About

Angela T Anderson, MD, is an Assistant Professor of Clinical Psychiatry and an Attending Physician at the Children's Hospital of Philadelphia. She holds a B.S. in Psychology and Biomedical Engineering Systems from Tufts University and earned her M.D. from Albert Einstein College of Medicine. Her professional work includes producing educational content on mental health topics such as anxiety and depression for teens and young adults, serving as an executive producer for related YouTube videos. Her research and professional contributions also encompass promoting diversity, equity, and inclusion through anti-racism initiatives, including organizing book clubs and supporting colleagues' mental health during racial pandemics. She has been involved in various scholarly activities, including presentations at the Society of Pediatric Psychology Annual Conference and media interviews on mental health topics.

Research topics

• Medicine
• Internal medicine
• Urology
• Biology
• Endocrinology

Selected publications

• Microbiota and kidney disease: the road ahead

  Nature Reviews Nephrology · 2025-07-28 · 19 citations

  reviewOpen access
  PublisherOA PDFDOI

• Time-Updated Estimated GFR Variability Is Associated With Mortality, Cardiovascular Disease, and End-Stage Kidney Disease in Patients With CKD: Findings From the CRIC Study

  American Journal of Kidney Diseases · 2025-03-05 · 5 citations

  articleOpen access
  PublisherOA PDFDOI

• #1172 Association between blood pressure and chronic kidney disease progression in patients with advanced chronic kidney disease: findings from CRIC and KNOW-CKD study

  Nephrology Dialysis Transplantation · 2025-10-01

  article

  Abstract Background and Aims Blood pressure (BP) control is important in the management of chronic kidney disease (CKD). However, in patients with advanced CKD, the benefits of BP control in delaying the progression of CKD remains uncertain. We aimed to explore the association of BP levels with kidney outcomes in patients with advanced CKD. Method We analyzed 2,939 participants with chronic kidney disease (CKD) G3b to G5 (estimated glomerular filtration rate [eGFR] <45 ml/min/1.73 m2) without kidney replacement therapy (KRT) from the Chronic Renal Insufficiency Cohort (CRIC) study and the KoreaN Cohort Study for Outcome in Patients With Chronic Kidney Disease (KNOW-CKD). The main predictors were baseline and time-updated systolic BP (SBP) and diastolic BP (DBP). The primary outcome was a composite kidney outcome of ≥50% decline in eGFR from baseline measurement or the initiation of KRT. In the analyses, multivariate cause-specific hazards models and marginal structural models were fitted for baseline and time-updated BPs, respectively. Results During 17755 person-years of follow-up (median, 4.7 years), the composite outcome occurred 1,627 (55.4%) participants. Compared with baseline SBP <120 mmHg, the hazard ratios (HRs) (95% CIs) for 120–129, 130–139, and ≥140 mmHg were 1.33 (1.15–1.54), 1.48 (1.27–1.72), and 1.82 (1.58–2.10), respectively. This association was more evident in analysis with time-updated SBP, where the corresponding HRs (95% CIs) were 1.29 (1.09–1.54), 1.75 (1.46–2.10), and 2.79 (2.36–3.29), respectively. Furthermore, the slopes of eGFR decline were −1.20 (−1.36 to −1.04), −1.77 (−1.97 to −1.57), −2.11 (−2.35 to −1.88), and −2.48 (−2.70 to −2.27) for respective SBP categories. Additional analyses with DBP also showed similar results. Conclusion In patients with advanced CKD, higher BP levels were associated with an increased risk of CKD progression.

