Clinical Focus

  • Internal Medicine

Academic Appointments

Honors & Awards

  • Member, Alpha Omega Alpha (2007)
  • ACP Chapter Outstanding Associate Award, American College of Physicians, Northern California (2009)
  • Semi-finalist for Top Innovations Project, Society of Hospital Medicine Annual Meeting (2010)
  • Community Service Award, UCSF Internal Medicine Residency Program (2010)
  • Fellowship (FACP), American College of Physicians (2013)

Professional Education

  • Residency: UCSF Graduate Medical Education Office (2010) CA
  • Medical Education: Yale School Of Medicine Office of Student Affairs (2007) CT
  • Fellowship: Stanford University Hospital -Clinical Excellence Research Center (2014) CA
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2010)
  • Internship: UCSF Medical Center (2008) CA
  • Postdoctoral Fellowship, Clinical Excellence Research Center, Stanford University (2014)
  • Internal Medicine Residency, University of California-San Francisco (2010)

Community and International Work

  • Attending Physician, San Francisco Free Clinic, San Francisco, CA

    Partnering Organization(s)

    San Francisco Free Clinic


    Bay Area

    Ongoing Project


    Opportunities for Student Involvement


All Publications

  • Better Health, Less Spending Delivery Innovation for Ischemic Cerebrovascular Disease STROKE Kalanithi, L., Tai, W., Conley, J., Platchek, T., Zulman, D., Milstein, A. 2014; 45 (10): 3105-?

    View details for DOI 10.1161/STROKEAHA.114.006236

    View details for Web of Science ID 000342794700056

    View details for PubMedID 25123221

  • What can be achieved by redesigning stroke care for a value-based world? Expert review of pharmacoeconomics & outcomes research Tai, W. n., Kalanithi, L. n., Milstein, A. n. 2014: 1–3


    Stroke results in significant healthcare costs and decreased quality of life. Thoughtful healthcare delivery redesign can help solve this problem through lower-cost, higher-quality care. The dominant fee-for-service reimbursement system may not incentivize delivery systems to invest in new cost-saving delivery innovations. Furthermore, lack of transparency hinder development of new systems of care. However, emerging payment models, including bundled payments and prospective payment, promote adoption of value-based stroke care methods. Both prevention and treatment of stroke offer opportunities to improve value-for-money via adoption of a package of emerging innovations. In order to encourage such adoption, alignment of incentives is crucial.

    View details for PubMedID 25095813

  • Better Health, Less Spending: Delivery Innovation for Ischemic Cerebrovascular Disease. Stroke; a journal of cerebral circulation Kalanithi, L. n., Tai, W. n., Conley, J. n., Platchek, T. n., Zulman, D. n., Milstein, A. n. 2014

    View details for PubMedID 25123221

  • The effect of a resident-led quality improvement project on improving communication between hospital-based and outpatient physicians. American journal of medical quality Kalanithi, L., Coffey, C. E., Mourad, M., Vidyarthi, A. R., Hollander, H., Ranji, S. R. 2013; 28 (6): 472-479


    This article reports on a resident-led quality improvement program to improve communication between inpatient internal medicine residents and their patients' primary care physicians (PCPs). The program included education on care transitions, standardization of documentation, audit and feedback of documented PCP communication rates with public reporting of performance, rapid-cycle data analysis and improvement projects, and a financial incentive. At baseline, PCP communication was documented in 55% of patients; after implementation of the intervention, communication was documented in 89.3% (2477 of 2772) of discharges during the program period. The program was associated with a significant increase in referring PCP satisfaction with communication at hospital admission (baseline, 27.7% "satisfied" or "very satisfied"; postintervention, 58.2%; P < .01) but not at discharge (baseline, 14.9%; postintervention, 21.8%; P = .41). Residents cited the importance of PCP communication for patient care and audit and feedback of their performance as the principal drivers of their engagement in the project.

    View details for DOI 10.1177/1062860613478976

    View details for PubMedID 23526358

  • Intrauterine growth restriction and placental location JOURNAL OF ULTRASOUND IN MEDICINE Kalanithi, L. E., Illuzzi, J. L., Nossov, V. B., Frisbaek, Y., Abdel-Razeq, S., Copel, J. A., Norwitz, E. R. 2007; 26 (11): 1481-1489


    The purpose of this study was to determine whether an association exists between intrauterine growth restriction (IUGR) and second-trimester placental location.A case-control study was performed in well-dated singleton pregnancies with (n = 67) and without (n = 205) IUGR (defined as estimated fetal weight <10th percentile for gestational age at the last sonographic examination) to investigate the association between IUGR and placental location. Placental location was determined by sonography at 16 to 20 weeks' gestation. Maternal, perinatal, and delivery characteristics were abstracted from medical records. Group comparisons were made by the Student t test, chi(2) analysis, the Fisher exact test, the Wilcoxon test, and analysis of variance. Multivariable logistic regression analysis was used to determine the relationship between IUGR and placental location.In both groups, the most common placental locations in the second trimester were anterior and posterior. After adjusting for potential confounders (including race, chronic hypertension, and hypertensive disorders of pregnancy), IUGR pregnancies were nearly 4-fold more likely to have lateral placentation (odds ratio, 3.8; 95% confidence interval, 1.3-11.2) compared with anterior or posterior placentation.Pregnancies complicated by IUGR are significantly more likely than non-IUGR pregnancies to have lateral placentation in the second trimester.

