Pranav Garimella, MBBS, MPH, is chief medical officer of the American Kidney Fund.

Pranav Garimella, MBBS, MPH

APOL1-Mediated Kidney Disease: From Genetic Discovery to the Edge of Precision Medicine


A decade and a half after APOL1 was linked to kidney disease, clinicians are still grappling with misdiagnosis, unpredictable progression, and uneven access to genetic insight, just as targeted therapies begin to emerge.

Kirk Campbell, MD, Professor of Medicine and Chief of the Renal Division at the University of Pennsylvania Perelman School of Medicine.

Pranav Garimella, MD, Chief Medical Officer of the American Kidney Fund,

Kristin Meliambro, MD, is an Associate Professor in the Department of Medicine, Division of Nephrology at the Icahn School of Medicine at Mount Sinai.

Katalin Susztak, MD, PhD, is a Professor of Medicine and Genetics at the University of Pennsylvania

John Cijan He, MD, PhD, Professor of Medicine and Pharmacological Sciences and Chief of the Division of Nephrology at the Icahn School of Medicine at Mount Sinai

A Genetic Discovery That Reshaped Kidney Disease Risk

In the span of roughly 16 years, APOL1 has moved from evolutionary curiosity to one of the most important genetic risk factors in nephrology.

The G1 and G2 variants, enriched in populations with West and Central African ancestry, rose in frequency because they confer protection against 

 infection. Today, they are recognized as among the strongest common genetic risk factors for kidney disease.

Approximately one-third of African Americans carry at least one high-risk APOL1 variant, and about 14% carry the high-risk genotype—two risk alleles in combinations such as G1/G1, G2/G2, or G1/G2. Globally, more than 100 million people in sub-Saharan Africa are estimated to carry two risk variants, with frequencies reaching 37% in parts of Ghana and 50% in southeastern Nigeria.

“It is a long time,” said Campbell. “But the fact that it took 13 years from the discovery of APOL1 kidney disease genetic association to the first proof-of-concept APOL1 inhibitor efficacy report should be celebrated.”

At the same time, Campbell emphasized ongoing uncertainty:

“There are still no approved APOL1-specific therapies, no consensus on population screening, limited ability to predict who among carriers will progress, and unresolved questions about ‘second hits,’” he said.

Rethinking a Default Diagnosis: Hypertension as Explanation — or Misclassification

Before APOL1 can be treated, it must be recognized—and that remains a persistent challenge.

Hypertensive nephrosclerosis has long served as a default diagnosis for chronic kidney disease in patients with hypertension, particularly Black patients. But emerging evidence suggests this label often obscures more specific and potentially treatable disease.

One biopsy-based study found that clinical criteria for nephrosclerosis had a sensitivity of just 0.13. Even optimized algorithms only reached 0.19, and roughly 40% of clinically diagnosed cases were found to have alternative diagnoses such as glomerulonephritis or interstitial nephritis.

Clinicians increasingly caution against treating hypertension as the primary explanation by default. “Hypertensive nephrosclerosis is often a diagnosis of exclusion,” Garimella noted. “Some patients labeled that way actually have APOL1-associated kidney disease, FSGS, or another primary kidney disorder.”

The reframing has clinical and psychological implications. Elevated blood pressure may in some cases be a consequence rather than a cause of kidney disease.

“Sometimes patients feel that explanation doesn’t fully make sense, especially if their hypertension hasn’t seemed severe,” Meliambro observed. “Recognizing that there may have been more going on can be validating rather than implying they did something wrong.”

The data on blood pressure management remain nuanced. Some studies show intensive blood pressure control does not necessarily slow progression in high-risk APOL1 carriers, while other data suggest a survival benefit with more intensive control compared with standard targets.

The introduction of a dedicated ICD code for APOL1-mediated kidney disease represents an important structural shift, enabling more precise diagnosis, counseling, and trial referral.

The Core Problem: Risk Without Prediction

While identifying APOL1 risk variants is now straightforward, predicting outcomes remains the central clinical challenge.

Carriers of two high-risk alleles face an estimated 15%–20% lifetime risk of kidney disease—meaning roughly 80% will never develop kidney failure.

“This represents a major knowledge gap,” Susztak explained. “If you receive a genotype result, you start asking: should I be doing something specific to prevent disease?”

