by using the insulin clamp technique at an insulin infusion rate of 6 pmol/min/kg). Glucose disposal rate averaged 26.6 +/- 1.5 mumol/min/kg, i.e., 20% lower than in normotensive controls (33.1 +/- 2.1 mumol/min/kg, P = .015) In the basal state, fasting plasma uric acid concentrations were higher in men than women (P < .001), were positively related to body mass index (r = 0.38, P = .02), waist/hip ratio (r = 0.35, P < .05), and serum triglyceride levels (r = 0.59, P = .0001), and negatively related to HDL cholesterol concentrations (r = -0.59, P = .0001) and glucose disposal rate (r = 0.42, P < .01). Uric acid clearance, on the other hand, was inversely related to body mass index (r = 0.41, P = .01), plasma uric acid (r = 0.65, P < .0001) and triglyceride concentrations (r = 0.39, P < .02), and directly related to HDL cholesterol levels (r = 0.52, P < .001). During insulin infusion, blood pressure, plasma uric acid and sodium concentration, and creatinine clearance did not change. In contrast, hyperinsulinemia caused a significant decrease in the urinary excretion of uric acid (2.67 +/- 0.12 to 1.86 +/- .14 mumol/min/1.73 m2, P = .0001), sodium (184 +/- 12 to 137 +/- 14 mumol/min/1.73 m2, P = .0001), and potassium (81 +/- 7 to 48 +/- 4 mumol/ min/1.73 m2, P = .0001). Both in absolute terms (clearance and fractional excretion rates) and percentagewise, these changes were similar to those found in normotensive subjects. Insulin-induced changes in urate excretion were coupled (r = 0.55, P < .0001) to the respective changes in sodium excretion. In hypertensive patients, higher uric acid levels and lower renal urate clearance rates cluster with insulin resistance and dyslipidemia. Despite insulin resistance of glucose metabolism, acute physiological hyperinsulinemia causes normal antinatriuresis, antikaliuresis, and antiuricosuria in these patients.
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            Serum uric acid. Its relationship to coronary heart disease risk factors and cardiovascular disease, Evans County, Georgia.

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              Correlates and consequences of asymptomatic hyperuricemia

               W. Fessel (1973)
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                978-3-8055-6818-0
                978-3-318-00390-1
                1660-8151
                2235-3186
                1999
                December 1998
                24 December 1998
                : 81
                : Suppl 1
                : 45-49
                Affiliations
                University of Wisconsin, Madison, Wisc., USA
                Article
                46298 Nephron 1999;81(suppl 1):45–49
                10.1159/000046298
                9873214
                © 1998 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
                References: 42, Pages: 5
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/46298
                Categories
                Paper

                Cardiovascular Medicine, Nephrology

                Renal failure, Nephropathy, Urate, Hyperuricemia

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