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Academic Appointments

Professional Education

  • Fellowship, Stanford University School of Medicine, Transplant Nephrology (2020)
  • Fellowship, Indiana University School of Medicine, Nephrology (2019)
  • Board Certification, American Board of Internal Medicine (2018)
  • Residency, Indiana University School of Medicine, Internal Medicine (2017)
  • Doctor of Medicine, Eastern Virginia Medical School (2014)
  • Bachelor of Arts, University of Virginia (2010)

Stanford Advisors


All Publications

  • Influence of Immunosuppression on Seroconversion Against SARS-Cov-2 in Two Kidney Transplant Recipients. Transplant infectious disease : an official journal of the Transplantation Society Wang, A. X., Quintero Cardona, O. n., Ho, D. Y., Busque, S. n., Lenihan, C. R. 2020: e13423


    Solid organ transplant recipients are at risk for infectious complications due to chronic immunosuppression. The outbreak of Coronavirus Disease 2019 (COVID-19) in United States has raised growing concerns for the transplant patient population. We seek to add to the current limited literature on COVID-19 in transplant recipients by describing the clinical course of two kidney transplant recipients with SARS-Cov-2 infection monitored by both RT-PCR and serology. Through careful adjustment of their immunosuppression regimen, both patients had excellent recovery with intact graft function and development of anti-SARS-Cov-2 antibodies.

    View details for DOI 10.1111/tid.13423

    View details for PubMedID 32701196

  • COVID-19 and Kidney Transplantation: Results from the TANGO International Transplant Consortium. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons Cravedi, P. n., Suraj, S. M., Azzi, Y. n., Haverly, M. n., Farouk, S. n., Pérez-Sáez, M. J., Redondo-Pachón, M. D., Murphy, B. n., Florman, S. n., Cyrino, L. G., Grafals, M. n., Venkataraman, S. n., Cheng, X. S., Wang, A. X., Zaza, G. n., Ranghino, A. n., Furian, L. n., Manrique, J. n., Maggiore, U. n., Gandolfini, I. n., Agrawal, N. n., Patel, H. n., Akalin, E. n., Riella, L. V. 2020


    Kidney transplant recipients may be at high risk of developing critical COVID-19 illness due to chronic immunosuppression and comorbidities. We identified hospitalized adult kidney transplant recipients at 12 transplant centers in the US, Italy and Spain who tested positive for COVID-19. Clinical presentation, laboratory values, immunosuppression and treatment strategies were reviewed and predictors of poor clinical outcomes were determined through multivariable analyses. Among 9,845 kidney transplant recipients across centers, 144 were hospitalized due to COVID-19 during the 9-week study period. 65% were male with a mean age of 60 (±12) years, 40% Hispanic and 25% African-American. Prevalent comorbidities included hypertension (95%), diabetes (52%), obesity (49%), heart (28%) and lung (19%) disease. Therapeutic management included antimetabolite withdrawal (68%), calcineurin inhibitor withdrawal (23%), hydroxychloroquine (71%), antibiotics (74%), tocilizumab (13%) and antivirals (14%). During a median follow-up period of 52 days (IQR: 16-66 days), acute kidney injury occurred in 52% cases, respiratory failure requiring intubation in 29%, and mortality was 32%. The 44 patients who died were older, had lower lymphocyte counts and eGFR, higher serum lactate dehydrogenase, procalcitonin and IL-6 levels. In sum, hospitalized kidney transplant recipients with COVID-19 have higher rates of acute kidney injury and mortality.

    View details for DOI 10.1111/ajt.16185

    View details for PubMedID 32649791

  • Simultaneous Coccidioidomycosis and Phaeohyphomycosis in a Kidney Transplant Recipient: A Case Report and Literature Review. Transplant infectious disease : an official journal of the Transplantation Society Puing, A. G., Couture-Cossette, A. n., Wang, A. X., Zygourakis, C. C., Cheng, X. n., Stevens, B. A., Banaei, N. n., Novoa, R. A., Ho, D. Y., Subramanian, A. n. 2020: e13365


    Advances in solid organ transplantation have improved the survival of end-stage organ disease at the expense of an increased risk for opportunistic infections. Unusual clinical presentations and the possibility of concurrent infections make diagnosing invasive fungal infection (IFI) more difficult. Here we present a case of simultaneous vertebral infection caused by Coccidioides immitis-posadasii and subcutaneous phaeohyphomycosis due to Nigrograna mackinnonii in a kidney transplant recipient. The diagnosis of both infections required invasive procedures to obtain tissue and a high index of suspicion that more than one IFI could be present. A multidisciplinary team approach for the management of immunocompromised patients with suspected or diagnosed IFI is warranted.