Traditional risk models have not resolved this. Polygenic risk scores have failed to improve prediction in APOL1 high-risk individuals. Clinical risk scores based on eGFR, proteinuria, age, and sex perform well in established disease but are not clinically meaningful in preserved kidney function, she said.

“Some work has suggested that the G1/G1 genotype might be associated with a higher risk of decline in GFR and also a younger age of developing kidney disease,” Meliambro noted, adding that this requires further validation. High-risk genotype is still defined as any two risk alleles.

To address this gap, researchers turned to proteomics.

In a study of approximately 1,400 African American individuals from the Penn Medicine Biobank—many with preserved kidney function and no proteinuria at baseline—researchers analyzed roughly 7,700 circulating proteins.

Using machine learning, they identified nine proteins that, combined with clinical variables, formed the APOL1 Proteomic Risk Score (APRS), achieving a time-dependent AUC of 86.5%.

Individuals in the highest-risk quintile had approximately a 60% probability of progressing to dialysis or transplant over 10 years, while those in the lowest-risk quintile had less than a 1% risk. The score outperformed both the Kidney Failure Risk Equation and polygenic risk scores.

“Some of these proteins are related to tissue damage in the kidney that is not reflected in creatinine levels or urinary protein,” Susztak said. “For example, markers like MMP7 and matrix proteins may reflect fibrosis or injury that isn’t detected with standard tests.”

Others reflect inflammatory and endothelial pathways.

The score has been validated in external cohorts, including UK Biobank and NIH-supported data, but remains a research tool.

“We need to incorporate this biomarker into clinical trials and demonstrate that it is actionable,” she said. “Currently, we can treat the disease but not cure it.”

What APOL1 Biology Is Revealing About Early Kidney Injury

Beyond prediction, APOL1 research is reshaping understanding of early disease biology.

“In African American patients, we know the APOL1 gene is a high-risk gene for what we call APOL1-mediated glomerular disease, which is essentially like FSGS,” said He. “When this gene is highly expressed, it can cause podocyte injury through specific cellular pathways.”

“Some of these proteins are related to tissue damage in the kidney that is not reflected in creatinine levels or urinary proteins,” Susztak said.

“Other proteins are linked to inflammation. APOL1 is strongly regulated by inflammation, so individuals with higher inflammatory states may be at greater risk.”

“And there are a few proteins related to endothelial injury that we are still working to understand.”

Together, these findings suggest injury may precede traditional clinical markers such as proteinuria or eGFR decline.

From Biology to Therapy: Precision Medicine Takes Shape

Mechanistic insight has enabled targeted drug development.

“Based on that mechanism, therapies have been developed to block the pathways activated by APOL1,” He said. “These inhibitors have shown promising results in reducing proteinuria in phase 2 studies, with ongoing phase 3 trials.”

Inaxaplin directly targets APOL1 pore formation in podocytes.

“This is a very specific, targeted therapy that inhibits the pore-forming function of the APOL1 protein,” Meliambro said. “It represents a true example of precision medicine in nephrology.”

Other approaches include antisense oligonucleotides and anti-inflammatory strategies.

Despite therapeutic advances, management remains standard CKD care.

“A two-risk-variant APOL1 genotype raises concern for progressive disease,” Garimella explained. “But the treatment backbone remains standard CKD care.”

That includes RAAS blockade, SGLT2 inhibitors when appropriate, blood pressure control, statins, and avoidance of nephrotoxins.

“APOL1 testing is worth considering when the result can change follow-up, trial eligibility, transplant donor counseling, or future targeted-treatment decisions,” Campbell said. “But it should come with counseling, and it should never replace a full kidney-disease workup.”

“Awareness only matters if it changes decisions such as diagnosis, counseling, testing, referral, or follow-up,” Garimella said.

The ICD code for APOL1-mediated kidney disease may help translate awareness into action.

Barriers to Integration and Uneven Adoption

Despite availability of testing, adoption remains inconsistent.

“It’s not necessarily ordering the test—it’s interpreting and explaining the results,” Meliambro said.

Barriers include lack of guidelines, limited genetic counseling infrastructure, and patient concerns about privacy and discrimination.

Equity Will Define the Impact of Precision Medicine

“Equitable access would require more than drug approval,” Campbell said. “It would require payer coverage for testing, counseling, nephrology referral, and medication.”

“Otherwise, we risk repeating the same inequities,” he said. “Patients with better access get tested and treated, while underserved populations remain underdiagnosed.”

