Causes and Prognosis of Decreased GFR by Race and Ethnicity

Chronic kidney disease disproportionately affects racial and ethnic minorities, but little is known about the determinants and consequences of decreased GFR (45-75 ml/min/1.73 m2) in these populations. Current studies are limited by non-representative populations, and gaps in knowledge about normal levels of measured GFR, appropriate methods to estimate GFR, associations of decreased GFR with development and progression of CKD and CVD, and effect modification by other biomarkers. Measurement of GFR in an ongoing longitudinal study of a representative, multi-racial and multi-ethnic population, with utilization of stored serum and urine for investigation of emerging biomarkers, is required to address these questions.


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Similar Ideas [ 4 ]


  1. Comment
    Helen Nickerson

    DNA would also be useful if these measurements and samples were to be collected

  2. Comment
    Bruce Molitoris
    ( Moderator )

    Excellent idea but will have to have reliable measured GFR. Also,why not quantify additional kidney functions such as serum erythropoetin and 1,25-D3 levels?

  3. Comment
    Harold Feldman
    ( Moderator )

    The study of racial and ethnic minorities with CKD is a very important goal. Adequate assessment of kidney function is likely to require more than GFR estimation. In addition to protein excretion, other metabolic parameters may be needed to provide a panel of measures that capture various aspects of renal function.

  4. Comment
    Vallabh (Raj) Shah

    Given the complexity of stages of CKD along with CVD, a multi-marker approach will be needed to add incremental value to clinical and imaging variables for prediction of progression of CKD. That a single molecule can unambiguously specify disease is a dangerous and unrealistic expectation. The development of 'signatures (profiling)' of bio-markers in etiologic pathways as opposed to measuring individual markers will facilitate identification of perturbed pathways and the

    development of new diagnostic and therapeutic interventions. We've to focus on signatures through high throughput metabolimics and or epigenomics now that GWAS didnt give us a magic bullet.


  5. Comment
    Bruce Carter

    Rather than just another "associational" study--useful perhaps for prediction/prognosis (some groups do better worse than others is not by itself as useful), such efforts should be used to better identify specific genetic differences that might someday yield more targeted therapies, (and specific molecules worthy of targeting.) Recent work such APOL1/MYH9 indicates potential mis-steps, but also new targets on the horizon. No "magic bullet"--but perhaps better aim.

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