Racial and Ethnic Discrepancy in Pulse Oximetry and Delayed Identification of Treatment Eligibility Among Patients With COVID-19.

Importance: Pulse oximetry guides triage and therapy decisions for COVID-19. Whether reported racial inaccuracies in oxygen saturation measured by pulse oximetry are present in patients with COVID-19 and associated with treatment decisions is unknown. Objective: To determine whether there is differential inaccuracy of pulse oximetry by race or ethnicity among patients with COVID-19 and estimate the association of such inaccuracies with time to recognition of eligibility for oxygen threshold-specific COVID-19 therapies. Design, Setting, and Participants: This retrospective cohort study of clinical data from 5 referral centers and community hospitals in the Johns Hopkins Health System included patients with COVID-19 who self-identified as Asian, Black, Hispanic, or White. Exposures: Concurrent measurements (within 10 minutes) of oxygen saturation levels in arterial blood (SaO2) and by pulse oximetry (SpO2). Main Outcomes and Measures: For patients with concurrent SpO2 and SaO2 measurements, the proportion with occult hypoxemia (SaO2<88% with concurrent SpO2 of 92%-96%) was compared by race and ethnicity, and a covariate-adjusted linear mixed-effects model was produced to estimate the association of race and ethnicity with SpO2 and SaO2 difference. This model was applied to identify a separate sample of patients with predicted SaO2 levels of 94% or less before an SpO2 level of 94% or less or oxygen treatment initiation. Cox proportional hazards models were used to estimate differences by race and ethnicity in time to recognition of eligibility for guideline-recommended COVID-19 therapies, defined as an SpO2 level of 94% or less or oxygen treatment initiation. The median delay among individuals who ultimately had recognition of eligibility was then compared. Results: Of 7126 patients with COVID-19, 1216 patients (63 Asian [5.2%], 478 Black [39.3%], 215 Hispanic [17.7%], and 460 White [37.8%] individuals; 507 women [41.7%]) had 32 282 concurrently measured SpO2 and SaO2. Occult hypoxemia occurred in 19 Asian (30.2%), 136 Black (28.5%), and 64 non-Black Hispanic (29.8%) patients compared with 79 White patients (17.2%). Compared with White patients, SpO2 overestimated SaO2 by an average of 1.7% among Asian (95% CI, 0.5%-3.0%), 1.2% among Black (95% CI, 0.6%-1.9%), and 1.1% among non-Black Hispanic patients (95% CI, 0.3%-1.9%). Separately, among 1903 patients with predicted SaO2 levels of 94% or less before an SpO2 level of 94% or less or oxygen treatment initiation, compared with White patients, Black patients had a 29% lower hazard (hazard ratio, 0.71; 95% CI, 0.63-0.80), and non-Black Hispanic patients had a 23% lower hazard (hazard ratio, 0.77; 95% CI, 0.66-0.89) of treatment eligibility recognition. A total of 451 patients (23.7%) never had their treatment eligibility recognized, most of whom (247 [54.8%]) were Black. Among the remaining 1452 (76.3%) who had eventual recognition of treatment eligibility, Black patients had a median delay of 1.0 hour (95% CI, 0.23-1.9 hours; P = .01) longer than White patients. There was no significant median difference in delay between individuals of other racial and ethnic minority groups and White patients. Conclusions and Relevance: The results of this cohort study suggest that racial and ethnic biases in pulse oximetry accuracy were associated with greater occult hypoxemia in Asian, Black, and non-Black Hispanic patients with COVID-19, which was associated with significantly delayed or unrecognized eligibility for COVID-19 therapies among Black and Hispanic patients. This disparity may contribute to worse outcomes among Black and Hispanic patients with COVID-19.

The role of aldosterone blockade in murine lupus nephritis.

BACKGROUND: The purpose of this study was to examine the effect of aldosterone receptor blockade on the immunopathogenesis and progression of nephritis in the (NZB x NZW) F1 murine lupus model. METHODS: Female NZB/W F1 mice (11 weeks old) were treated daily with 25 or 50 mg/kg oral spironolactone or vehicle. Proteinuria, renal function, and serum autoantibody levels were monitored. Renal histopathology, immune complex deposition, and immunohistochemistry were analyzed at various time points. Targeted microarray analysis was performed on renal tissue, with subsequent real-time PCR analysis of several differentially expressed genes. RESULTS: Treatment with spironolactone was well tolerated by the mice throughout the course of their disease progression, with no significant differences in azotemia or serum potassium levels between vehicle-treated and spironolactone-treated animals. By 36 weeks of age, fewer spironolactone-treated mice developed nephrotic range proteinuria as compared with the control mice (control 70.8%, 25 mg/kg spironolactone 51.3%, and 50 mg/kg spironolactone 48.6%). Compared with control mice, mice treated with 25 mg/kg spironolactone had significantly lower serum anti-single-stranded DNA levels (2,042 microg/ml versus 1,036 microg/ml; P = 0.03) and anti-double-stranded DNA levels (3,433 microg/ml versus 614 microg/ml; P = 0.05). Spironolactone-treated mice exhibited decreased histopathologic evidence of inflammation and tissue damage, as compared with control mice. Additionally, spironolactone treatment resulted in decreased expression in the kidney of several inflammatory and proapoptotic genes, including those encoding interferon-gamma, B lymphocyte stimulator (BlyS), tumor necrosis factor related apoptosis inducing ligand (TRAIL), tumor necrosis factor related weak inducer of apoptosis (TWEAK), and Fas ligand. CONCLUSION: Aldosterone receptor blockade is safe and well tolerated in progressive murine lupus nephritis, and it results in decreased levels of clinical proteinuria, lower serum levels of autoantibodies, and decreased kidney damage. It appears to modulate inflammatory changes during the progression of glomerulonephritis and may also have a previously undescribed role in attenuating apoptosis.