The Kidneys in Black and White: Inheriting Medical Racism
“Black people have higher average muscle mass compared to white people.”
When my medical school classes echoed this statement from the National Kidney Foundation website, it shocked me. It is just one of many ‘scientific facts’ about black bodies that have been implicitly or explicitly taught in medical schools around the country for more than a century, enshrined in medical equations, and promoted by decades of peer-reviewed research. Questioned about the validity of these claims, however, some of our physician-educators hit a wall. “This is what the research has shown,” they responded. “Actually, it’s just complicated.”
What is rather uncomplicated is this: this ‘fact’ about black physical difference is used to justify differences in kidney function testing between black and white people in a measure called the eGFR. The estimated GFR (eGFR) is a measure of kidney function which stands for “estimated glomerular filtration rate” and is a first line test in assessing kidneys. Using this statement about muscle mass creates two ‘separate but equal’ equations for kidney function, and justifies worse kidney-health outcomes for black individuals. In fact, justifying use of race in eGFR equations is just one of the many eugenic myths masquerading as truth in medical education, serving to perpetuate and naturalize the mistreatment of black people in medicine.
Why Does the eGFR Matter?
One of the main functions of our kidneys is to filter the blood, and a low GFR means that substances (such as toxins) are not adequately filtered and instead build up in the bloodstream. A low GFR means poor kidney function, and so eGFR is usually the first line test when evaluating a patient’s kidneys. The estimated GFR is preferred over measured GFR (mGFR) tests which involve 24 hour urine collection and additional, often more invasive, testing. GFR is especially important in the staging of chronic kidney disease (CKD), which impacts about 14% of US Americans annually.
The eGFR equation relies on the measurement of a substance in blood serum called creatinine (SCr), which mainly comes from the natural breakdown of skeletal muscle. High SCr means that it is building up in the blood, meaning a low GFR and poor kidney function. There are several limitations with using SCr for estimation, including that meat, exercise, and medications can all artificially raise SCr. On top of that, testing methods can also confuse other molecules that appear in diabetic diseases or liver diseases for SCr (Poirrini et al. 2019).
There are 3 popular equations that have been used for the eGFR: the Cockcroft-Gault (CG) equation, the Modified Diet Renal Disease (MDRD) Study equation, and the Chronic Kidney Disease Epidemiology (CKD-Epi) equation. The MDRD multiplies the eGFR by 1.212 (versus 1.159 in the CKD-Epi) if the patient is black, as defined by self-reporting or physician perception (Levey 1999, 2010). The MDRD is also the most popularly used eGFR equation in clinical practice and in research (having been cited more than 14000 times). It uses this 1.212 multiplier justifying it with the fact that “this is due to higher average muscle mass and creatinine generation in African Americans” (Levey 2006).
Aside from the very basic question of “how do you determine how black someone has to be for this factor to be applied?,” multiplying by 1.212 (or 1.159) means that black people’s kidney functions are overestimated compared to white people’s. The racial calculus is nauseating.
This overestimation undoubtedly adds to a paradox noted by Nature and other publications: although black people have lower rates of Stage 3 chronic kidney disease (CKD) compared to white people, they have higher rates of Stage 4 CKD and end-stage renal disease (NIDDK 2016, Delanaye & Mariat, 2013). So, although black people are less likely to be diagnosed with earlier stages of kidney disease, they disproportionately feel the burden of its later manifestations. The most insidious thing about CKD is that is it is a progressive, non-reversible disease. So when doctors tell a black patient who actually has CKD that they are above the GFR threshold, and don’t refer them for more intensive treatment or monitoring, this paradox emerges. Compound onto this structural issues which affect black people’s access to kidney transplants (Ariola, 2017), and you have an equation that helps kill black people. All this justified by the implacable conviction that black bodies are different from white bodies.
