Mallika Mendu, MD, MBA MedicalDirector of Clinical Operations Brigham and Women’s Hospital

Re-evaluation of Race Multiplier in Estimating Kidney Disease Interview with:


Dr. Mendu

Mallika Mendu, MD, MBA
MedicalDirector of Clinical Operations
Brigham and Women’s Hospital What is the background for this study? What are the main findings?

Response: African-Americans with chronic kidney disease have poorer outcomes with respect to hypertension control, timely nephrology referral, progression to end stage renal disease, placement of vascular access and transplantation compared to other racial groups. For the past two decades a race multiplier has been applied in equations that estimate glomerular filtration rate (a proxy for kidney function) for African-Americans. We sought to determine whether what the impact of the race multiplier term was on care delivered to African-Americans, by using our health system-wide CKD registry. We were particularly focused on advanced CKD patient outcomes, knowing that there are health disparities that could be potentially exacerbated.

The original CKD-EPI and MDRD studies showed an association between African-American race with higher measured GFR at the same blood creatinine concentration. However, there have been concerns raised about the application of the race multiplier to all African-American patients. First, there is no clear biological explanation for the association, the identification of Black race was unclear in some of the cohorts used in these studies, and there is vast genetic and ancestral heterogeneity among those who self-identify as black. The use of the race multiplier also ignores the fact that race is a social, not biological construct.

We found that with the removal of the race multiplier, up to one in every three African-American patients would be reclassified as having a more severe stage of CKD, with one-quarter of African-American patients going from stage 3 to stage 4. We also found that with the removal of the race multiplier, 64 patients would have had an eGFR <20, the threshold for referral for kidney transplant, and none of these patients were referred, evaluated or waitlisted for transplant. This is in contrast, to those African-American patients with an eGFR <20 with the race multiplier applied, who had a higher odds of being referred, evaluated or waitlisted for transplant compared to other racial groups (Odds ratio of 2.28, compared to White cohort). If the “race multiplier” when calculating eGFR is eliminated, does it mean than many more African Americans will be referred not just for transplant but for dialysis?

Response: If the race multiplier is eliminated, it means that African-American patients would be classified to a more severe stage of CKD, and in some patients, would fall below the eGFR <20 threshold for referral for transplant evaluation. In clinical practice, the decision to start a patient on dialysis or transplant a patient is not based on an eGFR value, but rather symptoms, trajectory of eGFR decline etc. If race is a social construct, then should everyone be screened for sickle cell, melanoma, Tay-Sachs? Isn’t your argument going against the prevailing push towards more personalized medicine based on genetics?

Our paper does not argue against the use of “precision medicine” which allows for tailoring of diagnosis and treatment, and we do not oppose the use of genetic ancestry to inform clinical decision making. For example, we state in the article that “There are examples of genetic inheritance informing kidney outcomes, such as the established association between the genetic mutation of apolipoprotein-1 (APOL1) and an increased risk of ESRD progression among some African-Americans with West African ancestry (33). Studies have indicated that APOL1 mutations account for over two-thirds of excess ESRD risk among African-Americans in the United States (34). Despite this evidence, most clinical laboratories are not performing APOL1 testing (35, 36).” What should readers take away from your report?

Response: The study provides important data at a time when health systems are considering the elimination of the race multiplier, and don’t have data on the potential implications. Our study provides this needed data. We also do seek to emphasize that there is real risk in potentially overestimating eGFR by using the race multiplier, in a population that already has disparate clinical outcomes. We advocate for at a minimum, full transparency with patients about the use of the race multiplier among providers and systems that continue to use it, and consideration of elimination of the race multiplier in tandem with the use of biomarkers less dependent on race such as Cystatin C. What recommendations do you have for future research as a result of this work?

Response: We recommend that multiple health systems leverage similar CKD registries and conduct analyses about the implications of race multiplier use on their patient populations. We also need to track the impact of removing the race multiplier in those health systems that have made this decision.

Any disclosures? I provide consulting for Bayer AG


Ahmed, S., Nutt, C.T., Eneanya, N.D. et al. Examining the Potential Impact of Race Multiplier Utilization in Estimated Glomerular Filtration Rate Calculation on African-American Care Outcomes. J GEN INTERN MED (2020).

Oct 16, 2020 @ 12:43 am