The decision to hold a major consensus meeting in Accra reflects the field’s shifting center of gravity.

“This is a rapidly evolving field,” Meliambro said. “There has been substantial research progress. But there are still many unresolved questions—especially around predicting disease progression and translating this knowledge into improved patient outcomes.”

“There is significant investment and enthusiasm,” she added. “Hopefully that will lead to meaningful breakthroughs in the near future.”

Campbell reports relevant disclosures with NIH, National Kidney Foundation. Garimella reports relevant disclosures with NIH. Meliambro reports no relevant disclosures identified. Susztak reports relevant disclosures with NIH. He reports no relevant disclosures identified.

Genovese G, Friedman DJ, Ross MD, et al. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science. 2010;329(5993):841-845. doi:10.1126/science.1193032

Tzur S, Rosset S, Shemer R, et al. Missense mutations in the APOL1 gene are highly associated with end stage kidney disease risk previously attributed to the MYH9 gene. Hum Genet. 2010;128(3):345-350. doi:10.1007/s00439-010-0861-0

Friedman DJ, Pollak MR. APOL1 nephropathy: from genetics to clinical applications. Clin J Am Soc Nephrol. 2021;16(2):294-303. doi:10.2215/CJN.15161119

Gbadegesin RA, Ulasi I, Ajayi S, et al. APOL1 bi- and monoallelic variants and chronic kidney disease in West Africans. N Engl J Med. 2025;392:228-238. doi:10.1056/NEJMoa2403840

Hallan S, Øien CM, Garborg K, et al. Hypertensive nephrosclerosis: wider kidney biopsy indications may be needed to improve diagnostics. J Intern Med. 2021;289(4):527-540. doi:10.1111/joim.13146

Ojo A, Ulasi I, Freedman BI, et al. APOL1 kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. Published online June 23, 2025. doi:10.1016/j.kint.2025.04.029

Li C, et al. Proteomic risk score for early prediction of kidney disease progression in individuals with APOL1 high-risk genotypes. Nat Med. Published online April 15, 2026. doi:10.1038/s41591-026-04337-2

Egbuna O, Zimmerman B, Manos G, et al. Inaxaplin for proteinuric kidney disease in persons with two APOL1 variants. N Engl J Med. 2023;388(11):969-979. doi:10.1056/NEJMoa2202396

Vertex Pharmaceuticals Incorporated. Vertex advances inaxaplin (VX-147) into phase 3 portion of adaptive phase 2/3 clinical trial for the treatment of APOL1-mediated kidney disease. Press release. April 1, 2024. Accessed May 1, 2026. https://news.vrtx.com/news-releases/news-release-details/vertex-advances-inaxaplin-vx-147-phase-3-portion-adaptive-phase

Vertex Pharmaceuticals Incorporated. Vertex announces key advancements across kidney portfolio. Press release. September 25, 2025. Accessed May 1, 2026. https://news.vrtx.com/news-releases/news-release-details/vertex-announces-key-advancements-across-kidney-portfolio

Maze Therapeutics. Maze Therapeutics doses first patient in phase 2 HORIZON clinical trial evaluating MZE829 as a potential treatment for APOL1 kidney disease. Press release. February 7, 2025. Accessed May 1, 2026. https://ir.mazetx.com/news-releases/news-release-details/maze-therapeutics-doses-first-patient-phase-2-horizon-clinical

Maze Therapeutics. Maze Therapeutics announces positive topline data from phase 2 HORIZON trial of MZE829. Press release. March 25, 2026. Accessed May 1, 2026. https://ir.mazetx.com/news-releases/news-release-details/maze-therapeutics-announces-positive-topline-data-phase-2

Articles

APOL1 G1/G2 variants, selected for trypanosome resistance, are prevalent in people with West/Central African ancestry and drive substantial CKD and FSGS risk, yet progression remains poorly predictable. Hypertensive nephrosclerosis frequently misclassifies underlying glomerular or interstitial disease, prompting calls for more precise workups and use of the new APOL1-mediated kidney disease ICD code. A nine-protein APOL1 Proteomic Risk Score stratifies 10-year kidney failure risk far better than existing models. Targeted APOL1 inhibitors (eg, inaxaplin) and other modalities are advancing, while equitable access to testing, counseling, and therapy lags.

