
Rennie L. Rhee
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2013–2026
About
Rennie L. Rhee, MD, MSCE, is an Assistant Professor of Medicine (Rheumatology) at the Hospital of the University of Pennsylvania. She specializes in the diagnosis and management of vasculitis and is a member of the Penn Vasculitis Center. Dr. Rhee is also the Director of the Penn Giant Cell Arteritis Fast-Track Program and serves as the Program Director for the Penn Vasculitis Fellowship at the Perelman School of Medicine, University of Pennsylvania. Her research program encompasses clinical and translational studies aimed at understanding disease pathogenesis and heterogeneity in autoimmune vasculitis. Her current work focuses on investigating the airway epithelium and microbiome in vasculitis, as well as identifying novel biomarkers. Dr. Rhee has led the development of a biorepository of nasal swab samples from patients with ANCA-associated vasculitis, relapsing polychondritis, and healthy controls, integrating molecular sequencing and culture-based approaches to explore immune interactions. She is also involved in multidisciplinary efforts to develop imaging biomarkers for giant cell arteritis, including vessel wall MRI. Her contributions include developing clinical programs and advancing research in vasculitis, with a focus on improving diagnosis and understanding of disease mechanisms.
Research topics
- Medicine
- Pathology
- Surgery
- Internal medicine
- Intensive care medicine
- Immunology
Selected publications
ACR Open Rheumatology · 2026-05-01
articleOpen accessSenior authorOBJECTIVE: There is a need for measures of disease severity for giant cell arteritis (GCA), which may enable identification of high-risk subgroups (eg, ophthalmic complications) and individualized approaches to therapy. We derived a continuous score using data from cranial vessel wall magnetic resonance imaging (VW-MRI) to quantify vascular burden in GCA and assessed the score's association with ophthalmic manifestations. METHODS: Patients with suspected new or relapsing GCA underwent cranial VW-MRI plus dedicated orbital MRI. A radiologist assessed VW-MRI enhancement of seven cranial structures bilaterally. Using a generalized linear mixed-effects model, a continuous MRI-derived patient-level score (range 1-10) of disease extent was developed: the Cranial Artery MRI Score for GCA (CAMRIS-GCA). CAMRIS-GCA was compared between clinical diagnosis (ocular GCA, nonocular GCA, or non-GCA) and patients with versus without ocular inflammation on MRI (defined as ophthalmic artery or optic nerve sheath enhancement). RESULTS: Seventy-four patients (17 ocular GCA, 16 nonocular GCA, and 41 non-GCA) were included. CAMRIS-GCA increased linearly across clinically defined groups of non-GCA, nonocular GCA, and ocular GCA (CAMRIS-GCA median 0.6 [interquartile range (IQR) 0-1.7] vs median 2.5 [IQR 0.5-6.6] vs median 4.8 [IQR 2.1-8.5]; P < 0.01). Patients with orbital inflammation on MRI (with or without visual symptoms) had a higher median CAMRIS-GCA compared to patients with negative orbital MRI (median 6.7 [IQR 5.6-8.5] vs median 0.4 [IQR 0-1.6]; P < 0.01). CONCLUSION: This proof-of-concept study introduces a quantitative MRI-derived vascular burden score in GCA and demonstrates its association with ophthalmic involvement. These early findings suggest that cranial VW-MRI may offer a prognostic value in identifying patients at risk for vision-threatening disease.
2025-06-09
book-chapterSenior authorGiant cell arteritis has a high incidence of ocular complications and visual morbidity. In contrast, ophthalmologic disease is less common in Takayasu arteritis and rare in other systemic non-ANCA vasculitides. This chapter will primarily focus on ophthalmologic disease in giant cell arteritis, including its manifestations, pathophysiology, diagnosis, and treatment. The chapter concludes with a brief description of the ocular manifestations that occur in Takayasu arteritis and other systemic vasculitides, including IgA vasculitis, cryoglobulinemic vasculitis, hypocomplementemic urticarial vasculitis syndrome, and polyarteritis nodosa.