  PublisherDOI

• Primary Prevention Aspirin, Lipoprotein(a), and Cardiorenal Outcomes in Chronic Kidney Disease

  JACC Advances · 2025-08-20 · 4 citations

  articleOpen access

  BACKGROUND: Chronic kidney disease (CKD) is a risk-enhancing factor for cardiovascular disease (CVD) and is associated with higher lipoprotein(a) (Lp[a]) levels. While aspirin may reduce Lp(a)-related prothrombotic risk, the role of primary prevention aspirin for persons with CKD and elevated Lp(a) is unclear. OBJECTIVES: The aim of the study was to assess the association of aspirin use with cardiovascular, renal, and bleeding outcomes stratified by Lp(a) level among individuals with CKD without clinical CVD. METHODS: There were 2,552 participants without clinical CVD in the Chronic Renal Insufficiency Cohort. Lp(a) was measured at baseline and not reported to clinicians. Aspirin use was self-reported and longitudinally assessed at each follow-up visit. Cox proportional hazards regression assessed the association of aspirin use with myocardial infarction (MI), stroke, end-stage renal disease (ESRD), and major bleeding events, stratified by Lp(a) ≥50 vs <50 mg/dL. RESULTS: . Over a median follow-up of 15.7 years, aspirin use was associated with a 38% lower risk of MI (HR: 0.62; 95% CI: 0.42-0.91) and a 28% lower risk of ESRD (HR: 0.72; 95% CI: 0.59-0.89) among individuals with Lp(a) ≥50 but not Lp(a) <50 mg/dL (MI, HR: 1.38; 95% CI: 1.07-1.77; ESRD, HR: 0.98; 95% CI: 0.84-1.15). Aspirin use was not significantly associated with stroke or major bleeding in either Lp(a) group. CONCLUSIONS: Individuals with CKD and elevated Lp(a) without clinical CVD may derive net benefit from low-dose aspirin for the primary prevention of MI and ESRD.

  PublisherDOI

• Abstract 4365177: Higher Self-Efficacy Reduces Hospitalization Risk in a Cohort of Adults With Chronic Kidney Disease

  Circulation · 2025-11-03

  article

  Background: Adults with chronic kidney disease (CKD) face a higher risk of hospitalization than the general population. Self-efficacy, an individual’s belief in their ability to manage their health, is a potentially modifiable factor that may reduce this risk. Research Question/Hypothesis: We examined the association between self-efficacy and hospitalization risk in adults with CKD, hypothesizing that higher self-efficacy would be linked to lower hospitalization risk. Methods: We analyzed data from the Chronic Renal Insufficiency Cohort study. Self-efficacy was assessed using the 5-item Manage Disease in General Scale, between 2013–2018. This scale evaluates participants’ confidence in managing tasks and activities related to their condition, seeking medical care, and coping with health-related emotional stress. Participants were followed until death, study withdrawal, or October 2024. Poisson regression was used to examine the association between self-efficacy and hospitalization risk, with stratification by sex and race/ethnicity. Models were adjusted for clinical center, age, sex, race/ethnicity, education, income, hypertension, diabetes, cardiovascular disease, estimated glomerular filtration rate, proteinuria, and frailty. Results: Among 3,862 participants who completed the self-efficacy assessment (mean age [SD]: 65 [10] years; 44% female; 41% White, 42% Black, 13% Hispanic), 44% reported high self-efficacy (score ≥9 out of 10). Those with high self-efficacy were less likely to have low income, diabetes, or frailty. Over a mean follow-up of 7.2 years, 18,939 hospitalizations occurred (21% cardiovascular-related, 79% non-cardiovascular). In fully adjusted models, higher self-efficacy was associated with a lower risk of hospitalization in the full cohort (Incidence Rate Ratio [IRR]: 0.87; 95% CI: 0.84–0.91), as well as in men (IRR: 0.77; 95% CI: 0.74–0.81), and in Black (IRR: 0.90; 95% CI: 0.86–0.94), Hispanic (IRR: 0.82; 95% CI: 0.71–0.96), and White (IRR: 0.84; 95% CI: 0.79–0.89) subgroups. Conclusion: In this large, diverse cohort of adults with CKD, higher self-efficacy was independently associated with a lower risk of hospitalization, even after adjusting for confounders. While these findings suggest a potential protective role of self-efficacy, residual confounding cannot be ruled out. Further research is needed to determine whether enhancing self-efficacy can causally reduce hospitalization risk in this high-risk population.

