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      Uromodulin concentrations are not associated with incident CKD among persons with coronary artery disease

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          Abstract

          Background

          A common variant of the UMOD gene was linked with prevalent chronic kidney disease (CKD) in large, genomics consortia. One community-based study found that urine concentrations of the uromodulin protein forecast risk of incident CKD. This study within persons with known coronary artery disease (CAD) evaluated whether uromodulin concentrations could distinguish CKD risk.

          Methods

          In the Heart and Soul Study, the UMOD snp (12917707) was genotyped in 879 individuals with baseline creatinine clearance (CrCl) measured from a 24-hour urine collection. Uromodulin protein was measured from stored urine specimens among a subset of 120 participants, balanced by genotype. Incident CKD cases (N = 102) were defined by an initial CrCl > 70 ml/min and a 5-year follow-up CrCl <60 ml/min; controls (N = 94) were matched on age, sex, and race.

          Results

          Among 527 self-described White participants with DNA, 373 (71%) were homozygous for the dominant allele (G/G), 133 (25%) were heterozygous (G/T) and only 21 (4%) were homozygous for the minor allele (T/T). The T/T genotype had an approximately 11 ml/min higher CrCl than the other 2 groups, but this difference did not reach statistical significance (p = 0.20). The T/T genotype had significantly lower uromodulin levels than the common G/G genotype, and the G/T genotype had intermediate levels. However, uromodulin concentrations were similar between cases and controls (44 vs. 48 mg/dL, p = 0.88).

          Conclusions

          This study among a cohort of persons with established CAD found no association between urine uromodulin and incident CKD, although UMOD genotype was associated with urine uromodulin concentrations.

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          Estimating GFR using serum cystatin C alone and in combination with serum creatinine: a pooled analysis of 3,418 individuals with CKD.

          Lesley Stevens, Josef Coresh, Christopher H Schmid … (2008)
          Serum cystatin C was proposed as a potential replacement for serum creatinine in glomerular filtration rate (GFR) estimation. We report the development and evaluation of GFR-estimating equations using serum cystatin C alone and serum cystatin C, serum creatinine, or both with demographic variables. Test of diagnostic accuracy. Participants screened for 3 chronic kidney disease (CKD) studies in the United States (n = 2,980) and a clinical population in Paris, France (n = 438). Measured GFR (mGFR). Estimated GFR using the 4 new equations based on serum cystatin C alone, serum cystatin C, serum creatinine, or both with age, sex, and race. New equations were developed by using linear regression with log GFR as the outcome in two thirds of data from US studies. Internal validation was performed in the remaining one third of data from US CKD studies; external validation was performed in the Paris study. GFR was measured by using urinary clearance of iodine-125-iothalamate in the US studies and chromium-51-EDTA in the Paris study. Serum cystatin C was measured by using Dade-Behring assay, standardized serum creatinine values were used. Mean mGFR, serum creatinine, and serum cystatin C values were 48 mL/min/1.73 m(2) (5th to 95th percentile, 15 to 95), 2.1 mg/dL, and 1.8 mg/L, respectively. For the new equations, coefficients for age, sex, and race were significant in the equation with serum cystatin C, but 2- to 4-fold smaller than in the equation with serum creatinine. Measures of performance in new equations were consistent across the development and internal and external validation data sets. Percentages of estimated GFR within 30% of mGFR for equations based on serum cystatin C alone, serum cystatin C, serum creatinine, or both levels with age, sex, and race were 81%, 83%, 85%, and 89%, respectively. The equation using serum cystatin C level alone yields estimates with small biases in age, sex, and race subgroups, which are improved in equations including these variables. Study population composed mainly of patients with CKD. Serum cystatin C level alone provides GFR estimates that are nearly as accurate as serum creatinine level adjusted for age, sex, and race, thus providing an alternative GFR estimate that is not linked to muscle mass. An equation including serum cystatin C level in combination with serum creatinine level, age, sex, and race provides the most accurate estimates.
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            Cardiovascular disease and subsequent kidney disease.

