Dr. Kurt Hafer is a board-certified physician and Fellow of the American College of Physicians (FACP) practicing Primary Care Internal Medicine exclusively at Stanford Concierge Medicine.
Dr. Hafer grew up in Chapel Hill, NC and attended Pomona College, where he received his undergraduate degree in Psychology. After completing post-baccalaureate pre-medical coursework at the University of Michigan (UM) in Ann Arbor, he worked as a neuro-endocrine peptide researcher at UM.
In 1999, Dr. Hafer graduated from The University of Chicago Pritzker School of Medicine. He completed a Primary Care Internal Medicine Residency at Santa Clara Valley Medical Center (SCVMC) in San Jose in 2002. Between 2002 to 2012 he was a Teaching Attending Physician at SCVMC as well as an adjunct Stanford physician, training medical students and residents in Internal Medicine.
Dr. Hafer joined Stanford in 2012 as the founding Medical Director of the Stanford Primary Care, Portola Valley Clinic -- Stanford's first new primary care clinic in many years. His five years of leadership at the Portola clinic included incorporating the latest technologies into primary care, adopting active population health panel management, LEAN management practices, embedded specialists and evidence-based, best-care practices as a viable model for the future of Stanford Primary Care.
In January 2017, Dr. Hafer joined Stanford Concierge Medicine as Medical Director. In addition to caring for his patients, his duties include directing the clinic and expanding clinic offerings in mental health, wellness, and piloting Primary Care Genetics and Pharmacogenomics screening programs as a test bed for Stanford Primary Care.
While at Stanford, Dr. Hafer has served as a lecturer for the American College of Physician's Internal Medicine Maintenance of Certification Course held in San Francisco, and has been a Reviewer for the American College of Physicians on multiple projects. He has served on numerous Stanford Healthcare committees and worked with teams on numerous projects, including Stanford's Primary Care 2.0 Redesign, Hypertension Center of Excellence Clinical Integration Team, The Virtual Hypertension Monitoring Project, and Stanford's Primary Care Precision Health program design team. He has directed pilots of TeleHealth phone and video visits, integration of specialty care MDs into our primary care clinics. He led a successful Clinical Effectiveness Leadership Training (CELT) project using clinical pharmacists embedded in primary care clinics to more effectively manage diabetes and high blood pressure between MD visits. He has also served as the Physician Leader for Stanford's Realizing Improvement through Team Empowerment (RITE) Quality Improvement Program.
He currently serves as a Physician Member on the Global Executive Services (GES) Network Steering Committee, part of the Vizient University Health System Consortium.
When not caring for patients, Dr. Hafer enjoys spending time outdoors with family and friends. He is married to a Stanford University History Professor, has a daughter who graduated from Stanford and is now a medical student at UCLA as well as a son who is studying engineering at Stanford. He is an avid lifelong cyclist (road and MTB, logging over 8k miles annually), hiker, has a passion for tinkering with vintage Datsuns and enjoys wearing vintage watches.
Dr. Hafer believes that a combination of truly knowing his patients as individuals, excellent patient-physician communication, and comprehensive preventive care allows him to provide exceptional care for his patients.
- Primary Care Internal Medicine
- Internal Medicine
Clinical Assistant Professor, Medicine - Primary Care and Population Health
Medical Director, Stanford Concierge and Executive Medicine (2017 - Present)
Medical Director, Stanford Primary Care, Portola Valley (2012 - 2017)
Honors & Awards
FACP, Fellow of the American College of Physicians (2018)
Boards, Advisory Committees, Professional Organizations
Member, Vizient Global Executive Services (GES) Network Steering Committee (2018 - Present)
Co-Director, Stanford Healthcare CELT/RITE Alumni Network (2017 - 2020)
Physician Director, Stanford HealthCare Realizing Improvement Through Education (RITE) Course Cohorts 7 & 9 (2017 - 2019)
Member, Stanford Healthcare CELT/RITE Advisory Council (2016 - 2020)
Member, American College of Physicians (ACP) (2001 - Present)
Residency: Santa Clara Valley Medical Center (2002) CA
Medical Education: Pritzker School of Medicine University of Chicago Registrar (1999) IL
Board Certification: American Board of Internal Medicine, Internal Medicine (2004)
B.A., Pomona College, Claremont, CA, Psychology (1988)
Community and International Work
Volunteer Teaching Medicine Attending
Pacific Free Clinic in San Jose at Overfelt High School
Opportunities for Student Involvement
Genetically determining individualized clinical reference ranges for the biomarker tryptase can limit unnecessary procedures and unmask myeloid neoplasms.
Serum tryptase is a biomarker used to aid in the identification of certain myeloid neoplasms, most notably systemic mastocytosis, where baseline (BST) levels >20 ng/mL are a minor criterion for diagnosis. Whereas clonal myeloid neoplasms are rare, the common cause for elevated BST is the genetic trait hereditary alpha-tryptasemia (HαT) caused by increased germline TPSAB1 copy number. To date, the precise structural variation and mechanism(s) underlying elevated BST in HαT and the general clinical utility of tryptase genotyping, remain undefined. Through cloning, long-read sequencing, and assembling of the human tryptase locus from an individual with HαT, and validating our findings in vitro and in silico, we demonstrate that BST elevations arise from over-expression of replicated TPSAB1 loci encoding canonical α-tryptase protein due to co-inheritance of a linked over-active promoter element. Modeling BST levels based upon TPSAB1 replication number we generate new individualized clinical reference values for the upper limit of 'normal'. Using this personalized laboratory medicine approach, we demonstrate the clinical utility of tryptase genotyping, finding that in the absence of HαT, BST levels >11.4 ng/mL frequently identify indolent clonal mast cell disease. Moreover, substantial BST elevations (e.g., >100 ng/mL) which would ordinarily prompt bone marrow biopsy, can result from TPSAB1 replications alone and thus be within 'normal' limits for certain individuals with HαT.
View details for DOI 10.1182/bloodadvances.2022007936
View details for PubMedID 36170795