    View details for Web of Science ID 000250639500003

    View details for PubMedID 17957042

  • Bactericidal/permeability-increasing protein's signaling pathways and its retinal trophic and anti-angiogenic effects FASEB JOURNAL Yamagata, M., Rook, S. L., Sassa, Y., Ma, R. C., Geraldes, P., Goddard, L., Clermont, A., Gao, B., Salti, H., Gundel, R., White, M., Feener, E. P., Aiello, L. P., King, G. L. 2006; 20 (12): 2058-2067


    Bactericidal/permeability-increasing protein (BPI) was originally identified as a lipopolysaccharide (LPS) binding protein with gram-negative bactericidal activity in the leukocytes. In this study, we characterized the previously unknown effects of BPI in the eye and the molecular mechanisms involved in its action. BPI mRNA was detected in bovine retina; retinal pigment epithelium; and primary cultures of bovine retinal pigment epithelial cells (RPE), pericytes (RPC), and endothelial cells (REC); while BPI protein was measured in human vitreous and plasma. BPI, but not control protein thaumatin, activated extracellular regulated kinase (ERK) and AKT, and increased DNA synthesis in RPE and RPC but not in REC. A human recombinant 21 kDa modified amino-terminal fragment of BPI (rBPI21) reduced H2O2-induced apoptosis in RPE and inhibited vascular endothelial growth factor (VEGF)-stimulated ERK phosphorylation in REC when preincubated with VEGF. Intraperitoneal (i.p.)-injected rBPI21 reduced ischemia-induced retinal neovascularization and diabetes-induced retinal permeability. Since BPI has unusual dual properties of promoting RPC and RPE growth while suppressing VEGF-induced REC growth and vascular permeability, the mechanistic understanding of BPI's action may provide novel therapeutic opportunities for diabetic retinopathy and age-related macular degeneration.

    View details for DOI 10.1096/05-5662com

    View details for Web of Science ID 000241156900014

    View details for PubMedID 17012258

  • Hepatocyte growth factor induces retinal vascular permeability via MAP-kinase and PI-3 kinase without altering retinal hemodynamics INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE Clermont, A. C., Cahill, M., Salti, H., Rook, S. L., Rask-Madsen, C., Goddard, L., Wong, J. S., Bursell, D., Bursell, S. E., Aiello, L. P. 2006; 47 (6): 2701-2708


    Although vascular endothelial growth factor (VEGF) is a key mediator of retinal vascular permeability (RVP), there may be additional humoral contributors. Hepatocyte growth factor (HGF) induces endothelial cell separation, regulates expression of cell adhesion molecules and is increased in the vitreous fluid of patients with proliferative diabetic retinopathy. The purpose of this study was to evaluate the in vivo effects of HGF on RVP and retinal hemodynamics and delineate the signaling pathways.RVP was assessed by vitreous fluorescein fluorophotometry in rats. Time course and dose-response were determined after intravitreal HGF injection. MAP kinase (MAPK), phosphatidylinositol 3-kinase (PI-3 kinase), and protein kinase C (PKC) involvement were examined by using selective inhibitors. Retinal blood flow (RBF) and mean circulation time (MCT) were evaluated by video fluorescein angiography.HGF increased RVP in a time- and dose-dependent manner. HGF-induced RVP was evident 5 minutes after injection, and reached maximal levels after 25 minutes (+107% versus vehicle, P=0.002). This effect was comparable to that of maximum VEGF stimulation (134%+/-128% at 25 ng/mL). Selective inhibitors of MAPK (PD98059) and PI-3 kinase (LY294002) suppressed HGF-induced RVP by 86%+/-44% (P=0.015) and 97%+/-59% (P=0.021), respectively. Non-isoform-selective inhibition of PKC did not significantly decrease HGF-induced RVP. Although VEGF increases RBF and reduces MCT, HGF did not affect either.HGF increases RVP in a time- and dose-dependent manner at physiologically relevant concentrations with a magnitude and profile similar to that of VEGF, without affecting retinal hemodynamics. Thus, HGF may represent another clinically significant contributor to retinal edema distinct from the actions of VEGF.

    View details for DOI 10.1167/iovs.05-0071

    View details for Web of Science ID 000237949000059

    View details for PubMedID 16723489