Estimated glomerular filtration rate among intensive care unit survivors: From the removal of race coefficient to cystatin C-based equations.

PURPOSE: Black race coefficient used in serum creatinine (sCr)-based estimated glomerular filtration rate (eGFR) calculation may perpetuate racial disparities. Among intensive care unit (ICU) survivors, sCr overestimates kidney function due to sarcopenia. Cystatin C (cysC) is a race- and muscle mass-independent eGFR marker. We investigated the impact of removing the race coefficient from sCr-based eGFR and compared cysC- and sCr-based eGFR in ICU survivors. MATERIALS AND METHODS: Among 30,920 patients from 2 institutions in the Bronx and Boston, eGFR was calculated at hospital discharge using sCr-based equations with and without race coefficient (eGFRsCr2009 and eGFRsCr2021). In a subset with available cysC between ICU admission and 1-year follow-up, sCr- and cysC-based estimates were compared. RESULTS: eGFRsCr2021 was higher than eGFRsCr2009 by a median of 4 ml/min/1.73 m2 among non-Black patients and lower by a median of 8 ml/min/1.73 m2 among Black patients. Removing race coefficient reclassified 12.9% of non-Black subjects and 16.1% of Black subjects to better and worse eGFR category, respectively, and differentially impacted the prevalence of kidney dysfunction between the institutions due to differences in racial composition. Among 51 patients with available cysC (108 measurements), cysC-based estimates were lower than sCr-based estimates (median difference 9 to 16 ml/min/1.73 m2), resulting in reclassification to worse eGFR category in 34% to 53.5% of measurements. CONCLUSIONS: Among ICU survivors, removal of race coefficient leads to lower eGFR in Black patients and may contribute to overestimation of kidney function in non-Black patients. While cysC is rarely used, estimates based on this marker are significantly lower than those based on sCr.

Molecular Mechanisms of Injury in HIV-Associated Nephropathy.

HIV-associated nephropathy (HIVAN) is an important cause of secondary focal glomerulosclerosis that occurs primarily in persons of African ancestry with advanced HIV disease. Although HIVAN is characterized by severe proteinuria and rapid progression to end stage renal disease without treatment, the phenotype is markedly attenuated by treatment with antiretroviral medications. HIV infection of glomerular and tubular epithelial cells and subsequent viral gene expression is a key contributor to HIVAN pathogenesis and the kidney can serve as reservoir for HIV strains that differ those in blood. HIV gene expression in renal epithelial cells leads to dysregulation of cellular pathways including cell cycle, inflammation, cell death, and cytoskeletal homeostasis. Polymorphisms in the APOL1 gene explain the marked predilection of HIVAN to occur in persons of African descent and HIVAN. Since HIVAN has the strongest association with APOL1 genotype of any of the APOL1-associated nephropathies, studies to determine the mechanisms by which HIV and APOL1 risk variants together promote kidney injury hold great promise to improve our understanding of the pathogenesis of APOL1-mediated kidney diseases.