Clinical Assistant Professor, Medicine - Nephrology
Fellowship: Stanford University Nephrology Fellowship (2017) CA
Fellowship: Stanford University Nephrology Fellowship (2015) CA
Board Certification: American Board of Internal Medicine, Nephrology (2015)
Board Certification: American Board of Internal Medicine, Internal Medicine (2014)
Residency: University of Chicago Medical Center Internal Medicine Residency (2013) IL
Medical Education: University of Colorado School of Medicine (2010) CO
Kidney transplant outcomes and function following simultaneous heart kidney transplant compared to solitary kidney transplant from the same donor
WILEY. 2020: 89
View details for Web of Science ID 000505634300187
What Solid Organ Transplant Healthcare Providers should know about Renin-Angiotensin-Aldosterone System Inhibitors and COVID-19.
The data on the outcomes of solid organ transplant recipients who have contracted coronavirus disease 2019 (COVID-19) are still emerging. Kidney transplant recipients are commonly prescribed renin-angiotensin-aldosterone system (AAS) inhibitors given the prevalence of hypertension, diabetes, and cardiovascular disease. As the angiotensin-converting enzyme 2 (ACE2) facilitates the entry of coronaviruses into target cells, there have been hypotheses that preexisting use of Renin-Angiotensin-Aldosterone System (RAAS) inhibitors may increase the risk of developing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Given the common use of RAAS inhibitors among solid organ transplant recipients, we sought to review the RAAS cascade, the mechanism of SARS-CoV-2 entry, and pertinent data related to the effect of RAAS inhibitors on ACE2 to guide management of solid organ transplant recipients during the COVID-19 pandemic. At present there is no clear evidence to support the discontinuation of RAAS inhibitors in solid organ transplant recipients during the COVID-19 pandemic.
View details for DOI 10.1111/ctr.13991
View details for PubMedID 32446267
Longitudinal Changes in Kidney Function Following Heart Transplantation: Stanford Experience.
Many heart transplant recipients experience declining kidney function following transplantation. We aimed toquantify change in kidney function in heart transplant recipients stratified by pre-transplant kidney function. 230 adult heart transplant recipients between May 1, 2008 and December 31, 2014 were evaluated for up to 5 years post-transplant (median 1 year). Using 19,398 total eGFR assessments, we evaluated trends in estimated glomerular filtration rate (eGFR) in recipients with normal/near normal (eGFR >45 mL/min/1.73m2 ) versus impaired (eGFR <45 mL/min/1.73m2 ) kidney function and the likelihood of reaching an eGFR of 20 mL/min/1.73m2 after heart transplant. Baseline characteristics were similar. Immediately following heart transplant, the impaired pre-transplant kidney function group showed a mean eGFR gain of 9.5mL/min/1.73m2 (n=193) versus a mean decline of 4.9 mL/min/1.73m2 (n=37) in the normal/near normal group. Subsequent rates of eGFR decline were 2.2 mL/min/1.73m2 /yrversus2.9 mL/min/1.73m2 /yr, respectively. The probability of reaching an eGFR of 20 mL/min/1.73m2 or less at 1, 5, and 10 years following heart transplant was 1%, 4% and 30% in the impaired group, and <1%, <1%, and 10% in the normal/near normal group. Estimates of expected recovery in kidney function and its decline over time will help inform decision making about kidney care after heart transplantation. This article is protected by copyright. All rights reserved.
View details for DOI 10.1111/ctr.13414
View details for PubMedID 30240515