I cannot imagine, as a physician, sitting down with a black patient and telling them they will not receive optimal treatment because of their perceived race. “I’m sorry, but according to this equation, you do not qualify for further treatment. You see, it’s because scientific data has demonstrated that the black race has more muscle mass, on average, than the white race. Yes, if you were white, it would be different.” It’s no wonder black patients in this country mistrust the medical and scientific establishments; from Tuskegee to the eGFR, medical racism sits unquestioned.
Even in the face of contradictory evidence (published in Nature, for goodness’ sake), clinicians in the USA are still using eGFR to guide clinical decision-making. So, if more science isn’t the answer, how do we cut the eGFR’s Gordian knot? The tools of the social sciences, like those of Critical Race Theory (CRT) and Social Theory, offer us an answer. CRT theorists Delgado & Stefancic (2017) use revisionist interpretations, for example, to provide a “view of history or an event that challenges the accepted one” and encourage the use of “counter-stories to challenge, displace, or mock these pernicious narratives and beliefs”. Social theorists like Michel Foucault, moreover, use a genealogical (or archaeological) methods to analyze the historical progression of ideas and asking how they could have emerged.
Below, I trace the genealogy of the claim that black people have more muscle mass. Using the technique of backward citation tracing — using study citations and marginalia to track the academic lineage of an idea — I excavate a selective history of an unscientific, and indeed racist, lineage of thought in kidney science. To understand the birth of the eGFR, we must first explore the birth of eugenics, PE classes, and ancient hippopotamuses.
Genealogy of the eGFR
In Medical Apartheid, historian Harriet Washington articulates that:
“Use of the term race to denote biologically different types of mankind evolved only in the eighteenth century [with] the study of animal breeding … Not coincidentally, this period coincided with the growth of the slave trade, when the biological distinctiveness of men became economically important.”
Slave owners used the language of science to fabricate differences between the races. Tropes like “blacks were magnificent physical specimens with the minds of children” which subjugated black people on the basis of their dichotomy “between physicality and intellect, bestiality and humanity.” This language was used, ultimately, as the popular basis for the further segregation (socially, economically, morally) of black people in postbellum America (Dain, 2003; Ch8). Through science, this America strove to measure moral and intellectual worth through bodies.
Several key figures pioneered this cause. Although famous for the “nature vs. nurture” debate and the bell curve, respectively, the “founding fathers of sociology”, Adolphe Quetelet (1796–1894) and Francis Galton (1822–1911) also established the fields of Anthropometry and Eugenics, respectively.
Quetelet had lofty dreams of a society in which morality could be distilled down to numbers. These ‘moral statistics’ would eventually bring us theories of probability and the statistical analysis behind crime (Wright 2009). Most important to this pursuit was the measurement of the ‘average man’ which would then allow for study of it’s deviations therefrom. This ‘scientific’ process, which involved measuring individuals from their head to their toes with the use of calipers and, later, photography, called itself Anthropometry — literally, the measure of man. Explicit in Quetelet’s premises was the assertion that Western Europe constituted ‘higher civilizations’ compared to those of Asia and Africa (Wright 2009). Unsurprisingly, these statistics, later brought into physical anthropology, would serve to maintain white superiority.
This sort of statistical reasoning was reinforced in Galton’s work, when he pioneered the use of questionnaire and survey data. Galton used these surveys, among other tools, for his project of eugenics — “the science which deals with all influences that improve the inborn qualities of a race”. This was no fringe science at the time: Galton spoke at several international conferences and published in prestigious publications such as Nature . In fact, the reception of his piece in Nature foreshadowed the many developments of anthropometry from then on, that “sociology should be founding its science of eugenics upon anthropology, psychology, and physiology” (Galton 1904). These disciplines indeed devoted themselves to reifying racial difference.
