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      Impact of Birth Weight on Familial Aggregation of End-Stage Renal Disease

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          Abstract

          Background: Birth weight (BW) and family history (FH) of end-stage renal disease (ESRD) have been shown to have an independent association with development of subsequent ESRD. This study was undertaken to determine the effects of BW (low BW suggesting a congenital reduction in functional nephron number) on the observed familial aggregation of ESRD. Methods: Cases were identified from the ESRD Network 6 ‘Family History of ESRD’ Study and BW was determined from birth certificate records maintained at the Office of Vital Records, South Carolina Department of Health and Environmental Control. BW and FH of ESRD data were available in 387 patients who initiated dialysis therapy between 1993 and 1997. Multiple logistic regression analysis was performed to assess the risk of low BW (<2,500 g) and high BW (≧4,000 g) on FH of ESRD. Results: A FH of ESRD in first or second-degree relatives was present in 24% of cases. No significant differences were observed in the frequency of a positive FH of ESRD in those with low BW compared to those with normal BW. There was a significant reduction in the prevalence of a FH of ESRD in those with high BW, compared to those with a normal BW (risk ratio 0.32, CI 0.11–0.94). Conclusion: The clustering of either high BW or low BW within multiply affected ESRD families does not account for the observed familial aggregation of ESRD. In addition, high BW was associated with a reduced familial aggregation of ESRD.

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          Most cited references 2

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          Genetic susceptibility to end-stage renal disease.

          New methods have been developed to uncover the genotypes that result in complex diseases. End-stage renal disease is a complex disease, without a simple correspondence between genotype and phenotype. Both population-based and family-based epidemiological studies and analysis of model organisms suggest that the pathogenesis of end-stage renal disease may have a genetic component. A number of studies have analyzed candidate nephropathy genes with little success, but recently several well-designed studies of multiplex families with diabetic nephropathy have identified candidate nephropathy susceptibility loci. To date, kidney disease-oriented research has focused on effector mechanisms responsible for the initiation and progression of chronic renal disease. However, because end-stage renal disease is a complex disease, interruption of a single effector pathway is unlikely to result in significant therapeutic benefit. Further understanding of the pathogenesis of kidney disease and the development of new kidney disease therapies will require continued application of genetic and genomic tools to kidney disease research.
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            A Low-Calorie Unrestricted Protein Diet Attenuates Kidney Damage in Uninephrectomized Spontaneously Hypertensive Rats

            Background/Aims: Uninephrectomized, spontaneously hypertensive rats (UNX-SHR) develop glomerular hyperfiltration, hyperfusion, and interstitial infiltrate of the remnant kidney. Consequently, UNX-SHR is a useful animal model to investigate mechanisms involved in the progression of hypertensive renal disease. Methods: Body weight; tail systolic blood pressure (SBP); urine excretion of protein, urea, and electrolytes; and serum biochemistry were determined in UNX-SHR at 2 months of age prior to uninephrectomy (week 0), prior to treatment (week 8) with a low-calorie (LC) or control diet, and one month after diet treatment (week 12). The LC diet was modified to allow equal intake of protein, sodium phosphorus, and other nutrients in both groups. Results: UNX-SHR treated with the LC diet had significantly lower body weights and SBP at the end of the experiment than did the controls (p < 0.0001). Changes in serum biochemistry and 24-hour urinary excretion of protein, sodium, potassium, and urea nitrogen in both groups were not statistically significant. The final glomerular filtration rate and renal plasma flow were similar in both groups, but the LC diet significantly reduced the glomerular damage index (0.0007), mesangial expansion index (p < 0.002), volume of interstitium per cortex (p < 0.0003), tubular interstitium volume fraction (p < 0.0008), glomerular volume (p < 0.02), and remnant kidney weight (p < 0.01). Conclusion: We demonstrated that in UNX-SHR, the prevention of renal damage by LC diet may involve diminished glomerular growth and interstitial infiltrate without changes in renal hemodynamics. Consequently, LC diet, regardless of protein ingestion, may be an important tool in the prevention of renal damage in hypertension. Additional studies of obese-hypertensive rats may confirm the beneficial effect of a LC diet and weight reduction on the renal damage of obesity-hypertension.
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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
              2003
              April 2003
              17 January 2003
              : 23
              : 2
              : 117-120
              Affiliations
              aDepartment of Biometry and Epidemiology, Medical University of South Carolina, Charleston, S.C.; bSoutheastern Kidney Council, Inc./ESRD Network 6, Raleigh, N.C., and cDepartment of Internal Medicine/Section on Nephrology, Wake Forest University School of Medicine, Winston-Salem, N.C., USA
              Article
              68037 Am J Nephrol 2003;23:117–120
              10.1159/000068037
              12481151
              © 2003 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: 2, References: 29, Pages: 4
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/68037
              Categories
              Original Article: Bench to Bedside

              Cardiovascular Medicine, Nephrology

              Birth weight, Familial aggregation, End-stage renal disease

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