Upper Respiratory Microbiome in Vasculitis
Rheumatic Disease Clinics of North America · 2025-03-05
reviewOpen accessSenior authorCorrespondingApollo (University of Cambridge) · 2025-07-15
articleOpen accessPublication status: Published
Longitudinal Changes on Cranial Magnetic Resonance Imaging in Relapsing Giant Cell Arteritis
SSRN Electronic Journal · 2025-01-01
preprintOpen accessSenior authorLongitudinal changes on cranial magnetic resonance imaging in relapsing giant cell arteritis
Seminars in Arthritis and Rheumatism · 2025-08-14 · 1 citations
articleSenior authorcyMAEv2: learning robust cell representations in mass cytometry without supervision 4582
The Journal of Immunology · 2025-11-01
articleOpen accessAbstract Description Batch effects in cytometry lead to inconsistent protein expression measurements and prevent researchers from integrating data from the most well-controlled studies. To address these challenges, we present cyMAEv2, an enhanced self-supervised learning model to generate robust cell representations in mass cytometry data. Compared to existing approaches, cyMAEv2 introduces 1) Enhanced Data Diversity and 2) Learning Cell Population Distributions. The model learns both protein expression distributions and their percentile distributions of eight distinct cohorts without cell type label. Validation was performed using two testing sets from 8 cohorts 1) a healthy donor set (HD), containing data with similar biological variations but different technical variations and; 2) an all-cohort set (ALL), which includes both healthy and diseased samples, reflecting differing biological variations. We used simplified single-cell integration benchmarking (scIB) metrics, to quantify conservation of biological variance (AvgBIO) and the removal of batch effects (AvgBATCH). For the HD set, cyMAEv2 achieved AvgBIO=0.833 and AvgBATCH=0.780, showing gains of + 0.066 AvgBIO and +0.175 AvgBATCH compared to using the original data. For the ALL set, cyMAEv2 achieved AvgBATCH=0.685, showing +0.071 gain from original data. These results demonstrate its ability to preserve biological integrity while mitigating batch effects. We believe this study marks a significant step forward for cytometry data integration. Funding Sources Supported by NIH AI082630, QuantumLeap Healthcare Collaborative fund, the University of Pennsylvania Perelman School of Medicine COVID Fund. Topic Categories Computational and Systems Immunology (COMP)
ACR Open Rheumatology · 2025-05-01 · 2 citations
articleOpen accessOBJECTIVE: Relapsing polychondritis (RP) is a rare, heterogeneous, multisystem disease lacking standard treatment guidelines. This study describes clinical manifestations in association with approaches to treatment. METHODS: Adults with physician-diagnosed RP were recruited into a multicenter observational cohort study. Clinical manifestations, organ damage, and medication history were recorded at the baseline study visit. Treatments received for RP at any time point before the initial visit were categorized into three groups: group 1 was treated with glucocorticoids (GCs) or no drugs, group 2 was treated with nonbiologic immunosuppressive (IS) drugs excluding JAK inhibitors (JAKis) with or without GCs, and group 3 was treated with JAKis or biologic IS drugs with or without nonbiologic IS drugs or GCs. RESULTS: Included in the study were 195 patients with RP who were predominantly female (167, 86%) and White (174, 89%), with a mean age of 49 ± 13years. All patients had ear, nose, or airway involvement, and 163 (83%) had musculoskeletal manifestations of RP. All patients had at least three clinical manifestations with median of 11 (range 3-19). GC treatment was given to 186 (95%) patients. Organ damage was seen in 80 (41%) patients. Treatment groups 1, 2, and 3 had 37 (19%), 55 (28%), and 103 (53%) patients, respectively. Patients in group 3 were more likely to have organ damage, arthritis, and subglottic stenosis. CONCLUSION: Patients with RP have a high burden of clinical manifestations with resultant damage. Physicians typically treat RP with GCs, and the use of other immunosuppressive medications is variable. Absence of a consensus approach to treatment underscores the need for clinical trials and treatment guidelines for RP.