  PublisherDOI

• Reprogramming of Cellular Plasticity via ETS and MYC Core-regulatory Circuits During Response to MAPK Inhibition in BRAF-mutant Colorectal Cancer

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-20

  preprintOpen access

  Abstract Background Aberrant enhancer dynamics play a critical role in the initiation and progression of colorectal cancer (CRC). BRAF V600E -mutated metastatic CRC may be a unique subtype, exhibiting a strong epigenetic phenotype. Interestingly, bromodomain 2, a reader protein for H3K27ac-marked enhancers, was found to be synthetically lethal in CRC with BRAF + EGFR inhibition. Design We evaluated the effectiveness of targeting aberrant enhancers with bromodomain and extraterminal (BET) + MAPK pathway inhibitors in patient-derived xenograft models of metastatic CRC, followed by comprehensive profiling of transcriptomic and chromatin dynamics upon BET inhibitor combination treatment. Results The combination of BET and standard MAPK inhibitors has demonstrated improved efficacy against BRAF V600E CRC and selective improvements against RAS-mutant CRC in vivo . We showed that BET + MAPK inhibition induced a profound downregulation of the MAPK signaling pathway compared to MAPK inhibition alone. The loss of activation signal on enhancers, as determined by H3K27ac, led to dysregulation of core-regulatory circuitries of CRC, especially loss of the auto-regulatory mechanism of the MAPK downstream E26 transformation–specific transcription factor family. Single nucleus multiome (RNA + ATAC) sequencing further distinguished differential transcriptomic and chromatin dynamics at cell type levels. Profound downregulation of well-differentiated cell types confirmed deep inhibition of MAPK signaling and downstream transcription factors. On the other hand, dedifferentiated cell populations were abundant after MAPK or combination inhibition, suggesting therapy-induced cell state switching and adaptation. Conclusion We are evaluating BET + BRAF + EGFR inhibition in patients with treatment-refractory BRAF V600E metastatic CRC. ClinicalTrial.gov identifier: NCT06102902 . What is already known on this topic Enhancer aberrations emerge as critical epigenetic features in the progression of colorectal cancer (CRC). However, the dynamics of active enhancer and the therapeutic potential of enhancer blockade, particularly in CRC tumors with BRAF V600E mutation, is not well understood. What this study adds This study demonstrates improved efficacy of BET inhibitor combination therapies in diverse patient-derived models and reveals epigenetic reprogramming driven cellular plasticity in BRAF V600E -mutated CRC. How this study might affect research, practice or policy Our findings support treatment with BET + BRAF + EGFR inhibitors for patients with BRAFV600E-mutant mCRC [ NCT06102902 ]. This study also highlights the potential of combining epigenetic agents to standard targeted therapy, offering a novel treatment option for this subset of patients.