    View details for DOI 10.1111/tid.13365

    View details for PubMedID 32533741

  • What Solid Organ Transplant Healthcare Providers should know about Renin-Angiotensin-Aldosterone System Inhibitors and COVID-19. Clinical transplantation Wong, S. Y., Brubaker, A. L., Wang, A. X., Taiwo, A. A., Melcher, M. L. 2020: e13991


    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

  • Difficult Patient Behavior in Dialysis Facilities. Blood purification Janosevic, D. n., Wang, A. X., Wish, J. B. 2019; 47 (1-3): 254?58


    Difficult behavior exhibited by dialysis patients is a spectrum that includes nonadherence, verbal or physical abuse, and threatening acts. Such behaviors may lead to harmful consequences to the patient, other patients, the facility, and staff and can culminate in involuntary discharge. It is important to recognize that these "difficult behaviors" may be due to underlying psychosocial or medical issues, which places an onus on care providers to explore further. According to the Conditions for Coverage (CfC) for dialysis facilities, it falls upon the medical director to coordinate and oversee policies for patient satisfaction, patient safety and rights, involuntary discharges, and adverse events and outcomes. Thus, medical directors are liable for their own actions, and their staff for which they have oversight, for harm or perceived harm to patients in response to difficult behaviors. Guidelines to deal with specific patient behavior scenarios have been published by the Decreasing Dialysis Patient Conflict National Task Force of the Forum of end-stage renal disease (ESRD) Networks. The common denominator for these difficult scenarios is impaired communication, and the majority of patient concerns involve issues with staff, policies, treatments, and diet. Involuntary discharge of a patient should always be viewed as a last resort, and there is a structured process described in the CfC that requires the involvement of the respective ESRD Network and the facility medical director. As physicians, we are bound by ethical and growing legal obligations to act in an appropriate, ethical, and fair manner to patients who are considered to be "difficult."

    View details for DOI 10.1159/000494592

    View details for PubMedID 30522106

  • Aldosterone deficiency prevents high-fat-feeding-induced hyperglycaemia and adipocyte dysfunction in mice. Diabetologia Luo, P. n., Dematteo, A. n., Wang, Z. n., Zhu, L. n., Wang, A. n., Kim, H. S., Pozzi, A. n., Stafford, J. M., Luther, J. M. 2013; 56 (4): 901?10


    Obesity is associated with aldosterone excess, hypertension and the metabolic syndrome, but the relative contribution of aldosterone to obesity-related complications is debated. We previously demonstrated that aldosterone impairs insulin secretion, and that genetic aldosterone deficiency increases glucose-stimulated insulin secretion in vivo. We hypothesised that elimination of endogenous aldosterone would prevent obesity-induced insulin resistance and hyperglycaemia.Wild-type and aldosterone synthase-deficient (As (-/-)) mice were fed a high-fat (HF) or normal chow diet for 12 weeks. We assessed insulin sensitivity and insulin secretion using clamp methodology and circulating plasma adipokines, and examined adipose tissue via histology.HF diet induced weight gain similarly in the two groups, but As (-/-) mice were protected from blood glucose elevation. HF diet impaired insulin sensitivity similarly in As (-/-) and wild-type mice, assessed by hyperinsulinaemic-euglycaemic clamps. Fasting and glucose-stimulated insulin were higher in HF-fed As (-/-) mice than in wild-type controls. Although there was no difference in insulin sensitivity during HF feeding in As (-/-) mice compared with wild-type controls, fat mass, adipocyte size and adiponectin increased, while adipose macrophage infiltration decreased. HF feeding significantly increased hepatic steatosis and triacylglycerol content in wild-type mice, which was attenuated in aldosterone-deficient mice.These studies demonstrate that obesity induces insulin resistance independently of aldosterone and adipose tissue inflammation, and suggest a novel role for aldosterone in promoting obesity-induced beta cell dysfunction, hepatic steatosis and adipose tissue inflammation.

    View details for DOI 10.1007/s00125-012-2814-8

    View details for PubMedID 23314847

    View details for PubMedCentralID PMC3593801

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