Oxalate is both a plant-derived molecule and a terminal toxic metabolite with no known physiological function in humans. It is predominantly eliminated by the kidneys through glomerular filtration and tubular secretion. Regardless of the cause, the increased load of dietary oxalate presented to the kidneys has been linked to different kidney-related conditions and injuries, including calcium oxalate nephrolithiasis, acute and chronic kidney disease. In this paper, we review the current literature on the association between dietary oxalate intake and kidney outcomes.

Key Points: A total of 8.42 million US adults have high CKD progression risk, and 4.77 million of them have eGFR >60 ml/min per 1.73 m². An individual's absolute risk of CKD progression is important in the diagnosis and prognostication of CKD. Background: CKD is currently defined using GFR or albuminuria. This is on the basis of the relative risk of mortality and kidney outcomes compared with a healthy population and does not consider an individual's absolute risk of CKD progression. Methods: Using National Health and Nutrition Examination Survey data from 1999 to 2020, we characterized the individual-level absolute 3-year risk of ≥40% decline in eGFR (ml/min per 1.73 m²) or kidney failure (3-year risk) among US adults. We categorized the 3-year risk and considered ≥5% as high risk. Results: Among 199.81 million US adults, 8.42 million (4%) had a 3-year risk ≥5%, including 1.04 million adults without CKD (eGFR ≥60 and albuminuria <30 mg/g). These high-risk adults without CKD as currently defined had risk factors including hypertension (98%), heart failure (72%), and diabetes (44%). A total of 15.51 million adults had CKD with preserved eGFR (eGFR ≥60 and albuminuria ≥30 mg/g)—3.73 million had a 3-year risk ≥5%, 41% of whom did not have diabetes and thus would not be screened for albuminuria using current screening recommendations. The 3-year risk of CKD progression was low (risk <5%) in 94% of the 5.66 million US adults with CKD stage G3a-A1 (eGFR 45 to <60 and albuminuria <30 mg/g). Conclusions: Assessment of the individual's absolute risk of CKD progression allowed further risk stratification of patients with CKD and identified individuals without CKD, as currently defined, who were at high risk of CKD progression. Podcast: This article contains a podcast at https://dts.podtrac.com/redirect.mp3/www.asn-online.org/media/podcast/JASN/2024_06_18_ASN0000000000000377.mp3

Key Points: Using multiple markers may improve GFR estimation especially in settings where creatinine and cystatin C are known to be limited. Panel eGFR is a novel multimarker eGFR equation consisting of age, sex, cystatin C, and nuclear magnetic resonance–measured creatinine, valine, and myo-inositol. eGFR-Cr and eGFR-Cr-CysC may underestimate measured GFR, while panel eGFR was unbiased among younger Black male individuals. Background: Using multiple markers may improve accuracy in GFR estimation. We sought to externally validate and compare the performance of a novel multimarker eGFR (panel eGFR) equation among Black and White persons using the Genetic Epidemiology Network of Arteriopathy cohort. Methods: We included 224 sex, race/ethnicity, and measured GFR (mGFR) category–matched persons, with GFR measured using urinary clearance of iothalamate. We calculated panel eGFR using serum creatinine, valine, myo-inositol, cystatin C, age, and sex. We compared its reliability with current eGFR equations (2021 CKD Epidemiology Collaboration creatinine [eGFR-Cr] and creatinine with cystatin C [eGFR-Cr-CysC]) using median bias, precision, and accuracy metrics. We evaluated each equation's performance in age, sex, and race subgroups. Results: In the overall cohort, 49% were Black individuals, and mean mGFR was 79 ml/min per 1.73 m². Panel eGFR overestimated mGFR (bias: −2.4 ml/min per 1.73 m²; 95% confidence interval [CI], −4.4 to −0.7), eGFR-Cr-CysC underestimated mGFR (bias: 4.8 ml/min per 1.73 m²; 95% CI, 2.1 to 6.7), while eGFR-Cr was unbiased (bias: 2.0 ml/min per 1.73 m²; 95% CI, −1.1 to 4.6). All equations had comparable accuracy. Among Black male individuals younger than 65 years, both eGFR-Cr (bias: 17.0 ml/min per 1.73 m²; 95% CI, 8.6 to 23.5) and eGFR-Cr-CysC (bias: 14.5 ml/min per 1.73 m²; 95% CI, 6.0 to 19.7) underestimated mGFR, whereas panel eGFR was unbiased (bias: 1.7 ml/min per 1.73 m²; 95% CI, −3.4 to 10.0). Metrics of accuracy for all eGFRs were acceptable in all subgroups except for panel eGFR in Black female individuals younger than 65 years (P30: 73.3%). Conclusions: Panel eGFR can be used to estimate mGFR and may have utility among Black male individuals younger than 65 years where current CKD Epidemiology Collaboration equations are biased.