Race, ancestry, and genetic risk for kidney failure

Nicholas, Susanne B.; Ford, Chandra L.; Norris, Keith C.

doi:10.1016/j.xcrm.2022.100726

Cited by 2 publications

(1 citation statement)

References 6 publications

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“…Although some papers are more circumspect [ 20 - 23 ], the systematic review identified fifty reviews, editorials, and commentaries in peer-reviewed journals [ 10 , 13 , 19 , 24 - 70 ] that argued for the abolition of race-based GFR cr estimation because Black race is: 1) a societal rather than biological construct [ 10 , 15 , 24 - 31 , 34 - 45 , 48 - 52 , 55 , 58 , 60 - 67 , 69 , 70 ]; 2) an imprecise proxy for genetic ancestry [ 13 , 24 - 26 , 29 , 31 , 43 , 44 , 46 - 50 , 60 - 65 , 67 , 70 ]; 3) poorly defined [ 10 , 13 , 19 , 34 , 39 , 43 , 44 , 48 - 52 , 55 , 62 , 63 , 67 - 69 ]; and 4) heterogeneous [ 10 , 26 , 29 , 30 , 34 , 35 , 44 , 46 , 52 , 66 , 67 ]. These articles also declared that the race correction: 5) lacked a physiological explanation [ 10 , 25 - 27 , 29 - 31 , 37 , …”

Section: Reviewmentioning

confidence: 99%

Retaining Race in Chronic Kidney Disease Diagnosis and Treatment

Williams

2023

Cureus

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The best overall measure of kidney function is glomerular filtration rate (GFR) as commonly estimated from serum creatinine concentrations (eGFR cr ) using formulas that correct for the higher average creatinine concentrations in Blacks. After two decades of use, these formulas have come under scrutiny for estimating GFR differently in Blacks and non-Blacks. Discussions of whether to include race (Black vs. non-Black) in the calculation of eGFR cr fail to acknowledge that the original race-based eGFR cr provided the same CKD treatment recommendations for Blacks and non-Blacks based on directly (exogenously) measured GFR. Nevertheless, the National Kidney Foundation and the American Society of Nephrology Task Force on Reassessing the Inclusion of Race in Diagnosing Kidney Disease removed race in CKD treatment guidelines and pushed for the immediate adoption of a race-free eGFR cr formula by physicians and clinical laboratories. This formula is projected to negate CKD in 5.51 million White and other non-Black adults and reclassify CKD to less severe stages in another 4.59 million non-Blacks, in order to expand treatment eligibility to 434,000 Blacks not previously diagnosed and to 584,000 Blacks previously diagnosed with less severe CKD. This review examines: 1) the validity of the arguments for removing the original race correction, and 2) the performance of the proposed replacement formula. Excluding race in the derivation of eGFR cr changed the statistical bias from +3.7 to -3.6 ml/min/1.73m 2 in Blacks and from +0.5 to +3.9 in non-Blacks, i.e., promoting CKD diagnosis in Blacks at the cost of restricting diagnosis in non-Blacks. By doing so, the revised eGFR cr greatly exaggerates the purported racial disparity in CKD burden. Claims that the revised formulas identify heretofore undiagnosed CKD in Blacks are not supported when studies that used kidney failure replacement therapy and mortality are interpreted as proxies for baseline CKD. Alternatively, a race-stratified eGFR cr (i.e., separate equations for Blacks and non-Blacks) would provide the least biased eGFR cr for both Blacks and non-Blacks and the best medical treatment for all patients.

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Section: Reviewmentioning

confidence: 99%

Retaining Race in Chronic Kidney Disease Diagnosis and Treatment

Williams

2023

Cureus

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Single-cell sequencing reveals homogeneity and heterogeneity of the cytopathological mechanisms in different etiology-induced AKI

Chen

Yuan

et al. 2023

Cell Death Dis

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Homogeneity and heterogeneity of the cytopathological mechanisms in different etiology-induced acute kidney injury (AKI) are poorly understood. Here, we performed single-cell sequencing (scRNA) on mouse kidneys with five common AKI etiologies (CP-Cisplatin, IRI-Ischemia-reperfusion injury, UUO-Unilateral ureteral obstruction, FA-Folic acid, and SO-Sodium oxalate). We constructed a potent multi-model AKI scRNA atlas containing 20 celltypes with 80,689 high-quality cells. The data suggest that compared to IRI and CP-AKI, FA- and SO-AKI exhibit injury characteristics more similar to UUO-AKI, which may due to tiny crystal-induced intrarenal obstruction. Through scRNA atlas, 7 different functional proximal tubular cell (PTC) subtypes were identified, we found that Maladaptive PTCs and classical Havcr1 PTCs but not novel Krt20 PTCs affect the pro-inflammatory and pro-fibrotic levels in different AKI models. And cell death and cytoskeletal remodeling events are widespread patterns of injury in PTCs. Moreover, we found that programmed cell death predominated in PTCs, whereas apoptosis and autophagy prevailed in the remaining renal tubules. We also identified S100a6 as a novel AKI-endothelial injury biomarker. Furthermore, we revealed that the dynamic and active immune (especially Arg1 Macro_2 cells) -parenchymal cell interactions are important features of AKI. Taken together, our study provides a potent resource for understanding the pathogenesis of AKI and early intervention in AKI progression at single-cell resolution.

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Race, ancestry, and genetic risk for kidney failure

Cited by 2 publications

References 6 publications

Retaining Race in Chronic Kidney Disease Diagnosis and Treatment

Retaining Race in Chronic Kidney Disease Diagnosis and Treatment

Single-cell sequencing reveals homogeneity and heterogeneity of the cytopathological mechanisms in different etiology-induced AKI

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