Identifying robust association between genetic variation and severe human CKD phenotypes has been hindered by lack of collections of patient sample collection of sufficient size to use effectively in GWAS. The community could address this issue by developing reproducible but simple clinical phenotyping criteria and collecting samples from ESRD patients in dialysis units. Contrast can be made to publicly available datasets of healthy volunteers with GWAS data. I am assuming, for example, that patients with diabetic nephropathy can be compared to healthy non-diabetic patients since the genetic architecture of type 2 diabetes common variants has been characterized.
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