Towards the late 19th and early 20th centuries, eugenics concepts and techniques were becoming integrated into various cultural institutions in the USA, especially physical education. With the increasing popularity of photography in this time, the study of the body to understand characteristics of criminality and race were increasingly emphasized. Scientists like anthropologist Earnest A Hooton and psychologist William H Sheldon were interested in using emerging photographic techniques to study the body scientifically, premised on the belief that the “size and shape of a person’s body indicators of intelligence, temperament, and moral worth” (Vertinsky 2007). It is no surprise, however, that these techniques served to substantiate “a priori beliefs about class, race, and gender … especially by encouraging certain physiques to be equated with superior mental and spiritual qualities” (Vertinsky, 2007). Hooton, inspired by Galton’s work, wrote extensively of the potential shortcomings to the incorporation of other races into ‘white civilization’ writing that the “race mixture raises the question of the inheritance of physical characteristics in the hybrid offspring, as well as their fertility, vitality, intelligence, and capacity for civilization.” (Hooton 1935, pg.505). Their laboratories, funded by Columbia and Harvard, provided the training and ideology for researchers to ensure that the spirit of eugenics would continue in the US American academic consciousness.
The US American public still lives with the strange aftermath of this anthropometric tradition. After World War I, individuals’ posture — literally how straight people could sit and stand — greatly concerned the general US American public. This concern mirrored the “wider anxieties about character, eugenic practices, and the need for better bodies for improved breeding” (Vertinsky 2007). Sheldon, Hooton, and others took it upon themselves to formalize the practice of anthropometry through a study of ‘posture photos’ — a series of more than 80,000 naked photos of every incoming freshman at elite universities around the USA (from the 1940s-1970s) in order to study the deterioration of posture in the USA. Naomi Wolf in the book The Beauty Myth (1990) and later Ron Rosenbaum in the New York Times (1995) wrote about the ensuing scandal when these photos were discovered, citing the public’s concerns about the project’s social darwinist and eugenic flavor, and eerie similarities to the Third Reich’s analysis of US American yearbooks for their own ends (Rosenbaum 1995; Vertinsky 2007). Nonetheless, few institutions objected to the collection of this scientific data.
The “Ivy League Photos” project later gave rise to Sheldon’s Atlas of Men, a nominally scientific compendium in which male bodies were categorized and correlated with psychiatric predispositions. The atlas categorizes people numerically between three ‘somatotypes’ (ie. types of bodies): endomorphs, mesomorphs, and ectomorphs; essentially fat, muscley, and thin, respectively [see picture below]. Each sub-type was then compared to an animal, and from that naturalist metaphor, a psychiatric observation was derived. For example, Atlas of Men ends its review of somatotypes with the “most magnificent … Somatotype 7 4 1 (Mesomorphic polar endomorphy at extreme ectopenia, 12-level.) … Ancient Hippopotamus … No giant water hog of old ever loved the shallow shores more dearly than does the human 7 4 1 of today” and that they display a “loss of inhibition, hence overexpression — manic euphoria … Thus the 7 4 1, when found in the mental hospital, is likely to turn out to be the very life of the place” (Sheldon 1954).
In other words, Sheldon states that heavyset people are more likely to become the ‘life of the place’ because they lack inhibition and are happier than the rest. A stereotype ‘proven’ statistically. This ‘constitutional science’ sought to bring together theories of nature (here body), nurture (environment), and connect them to individual predisposition to certain disease states, ranging from gallbladder disease to schizophrenic psychoses. Today, terms like ‘constitution’ are still thrown around in medical charts, in common speech (“she has a weak constitution”), and these somatotypes are still taught in physical education curricula (as they were in mine).