APOL1 research is driving precision nephrology, but prediction gaps and equity challenges still limit clinical impact.

APOL1-Mediated Kidney Disease: From Genetic Discovery to the Edge of Precision Medicine

For decades, a significant proportion of 

 in Black patients has been attributed to hypertension. This mislabeling may have obscured a distinct and underrecognized genetic driver, variants in the 

APOL1-mediated kidney disease (AMKD) affects an estimated 6 million African Americans who carry a high-risk genotype,¹ with approximately 13% of the self-identified African American population carrying two risk alleles that confer substantially elevated kidney disease risk.² Yet AMKD remains largely absent from routine clinical practice.

In recognition of the third annual AMKD Awareness Day, HCPLive spoke with Pranav Garimella, MD, Chief Medical Officer of the American Kidney Fund, about the scope of the misclassification problem embedded in the "hypertensive nephrosclerosis" diagnosis, the systemic and patient-level barriers slowing genetic testing uptake, and what nephrologists outside major academic centers should be doing differently — right now — for patients who carry two high-risk APOL1 variants.

The American Kidney Fund has described APOL1-mediated kidney disease as historically underdiagnosed, with many cases likely labeled as hypertension-associated kidney disease. How significant is that misclassification problem in practice, and how should nephrologists be rethinking patients currently labeled with 'hypertensive nephrosclerosis'?

The misclassification problem is real and clinically important. Hypertensive nephrosclerosis is often a diagnosis of exclusion, so some patients labeled that way actually have APOL1-associated kidney disease, FSGS, glomerulonephritis, or another primary kidney disorder. One biopsy-based study found that current clinical criteria for nephrosclerosis had very low sensitivity, 0.13, and even an optimized algorithm only rose to 0.19, while 40% of test-positive cases had other treatable diagnoses such as glomerulonephritis or interstitial nephritis.

In practice, that means nephrologists should be more skeptical of the label, especially in younger patients, those with proteinuria, hematuria, rapid eGFR decline, or an atypical course. Rather than accepting hypertension as the full explanation, we should rethink those cases as 'kidney disease with hypertension' and consider whether biopsy, genetic testing, or a broader workup is warranted.

Genetic testing for APOL1 is becoming more available, but uptake in clinical practice remains limited. What are the biggest barriers—clinical, systemic, or patient-level—to broader testing in high-risk populations, and where does responsibility for closing that gap ultimately fall?

Despite increasing availability of genetic testing, several barriers continue to limit its broader uptake in clinical practice. At the clinical level, many health care professionals remain uncertain about how to act on results, particularly if the downstream implications for treatment and monitoring are not clearly defined in guidelines. In addition, genetic testing is still not well integrated into routine clinical workflows.

At the patient level, awareness of APOL1 variants remains relatively low, even among high-risk populations. Concerns about genetic privacy, potential discrimination and mistrust of the healthcare system can further reduce uptake, particularly in communities that have historically been underserved or marginalized.

Addressing these gaps will require shared responsibility across stakeholders. Professional societies and researchers must develop consensus guidelines on monitoring, including incorporating genetic counseling services. To make meaningful progress, there needs to be equitable access, coverage for genetic counseling services, and an infrastructure. At the same time, community engagement and patient education are essential to building trust and awareness, requiring coordinated efforts across the care continuum.

The third annual APOL1-mediated kidney disease Awareness Day just passed. When you talk about 'awareness,' who is the primary target—patients, clinicians, or both? And what does meaningful awareness look like in practice versus awareness that doesn't change clinical care?

Both patients and clinicians. The American Kidney Fund is working to reach all of these audiences. Given how relatively recent the link between APOL1 and kidney disease was identified, we know that awareness among patients is low, and it's fair to say that health care professionals outside of nephrology likely have not received specialized education about AMKD.

For patients, awareness means understanding that APOL1 can be relevant to kidney disease risk and knowing when to ask questions or seek testing. For clinicians, especially outside nephrology, it means recognizing when APOL1 or AMKD should be part of the differential and when a "hypertensive nephrosclerosis" label deserves a second look. The new ICD code for AMKD is a big step forward as it gives clinicians a formal way to name APOL1-mediated kidney disease instead of forcing patients into nonspecific labels like hypertensive nephrosclerosis. In practice, that should improve recognition, data capture, family counseling, and trial referral.