            Hocine Tighiouart, Mohamed ElSayed, Rifaat D Salem … (2007)
            Chronic kidney disease is a risk factor for cardiovascular disease (CVD); however, it is uncertain if CVD is a risk factor for progression or development of kidney disease. Individual patient data were pooled from 2 longitudinal, community-based, limited-access studies, the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study. Baseline CVD was defined by stroke, angina, claudication, transient ischemic attack, coronary angioplasty or bypass, and recognized or silent myocardial infarction. Study outcomes included kidney function decline, defined by an increase in serum creatinine level of at least 0.4 mg/dL (>or=35.4 micromol/L), and development of kidney disease, defined by an increase in serum creatinine level of at least 0.4 mg/dL (>or=35.4 micromol/L) in which the baseline serum creatinine level was less than 1.4 mg/dL (<123.8 micromol/L) in men and less than 1.2 mg/dL (<106.1 micromol/L) in women and the final serum creatinine levels exceeded these levels. Secondarily, kidney function decline was defined by an estimated glomerular filtration rate (eGFR) reduction of at least 15 mL/min per 1.73 m(2), and development of kidney disease was defined by an eGFR reduction of at least 15 mL/min per 1.73 m(2) in which the baseline eGFR was at least 60 mL/min per 1.73 m(2) and the final eGFR was below these levels. Multivariate logistic regression analysis was used to determine the association between CVD and outcomes. Among 13 826 individuals, the mean +/- SD baseline serum creatinine level was 0.9 +/- 0.2 mg/dL (79.6 +/- 17.7 micromol/L), and the mean +/- SD baseline eGFR was 89.8 +/- 20.1 mL/min per 1.73 m(2). In serum creatinine level-based models, 520 individuals (3.8%) experienced kidney function decline, and 314 individuals (2.3%) developed kidney disease during a mean +/- SD of 9.3 +/- 0.9 years of follow-up. Baseline CVD, present in 1787 individuals (12.9%), was associated with an increased risk of all outcomes (odds ratio, 1.70; 95% confidence interval, 1.36-2.13), an odds ratio of 1.75 (95% confidence interval, 1.32-2.32) for serum creatinine level, and odds ratios of 1.28 (95% confidence interval, 1.13-1.45) and 1.54 (95% confidence interval, 1.26-1.89) for eGFR for kidney function decline and development of kidney disease, respectively. Cardiovascular disease is independently associated with kidney function decline and with the development of kidney disease.
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              Uromodulin levels associate with a common UMOD variant and risk for incident CKD.

              Ya-Qin Fu, Shih-Jen Hwang, Josef Coresh … (2010)
              Common variants in the region of the UMOD gene, which encodes uromodulin (Tamm-Horsfall protein), associate with chronic kidney disease (CKD) and estimated GFR (eGFR). Whether uromodulin levels associate with UMOD variants or with the risk for developing CKD is unknown. We conducted an age- and gender-matched case-control study (n = 200) of incident CKD (eGFR <60 ml/min per 1.73 m(2)) within the Framingham Heart Study (FHS). Baseline urinary uromodulin concentrations were related to case-control status 9.9 yr later and to genotype at rs4293393. As a replication set, we tested the genotype association with uromodulin concentration in the Atherosclerosis Risk in Communities (ARIC) Study (n = 42). Geometric means of uromodulin concentrations were 51% higher in case than in control subjects (P = 0.016). The adjusted odds ratio of CKD per 1-SD higher concentration of uromodulin was 1.72 (95% confidence interval 1.07 to 2.77; P = 0.03) after accounting for CKD risk factors and baseline eGFR. We observed lower urinary uromodulin concentrations per each copy of the C allele at rs4293393 in both cohorts. In summary, elevated uromodulin concentrations precede the onset of CKD and associate with a common polymorphism in the UMOD region.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMC Nephrol
                Title: BMC Nephrology
                Publisher: BioMed Central
                ISSN (Electronic): 1471-2369
                Publication date Collection: 2011
                Publication date (Electronic): 14 January 2011
                Volume: 12
                Page: 2
                Affiliations
                [1 ]Division of General Internal Medicine, San Francisco VA Medical Center; San Francisco, CA, USA
                [2 ]Department of Medicine University of California, San Francisco; San Francisco, CA, USA
                [3 ]National Heart, Lung and Blood Institute's Framingham Heart Study, Framingham, MA; Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (CSF), USA
                [4 ]Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
                [5 ]Division of Metabolism and Endocrine Sections, San Francisco VA Medical Center; San Francisco, CA, USA
                Article
                Publisher ID: 1471-2369-12-2
                DOI: 10.1186/1471-2369-12-2
                PMC ID: 3031204
                PubMed ID: 21235779
                SO-VID: e1fc6916-3e13-44dc-9ccc-a09017b5bbc9
                Copyright © Copyright ©2011 Shlipak et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 8 September 2010
                Date accepted : 14 January 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Nephrology
                Data availability:
                ScienceOpen disciplines: Nephrology

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