Arthritis & Rheumatology · 2025-12-19
articleOpen accessObjective The objective of the study was to determine risk factors for relapse of antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis (AAV) after reinduction of remission with rituximab and discontinuation of maintenance therapy. Methods This is a post hoc analysis of the RITAZAREM clinical trial. Patients aged 15 years or older with AAV and a positive test for anti–proteinase‐3 or anti‐myeloperoxidase‐ANCA who achieved remission after reinduction with rituximab and glucocorticoids were randomized at month 4 to receive continued rituximab or azathioprine for a maintenance period up to 24 months, followed by observation until relapse or up to 48 months. Generalized estimating equations logistic regression identified baseline and time‐varying risk factors for relapse by the next visit for the two study phases: maintenance (months 4–24) and off‐treatment (months 24–48). Results Among 170 patients (median [interquartile range] age 59 [48–68] years, disease duration 5 [2–10] years), 99 relapses occurred (46 during maintenance). During maintenance, musculoskeletal involvement (odds ratio [OR]: 2.8, 95% confidence interval [CI]: 1.1–7.2; P = 0.03) and higher patient global assessment (OR: 1.1, 95% CI: 1.0–1.2; P = 0.04) were associated with relapse. During the off‐treatment phase, presence of CD19 + B cells (OR: 2.5, 95% CI: 1.2–5.1; P = 0.01) and reappearance of ANCA (OR: 3.2, 95% CI: 1.3–7.7; P = 0.01) were each associated with higher relapse risk. Multivariable analysis identified markers of inflammation (changes in platelets, white blood cells, and IgA) associated with relapse. Conclusion Risk factors for relapse in AAV vary by treatment phase. Monitoring markers of inflammation and immune reconstitution may identify patients at risk for relapse, particularly after treatment withdrawal.
Arthritis & Rheumatology · 2025-06-12 · 8 citations
articleOpen accessOBJECTIVE: To compare the efficacy of abatacept to placebo for the treatment of relapsing, nonsevere granulomatosis with polyangiitis (GPA). METHODS: In this multicenter trial, eligible patients with relapsing, nonsevere GPA were randomized to receive abatacept 125 mg subcutaneously once a week or placebo, both together with prednisone 30 mg/day (or equivalent), tapered and discontinued at week 12. Patients already taking methotrexate, azathioprine, mycophenolate, or leflunomide continued this medication at a stable dose. Patients achieving remission remained on their randomized assignment until relapse, early termination, or the common close date 12 months after enrollment of the last patient. Those who had a nonsevere relapse, had nonsevere worsening, or were not in remission by month 6 had the option to receive open-label abatacept. The primary end point was the rate of treatment failure, defined as relapse, disease worsening, or failure to achieve a Birmingham Vasculitis Activity Score for Wegener's Granulomatosis (BVAS/WG) of 0 or 1 by six months. RESULTS: Sixty-five patients were randomized; 34 received abatacept and 31 received placebo. No statistical difference in the treatment failure rate was found between those who received abatacept and those who received placebo (P = 0.853). Treatment with abatacept did not demonstrate any statistical difference from placebo in key secondary end points, including time to full remission (BVAS/WG = 0), duration of glucocorticoid-free remission, relapse severity, prevention of damage, and patient-reported quality-of-life outcomes. There was no difference in the frequency or severity of adverse events between treatment arms, including infection. CONCLUSION: In patients with relapsing, nonsevere GPA, abatacept did not reduce the risk of relapse, severe worsening, or failure to achieve remission.
Recent grants
Nasal Microbiome and Host Immunity in Granulomatosis with Polyangiitis
NIH · $957k · 2022–2022
Frequent coauthors
- 73 shared
Peter A. Merkel
- 62 shared
Nedaa Husainat
- 48 shared
Andy Abril
- 32 shared
Maria Ibarra
Children's Mercy Hospital
- 32 shared
Robert P. Sundel
Boston Children's Museum
- 28 shared
Reem A. Mustafa
University of Kansas Medical Center
- 27 shared
Philip Seo
Johns Hopkins University
- 26 shared
Carol A. Langford
Cleveland Clinic
Labs
Rennie L. Rhee LabPI
Awards & honors
- Penn Vasculitis Center Program Director
- Penn Giant Cell Arteritis Fast-Track Program (co-led)
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