Awareness only matters if it changes decisions such as diagnosis, counseling, testing, referral, or follow-up — not if it just increases familiarity with the term. Actionable awareness is the goal with the American Kidney Fund's efforts surrounding AMKD awareness.

With APOL1-targeted therapies in clinical trials, what should nephrologists outside of major academic centers be doing right now for a patient with two high-risk APOL1 variants—if anything differently today compared to standard chronic kidney disease management?

Nephrologists should treat the CKD phenotype, not just the genotype, using standard measures that slow progression: RAAS blockade when indicated, SGLT2 inhibitors when appropriate, BP control, statins when indicated, nephrotoxin avoidance, and sick-day counseling.

They should monitor closely if the patient is high risk. A two-risk-variant APOL1 genotype raises concern for progressive disease, so you should be more alert to rising albuminuria, falling eGFR, and faster-than-expected progression, but the treatment backbone remains standard CKD care.

Nephrologists should also discuss family member testing to identify other high-risk carriers who may need close monitoring as well, and refer to a clinical trial if eligible and if access exists.

Lastly, use shared decision-making. If discussing APOL1 results, explain that many people with two risk variants never develop kidney disease, so genotype is risk information, not an outcome. Partner with a clinical genetic counselor for better patient understanding.

Editor’s Note; Garimella reported no relevant financial disclosures.

Srinivasan V, So PN, Kwakyi EPK, Lerma EV, Wiegley N. APOL1 mediated kidney disease: a review and look toward the future. 

Pollak MR, Friedman DJ. APOL1 and APOL1-associated kidney disease: a common disease, an unusual disease gene — proceedings of the Henry Shavelle Professorship. 

APOL1 high-risk genotypes—present in ~13% of self-identified African Americans—may underlie kidney disease long attributed to hypertension, leaving millions with unrecognized AMKD. “Hypertensive nephrosclerosis” often functions as a low-specificity diagnosis of exclusion; biopsy data show poor clinical sensitivity and frequent alternative, treatable pathology. Broader APOL1 testing is slowed by unclear actionability, workflow gaps, limited counseling access, and privacy/mistrust concerns. A dedicated ICD code can improve recognition, data capture, counseling, and trial referral. Management remains phenotype-driven CKD care with intensified monitoring and shared decision-making.

Garimella, MBBS, unpacks what clinicians need to know about APOL1-mediated kidney disease, including misclassification, testing barriers, and management gaps. 

Beyond Hypertensive Nephrosclerosis: A Closer Look at APOL1-Mediated Kidney Disease

Rebuilding Trust, Increasing Living Donor Transplant In Black Kidney Candidates, With Pranav Garimella, MBBS, MPH

While recent national policy aimed to repay a historical debt for black kidney transplant candidates who were disadvantaged by race-based eGFR, the structural barriers to living donor kidney transplants remain.

“The study improved overall transplantation rates in persons who identify as Black, particularly for preemptive transplantation, but it did not increase living donor transplants,” Pranav Garimella, MBBS, MPH, Chief Medical Officer of the American Kidney Fund and an associate professor of medicine at UC San Diego, told HCPLive. “That highlights a persistent gap driven in part by historic mistrust in the medical system, and underscores the need to build trust and improve access to living donor transplantation.”

Historically, these patients had been marginalized by race-based kidney function equations for decades, which misrepresented the measure of their kidney function. The 2023 Organ Procurement and Transplantation Network (OPTN) national policy restored waitlisting time, and successfully saw an increase in transplants for Black kidney candidates of 

. Meanwhile, the OPTN data also pointed out that after the initial spike, 

transplant rates have begun to decline again

, with experts suggesting structural barriers remain a looming challenge in getting historically marginalized patients onto transplant lists.

While the number of patients who would benefit from a living donor kidney transplant continually outpaces the number of available organs, access remains disproportionately available to those based on their race.

For example, despite increased rates of end-stage kidney disease in patients who are black, these patient recive living donor kidney transplants significantly less frequently than those who are white. Furthermore, black patients are less likely to be referred for kidney transplant evaluation and less likely to be added to a waitlist.

“A critical bottleneck in transplantation is the limited availability of donor kidneys—especially from living donors—so expanding access through community engagement, supportive policies, and addressing financial concerns for donors will be essential to meaningfully increase transplant rates, particularly in historically marginalized populations,” concluded Garimella.