  PublisherOA PDFDOI

• APOL1 Risk Variants and Progression of CKD: A CRIC Follow-Up Study

  Journal of the American Society of Nephrology · 2025-10-01

  article
  PublisherDOI

• CNSC-79. MALIGNANT (NON-SUBEPENDYMAL) GLIOMAS IN PATIENTS WITH TUBEROUS SCLEROSIS: TWO CASES AND A LITERATURE REVIEW

  Neuro-Oncology · 2025-11-01

  review1st authorCorresponding

  Abstract Tuberous sclerosis complex (TSC) is a genetic disorder resulting from mutations in the TSC1/TSC2 tumor suppressor genes. It causes benign tumors in multiple organs including the brain with cortical tubers, subependymal nodules, white matter abnormalities, and low-grade subependymal giant cell astrocytomas (SEGAs). Reported cases of malignant gliomas in TSC patients, with two new cases, are presented below. A 49-year-old woman, with TSC, cortical tubers, epilepsy, and taking everolimus for renal angiomyolipoma, presented with new headaches; a glioblastoma was resected. She underwent radiation, temozolomide, and bevacizumab. She is stable 12 months after diagnosis. A 57-year-old male, with a history of TSC, epilepsy, and cortical tubers, presented with new headaches. An enhancing brain mass was resected as a glioblastoma. He experienced mesenteric ischemia and bowel infarction and died three weeks later. A 22-month-old male, with a malignant gemistocytic astrocytoma, diagnosed after presenting with lethargy and vomiting, survived five months after surgery and radiotherapy. A 17-year-old male had upper motor neuron signs, from a glioblastoma, which was resected and radiated. A 26-year-old male developed glioblastoma eight years after radiation and excision of a SEGA. He died four months after surgery and chemotherapy. A 5-year-old male, with TSC2, lived three years following surgery, chemotherapy, radiotherapy, and mTOR inhibition for glioblastoma. A 33-year-old female presented with behavioral changes and hemiparesis; a glioblastoma was resected. A 58-year-old male, with confusion, dysphasia, and hemiparesis, had a glioblastoma and survived one month. An 11-month-old male had a SEGA resected which recurred as a malignant SEGA; he remained recurrence-free five years after chemotherapy. A 54-year-old male, with TSC1, developed visual loss secondary to a glioblastoma. He received surgery, radiotherapy, chemotherapy, bevacizumab, and anti-PD-L1 antibody, surviving 12 months post-surgery. These cases raise the question of whether malignant gliomas, in patients with TSC, may be more frequent and appear earlier.

  PublisherDOI

• Sex Differences in Social, Behavioral, and Metabolic Risk Factors for Cardiovascular Disease Mortality among US Adults

  medRxiv · 2025-11-21 · 1 citations

  preprintOpen access

  Abstract Background Prevalence and associations of risk factors for cardiovascular disease (CVD) may differ between women and men, but previous findings are inconclusive. We investigated the simultaneous contributions of social determinants of health (SDOH), behavioral factors, and metabolic factors to CVD mortality among women and men in the US general population. Methods We included 50,808 participants aged ≥20 years from the National Health and Nutrition Examination Survey 1999-2018, linked to the National Death Index for CVD mortality follow-up through December 31, 2019. SDOH, behavioral factors, and metabolic factors were collected in each survey cycle. We estimated the simultaneous impact of SDOH, behavioral factors, and metabolic factors on CVD mortality in women and men using average population attributable fractions (PAFs), which consider both the prevalence and strength of association of all risk factors with CVD mortality in one model. Results During a mean 9.4-year follow-up, 2,589 CVD deaths were recorded (1,140 in women; 1,449 in men). Women had higher prevalence of unemployment and central obesity than men. Men had higher prevalence of no regular healthcare access, current smoking, heavy alcohol drinking, unhealthy diet, and high cholesterol than women. In fully adjusted models, associations of risk factors with CVD mortality were mostly similar among women and men. However, unemployment was more strongly associated with CVD mortality among men (hazard ratio [95% CI], 1.97 [1.62-2.39]) compared with women (1.19 [1.00-1.43; p-value for interaction &lt;0.001). In those older than age 60, sleep duration &lt;6 or &gt;8 hours/day was independently associated with CVD mortality among women but not men. Hypertension (14.3%), albuminuria (10.0%), low family income-to-poverty ratio (8.7%), leisure-time physical inactivity (6.6%), and diabetes (6.3%) were top population-level contributors to CVD mortality in men, while leisure-time physical inactivity (14.7%), albuminuria (11.7%), low family income-poverty ratio (10.0%), low estimated glomerular filtration rate (8.9%), and diabetes (6.5%) were top contributors among women. Conclusions Although the prevalence of CVD risk factors varied by sex, magnitudes of association with CVD mortality were mostly similar among women and men. SDOH and behavioral risk factors collectively accounted for a third of CVD deaths in both men and women living in the US. Clinical Perspective What Is New? Associations of a wide array of social determinants of health, behavioral factors, and metabolic factors with CVD mortality are similar among men and women in the US. However, prevalence of these risk factors and associated population attributable fractions vary by sex. Hypertension, lower kidney function, and leisure-time physical inactivity are top population-level contributors to CVD mortality among men, while leisure-time physical inactivity, low kidney function and diabetes are top population-level contributors among women. What Are the Clinical Implications? Low kidney function showed the largest absolute mortality rate in both men and women compared to other risk factors, and increased efforts targeting prevention of kidney disease are warranted. Sex-specific strategies may be warranted to target the primordial prevention of social determinants of health and behavioral factors to reduce the burden of CVD mortality.