Somatotyping and its history are disturbingly, and have received deserved attention elsewhere; for our purposes, however, I am interested in one of Sheldon’s assistants for Atlas of Men: CW Dupertuis. Dupertuis already had an extensive resume when he met Sheldon at a meeting of the USAmerican Association of Physical Anthropologists in the 1940s: he had worked at the Constitution Clinic at Columbia’s Medical Center, published the “Human Constitution in Clinical Medicine” textbook, and participated in Hooton’s physical anthropology projects at Harvard (Draper et al. 1944; Vertinsky, 1936). Depertuis, housed at Case Western (among other medical institutions) went on to provide anthropometric expertise to other research teams across the US. In part, this helped fill in a gap of Sheldon’s earlier research on “the relations between hereditary racial characteristics and morphology” which he believed “present problems of great importance to human society”. Preliminary series of 400 “northern Negroes” led Sheldon to suggest that Black (and Jewish) US Americans had an extreme distribution of somatotypes (most were either extremely thin, muscular, or fat), but that “among the Negroes it is the extreme second component that is most prominent” (Sheldon 1940). This second component was mesomorphy, the muscular somatotype. In other words he suggested that black individuals were more muscular than the general population, and using the language of constitutional medicine, Depertuis and Sheldon could prove this as scientific fact.
This takes us, finally, to three studies that use body measurement to assert that black bodies have more muscle mass, and propelled this idea into the MDRD equation we use today:
- Harsha et al. (1978), “Densitometry and Anthropometry of Black and White Children.” In a study of 242 youth in Louisiana, “Black children were found to have less body fat than White children”. In other words, between two boys of the same weight, one black and one white, the black child has more lean muscle and is therefore more dense. The study notes that “systematic anthropometric differences between the races have long been recognized” and that their “findings corroborate the view that the races differ somatically.” It should be no surprise that CW Dupertuis helped to “design the anthropometric aspect of this study”.
- Cohn et al. (1976), “Body elemental composition: comparison between black and white adults.” Using potassium (K) as a marker for lean muscle, the study noted that among a cohort of 47 black individuals, “although there were no significant differences in the height of the two groups, black men and women had significantly higher total-body potassium than the sex- and age-matched white population.” Thus, as the study suggests, equation modifiers should be used when estimating potassium (among other chemical markers) in black versus white individuals.
- Worrall et al. (1990), “Racial Variation in serum creatine kinase unrelated to lean body mass.” Not to be confused with creatinine (SCr), expression of creatine kinase (CK) — produced by nearly all tissues in the body, but especially by muscle — was investigated between black and white individuals. As the study title suggests, black overexpression of this serum creatine kinase was unrelated to their lean body mass (muscle), and instead related to something else. In fact, two case studies of black men in the article indicate that the rise in creatine kinase could instead be associated with “mild depressive illness” and “learned illness behavior in an under-achiever with academically successful siblings.” (It is unclear how ‘depressive illness’ or ‘learned illness behavior’ led to these differing results.) For the others in the study, this increased creatine kinase could be related to increased ‘muscle permeability’ or differences in ‘renal clearance’ among black people.
The insidious aspect of these studies is that these studies were supported by major grants (some through the US government), and still appear as ‘peer-reviewed’ articles today. They serve as just a few examples of an extensive literature that define black bodies against white bodies. The first two studies suggest that blacks are ‘denser’ than whites through increased muscle mass; and the third that even if it is not lean body mass, something on a biochemical level must be different between blacks and whites. Thus arises the logic for separate equations, so that black people may be spared ‘unnecessary treatment’ and so their medical anomalies may be explained away by their differing biologies.
This logic is exemplified by the MDRD equation. In fact, the three studies above are the only ones cited by Levey et al. (1999) when claiming that “previous studies have shown that on average, black persons have greater muscle mass than white persons.” The study, which uses data from the previous Modification of Diet in Renal Disease (MDRD) study (1999), set out to find a way to use serum creatinine concentration to produce an estimated GFR (as described before). The MDRD study led to the aforementioned 1.212 corrector for eGFR in black patients. In 2010, Levey developed the newer CKD-EPI (Chronic Kidney Disease Epidemiological Collaboration) equation which maintained a difference between black and white/other participants, but with a factor of 1.159 instead (Levey et al. 2010). No explanation was given to why this gap was reduced, but that it did help reduce the relatively higher prevalence of eGFR estimates in “women and Whites”, as some reviewers had criticized the MDRD equation for before.
