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      A Population-Based Assessment of the Familial Component of Chronic Kidney Disease Mortality

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          Abstract

          Background/Aim: While the familial nature of chronic kidney disease (CKD) has been recognized, it has primarily been defined from studies of first-degree relatives of selected sets of cases. The goal of this study is an evaluation of the familial clustering of end-stage renal disease (ESRD) and CKD mortality using a population-based genealogy of Utah. This is the first population-based analysis of the familial component of ESRD and non-ESRD CKD. Methods: We have defined two distinct patient groups for this analysis, using individuals with death certificates in the Utah Population Database indicating ESRD (n = 192) and non-ESRD CKD (n = 335) as the cause of death. Two measures of familiality were used: (1) relative risk (RR) of CKD or ESRD death in relatives of cases and (2) an average relatedness statistic, i.e., the Genealogical Index of Familiality. Results: The RR for dying with ESRD among the first-degree relatives of individuals dying with ESRD is estimated to be 10.1 (p = 0.0007, 95% confidence interval CI 2.76–25.95), but is not significantly elevated among second-degree relatives. The RR for dying with non-ESRD CKD among first- and second-degree relatives of individuals dying with non-ESRD CKD was 3.89 (p = 0.0051, 95% CI 1.43–8.46) and 3.11 (p = 0.04, 95% CI 0.85–7.95), respectively. The Genealogical Index of Familiality statistic demonstrated that the individuals dying with ESRD are significantly more related than expected in this population (p = 0.013); significant excess relatedness was also observed for individuals dying with non-ESRD CKD (p = 0.006), suggesting a familial component for both, with evidence for common environmental and genetic effects. Conclusion: The results of this analysis of individuals dying with ESRD and non-ESRD CKD supports a significant and independent familial component to both conditions, suggesting a heritable factor playing a role.

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          Most cited references 18

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          Cardiovascular complications in chronic kidney disease.

          The risk for cardiovascular disease (CVD) morbidity and mortality remains alarmingly high in all stages of chronic kidney disease (CKD). CVD often begins before end-stage renal disease (ESRD), and patients with reduced kidney function are more likely to die of CVD than to develop ESRD. Three pathological forms of CVD should be considered in patients with CKD: alterations in cardiac geometry, including left ventricular hypertrophy, atherosclerosis, and arteriosclerosis. All are highly prevalent in patients with CKD. Although patients with CKD share many of the same risk factors for CVD as the general population, there are a number of uremia-related risk factors, such as anemia and alterations in calcium/phosphorus metabolism, that also play a role in promoting CVD. Treatment of both traditional and uremia-related risk factors should be initiated in the earlier stages of CKD. Additional clinical trials with a goal to reduce CVD are urgently needed in CKD.
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            Heritability of GFR and albuminuria in Caucasians with type 2 diabetes mellitus.

            Elevated urinary albumin excretion and decreased glomerular filtration rate (GFR) are risk factors for cardiovascular death and end-stage renal disease in individuals with type 2 diabetes mellitus (DM). To determine the extent of familial aggregation of GFR and urine albumin-creatinine ratio (ACR), we calculated heritability (h2) estimates by using a variance component approach. Among 662 participants with DM from 310 families (422 DM-concordant sibling pairs), 51.8% (n = 343) were women, mean age was 62.3 +/- 9.2 (SD) years (median, 62.6 years), diabetes duration was 10.8 +/- 7.6 years (median, 9 years), GFR was 67.6 +/- 19.0 mL/min (median, 64.7 mL/min), and urine ACR was 139.7 +/- 631.4 mg/g (median, 13.1 mg/g). Estimated h2 of GFR was 0.75 +/- 0.10 (P < 0.0001) after adjusting for age, sex, mean arterial blood pressure, medications, and hemoglobin A(1c) level. These covariates accounted for only 2% of the total phenotypic variation in log GFR. Similarly, estimated h2 of ACR was 0.46 +/- 0.12 (P < 0.0001) when adjusting for these covariates, with covariates contributing only 9% of phenotypic variation. These data provide strong evidence that among Caucasians with type 2 diabetes, GFR and urine ACR show strong familiality, suggesting that genetic factors exhibit significant influences. Given their biological and clinical importance and the similarity of these estimates with other cardiovascular disease- and DM-related traits, efforts to map genes that influence GFR and urine ACR levels should have increased importance.
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              Familial predisposition to nephropathy in African-Americans with non-insulin-dependent diabetes mellitus.

              Nephropathy clusters in Pima Indian families with non-insulin-dependent diabetes mellitus (NIDDM), suggesting that susceptibility to nephropathy is distinct from NIDDM per se. The authors compared the family history of end-stage renal disease (ESRD) from 52 African-American patients with NIDDM-induced ESRD (cases) with 45 age-, sex-, and and race-matched non-insulin-dependent diabetics without nephropathy (controls) to assess whether the risk of renal disease was independent from NIDDM in African-Americans as well. Thirty-seven percent (19 of 52) of NIDDM-induced ESRD patients had either a first-, second-, or third-degree relative with ESRD, in contrast to only 7% (3 of 45) of diabetic controls. African-American individuals with NIDDM were at eightfold increased risk for developing subsequent ESRD in the presence of a close relative with ESRD (odds ratio = 8.06; 95% confidence interval, 2.2 to 29.6; P < or = 0.0005). No significant differences were observed in yearly income, years of formal education, total serum cholesterol level, prevalence of smoking, or hypertension between the groups. Diabetic control (assessed by glycosylated hemoglobin and random glucose levels) was suboptimal in nonrenal disease controls, suggesting that hyperglycemia alone fails to cause nephropathy in patients with NIDDM. Family size was unlikely to have influenced the results because diabetic cases had significantly fewer first-degree relatives than did diabetic controls. Familial clustering of ESRD is present in certain African-American families with NIDDM. Differences in family size and degree of diabetic control are unlikely to account for the differences observed between families.(ABSTRACT TRUNCATED AT 250 WORDS)
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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
                May 2006
                02 June 2006
                : 26
                : 2
                : 142-148
                Affiliations
                aDivision of Nephrology and Hypertension and Departments of bFamily and Preventive Medicine and cMedical Informatics, University of Utah School of Medicine, Salt Lake City, and dVeterans Affairs Salt Lake City Healthcare System, Salt Lake City, Utah, USA
                Article
                92280 Am J Nephrol 2006;26:142–148
                10.1159/000092280
                16557020
                © 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: 1, Tables: 4, References: 34, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/92280
                Categories
                Original Report: Patient-Oriented, Translational Research

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