  PublisherOA PDFDOI

• Differential Effect of Hospitalization on Cystatin C– and Creatinine-Based Estimated GFR

  Journal of the American Society of Nephrology · 2025-03-11 · 4 citations

  article

  Key Points Critical illness is known to acutely decrease eGFRdiff (estimation of GFR by cystatin C−estimation of GFR from serum creatinine [eGFRCr]), presumably because of loss of muscle mass falsely elevating eGFRCr. It is unknown whether this eGFRdiff effect occurs in all-cause hospitalizations and whether the effect persists after hospitalization. More hospitalization was associated with larger decreases in estimation of GFR by cystatin C compared with eGFRCr on measurements months after hospital discharge. Background Cystatin C has entered mainstream clinical care as a measure of kidney function, joining serum creatinine, which has been used for almost a century. However, many physicians notice that estimation of GFR from serum creatinine (eGFRCr) and estimation of GFR by cystatin C (eGFRCys) values can differ considerably. Hospitalization with critical illness is known to acutely decrease eGFRdiff (eGFRCys−eGFRCr). However, whether this effect occurs in all-cause hospitalizations and persists after hospitalization is unknown. Methods Among 5599 adult participants in the Chronic Renal Insufficiency Cohort study with serum creatinine and cystatin C measurements, we estimated the association of six categories of total days of hospitalization between annual study visits (never hospitalized, hospitalized &lt;7, 7 to &lt;14, 14 to &lt;28, 28 to &lt;42, and ≥42 days) and changes in eGFRCr, eGFRCys, and eGFRdiff between those study visits. Results Compared with no hospitalization between study visits, increasing days of hospitalization were associated with decreases in eGFRCys ( e.g ., −3.30 [95% confidence interval, −5.48 to −1.13] ml/min per 1.73 m 2 for ≥42 days of hospitalization, test for trend P &lt; 0.001), while eGFRCr remained relatively stable ( e.g ., −1.12 [−2.77 to 0.53] ml/min per 1.73 m 2 for ≥42 days of hospitalization, test for trend P = 0.21). The differential effect resulted in eGFRdiff becoming progressively more negative with more total days of hospitalization (test for trend P &lt; 0.001). Conclusions Prolonged or repeated hospitalization was associated with larger decreases in eGFRCys compared with eGFRCr on measurements months after hospital discharge.

  PublisherDOI

Recent grants

• The Gut Microbiome and The Metabolome in Chronic Kidney Disease

  NIH · $2.8M · 2024–2024

• NIH Grant K01DK092353

  NIH · $650k · 2016

• Continuation of the Chronic Renal Insufficiency Cohort (CRIC)

  NIH · $20.5M · 2001–2028

• Measures of Fibrosis and Clinical Outcomes in Chronic Kidney Disease

  NIH · $1.9M · 2015–2021

Frequent coauthors

• Harold I. Feldman

  University of Illinois Chicago

  524 shared

• Raymond R. Townsend

  501 shared

• Jiang He

  Central South University

  497 shared

• Radhakrishna R. Kallem

  University of Pennsylvania

  406 shared

• Jackson T. Wright

  Case Western Reserve University

  406 shared

• John W. Kusek

  University of Pennsylvania

  388 shared

• Mahboob Rahman

  377 shared

• Dawei Xie

  361 shared