The contemporary landscape of the eGFR continues to problematize eGFR, even beyond its use in black bodies. Two Nature reviews have prominently rebutted its utility. For one reviewer, the eGFR been inconsistently modified to account for racial differences between Japanese and Chinese populations (Delanaye & Mariat, 2013). Moreover, comparisons of the eGFR to mGFR (directly measured GFR) has pointed out that not only is eGFR innacurate (30–40% off in most cases), but that it “interestingly … has shown wider margins of error in non-white than in white populations” and moreover that the “ethnicity-specific corrective factors” did not improve the accuracy or precision of eGFR measurements” (Porrini et al. 2019). In other words, the racial corrective factor does not improve the accuracy of eGFR for non-white populations, and the use of epidemiological equations for individual application does not bear out in these analyses.
Perhaps the most damning evidence contrary to the use of race in eGFR is that this racial co-factor is not accurate to black populations in Africa (Delanaye & Mariat, 2011). If increased serum creatinine is a statistical reality, it is not then because of increased muscle mass, it is due to the particular treatment and circumstances of black individuals in the USA. In other words, the use of race in these equations conflates the experience of black people in the USA with their imagined separate biologies.
Galton, Quetelet, Hooton, Sheldon, and Depertuis would be quite pleased by their scientific legacies in medicine today given how their initial assertions about black bodies live on. The image below traces some of the influences of their ideas onto the modern eGFR equations. Their assertion that black bodies are fundamentally different and the reification of these differences into the US health infrastructure disenfranchises black individuals and is the embodiment of generations of (un)conscious scientific racism cloaked as scientific matter-of-fact. That black people are being diverted from treatment in the USA due to the eGFR and assertion that ‘blacks have more muscle mass than whites’ is a legacy of eugenics which still lives on in the USA today and is being exported to the world.
Conclusion
Scientific research, of course, does not exist in a vacuum. If you begin with a faulty premise borne of bias and perpetuate tainted research hypotheses, a couple of hundred papers and decades later your faulty premise looks like a solidified fact. Scientific research has given us many such ‘true’ findings about black people over the years: that they are intellectually inferior to other races due to smaller skulls, that black people can’t swim due to denser bones, and that they have more muscle mass. How do we refute something so embedded into the scientific and cultural landscape?
Physicians like Dr. Toni Martin hear a “snort of disbelief” when she explains the logic behind the eGFR equations to her black patients (Martin 2011). For black folks, the trope of science being used to harm black bodies is age-old. However, I disagree with Dr. Martin that we should contextualize use of these equations in clinical practice. At this point, there has already been enough scientific reevaluation, enough ‘clinical contextualizing’. Given the critical reappraisal of the information at hand, it is high time to reject the premise of racial biology and abolish use of these racial algorithms altogether.
There is, in fact, a movement within medicine today to remove race from eGFR equations, and using other molecular markers to estimate kidney function. Even so, these new markers (like Cystatin C) continue to be correlated with race in new scientific research. In Superior: The Return of Race Science, Angela Saini writes about the obstinacy of racist science in medicine, serving only to promote white supremacy and obscure the socioeconomic origins of racial disease differences.
Sure, it’s easy in the ‘everyday’ of clinical practice to unthinkingly stick to your medical society’s facts. Physicians are generally well-meaning fact-followers, after all. However, when these ‘facts’ are not based in science but instead racial pseudoscience, they cease to be supportable. Uncertainty still exists in using the eGFR because it cannot be supported on its shaky foundations. To that I say: listen to history and your patients, remain critical, and refuse to implement racist science.
At the end of these four years, I will make an oath, “to share my medical knowledge for the benefit of my patient and the advancement of healthcare”, “to approach [the profession] with awareness of [its] limitations,” and to not use that knowledge “to violate human rights and civil liberties”. However well-intentioned the medical community is, without a critical appraisal of how we construct knowledge, we risk perpetuating harm. I refuse to be complicit in perpetuating medical racism, and I beseech my medical colleagues to follow.