Editor’s Note: Garimella has relevant disclosures with Otsuka and the PKD Foundation.

Khazanchi R, Fleishman A, Eneanya ND, et al. Wait Time Modifications for Black Transplant Candidates Affected by Race-Based Kidney Function Estimation. 

. Published online September 2026:e260001. doi:

https://doi.org/10.1001/jamainternmed.2026.0001

Garimella P. How Rewriting Race-Based GFR Equations Changed Kidney Transplant Access, With Pranav Garimella, MBBS, MPH. HCPLive. Published March 31, 2026. 

https://www.hcplive.com/view/rewriting-race-based-egfr-equation-changed-kidney-transplant-access

Garimella P. OPTN Policy Gave Back Time, Increased Transplants for Black Kidney Candidates So Why Have Rates Plateaued? HCPLive. Published April 2, 2026. 

https://www.hcplive.com/view/optn-policy-gave-back-time-to-waitlisted-black-kidney-candidates-but-transplant-rates-are-declining

Suah A, Saunders MR. Racial Disparities in Living Donor Kidney Transplantation—How Can We Bridge the Gap? 

https://doi.org/10.1001/jamanetworkopen.2023.47808

Videos

Pranav discusses the necessity for addressing the structural barriers that remain for living donor kidney transplantations in black patients. 

OPTN Policy Gave Back Time, Increased Transplants for Black Kidney Candidates So Why Have Rates Plateaued?

national policy restored waitlisting time and saw an increase in 5.3 transplants per 1000 listings

 for Black kidney transplant candidates marginalized by race-based kidney function equations for decades.

New data from the Organ Procurement and Transplantation Network (OPTN) pointed out that transplant rates have begun to decline again, with experts suggesting structural barriers remain a looming challenge in getting historically marginalized patients onto transplant lists.

“The numbers for a long period of time have been stable, and we see this fight between 2023 and 2024 and over the last two years, once again, there has been a flattening of that curve, and that's because what the policy did was to repay a historical debt of inequity, and that has now been restored,” Pranav Garimella, MBBS, MPH, Chief Medical Officer of the American Kidney Fund and an associate professor of medicine at UC San Diego, told HCPLive. “The question now remains, how do we take this forward and improve access to transplantation for people who have historically been marginalized?”

The history of race-based GFR involves distinct values for patients who identified as black compared to other races. These were based on studies published in the 1990s, which found increased serum creatinine levels in black participants, which they attributed to increased average muscle mass, a historic clinical misconception and stereotype. As a result, race-based GFR equations systematically assigned a ~16–18% higher eGFR value to these patients, leading to an underestimation in the severity of kidney disease, thereby delaying treatment at crucial intervention windows.

In 2021, the National Kidney Foundation and American Society of Nephrology recommended the 2021 CKD-EPI Creatinine Equation, a race-free formula using serum creatinine, age, and sex, removing the variable “black” or “non-black”. The OPTN implemented a national policy in 2022, bolstering the CKD-EPI equation to improve accuracy and fairness in kidney care.

As recently as January 2023, the OPTN implemented a second national policy, which required the review and adjustment of waiting times for Black candidates who had been disadvantaged by the previous equation.

Despite the gains made by this national policy, 

barriers to kidney care and transplantation remain for historically marginalized patient populations.

“Even if we provide them with an updated GFR that makes them eligible, there are factors, financial economics, and social determinants that may not allow them to receive a transplant,” Garimella said. “While the policy itself has shown that it can result in meaningfully increased transplant access to patients who get to that transplant list, getting to that transplant list remains the challenge, and again, beyond people who identify as black.”

Another important facet of this data that Garimella points out is the increase in transplants for candidates who identified as Black, which did not reduce transplants from individuals of other races. He emphasizes that correcting this historical injustice does not mean taking away from others.

Uppal P, Benjamin Ira Golden, Panicker A, Khan OA, Burday MJ. The Case Against Race-Based GFR. 

https://doi.org/10.32481/djph.2022.08.014

Charles K, Mary Jane Lewis, Montgomery E, Reid M. The 2021 Chronic Kidney Disease Epidemiology Collaboration Race-Free Estimated Glomerular Filtration Rate Equations in Kidney Disease: Leading the Way in Ending Disparities. 

New OPTN data shows kidney transplant gains from race-free GFR and restored wait times stall, as structural barriers still limit equitable listing access.