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Race-free biomarkers to quantify kidney function: Health equity lessons learned from population-based research

American Journal of Kidney Diseases May 1, 2021

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Original investigation and perspective articles that describe the use and misuse of race in medicine have been increasingly featured in academic and lay media outlets.Specifically, race correction with regard to estimated glomerular filtration rate (eGFR) equations remains controversial owing to foundational equation studies that asserted Black individuals as inherently different than other racial groups.Despite the Human Genome Project confirming that racial groups are not genetically distinct, research studies continue to use race as a proxy for biological differences.Owing to the direct effects of structural racism, Black individuals are at higher risk of developing diabetes and hypertension—the 2 most frequent etiologies of chronic kidney disease (CKD) in the United States. Furthermore, Black individuals are less likely to receive nephrology care or kidney transplantation and have faster progression of CKD to kidney failure.Therefore, the use of a race correction factor that assigns Black individuals better kidney function than other racial groups without biological justification may compound existing disparities and lead to delays in preventative care, as well as to referral for kidney transplant evaluation.To advance health equity among Black Americans with kidney disease, a practical first step includes quantifying kidney disease using biomarkers that do not perform differently across racial groups.

In this issue of AJKD, Inker et al aimed to develop more accurate eGFR equations that do not include a specific Black race coefficient. The investigators used a panel of endogenous filtration markers including β2-microglobulin and β-trace protein, both filtered by glomeruli. Similar to cystatin C, these biomarkers have not been shown to differ significantly between individuals based on age, sex, or race but are more strongly associated with death compared to creatinine. The equations were tested among 14 CKD and non-CKD studies where participants had glomerular filtration rate (GFR) measured using iothalamate, iohexol, or Cr-EDTA. The newly developed eGFR equations used β2-microglobulin and β-trace protein in addition to cystatin C (3-marker panel) or cystatin C and creatinine (4-marker panel) and were tested with and without a Black race coefficient. These equations were then compared with validated CKD-EPI reference equations that used creatinine, cystatin C, or both biomarkers (eGFRcr, eGFRcys, and eGFRcr-cys, respectively).


Agency for Healthcare Research and Quality (AHRQ)