About

William Asch, MD, PhD, BA, is an Associate Professor of Medicine in Nephrology at Yale School of Medicine. His clinical, educational, administrative, and scholarly efforts are centered on solid organ transplantation, with a primary focus on kidney transplantation. He provides subspecialty consultative services to the liver, heart, and bone marrow transplant programs. As the Program Director of the Transplant Nephrology Fellowship Program and the Director of Pre-Transplant Operations at Yale, he established the policies, procedures, and documentation required for the fellowship program, which is accredited through the American Society of Transplantation and has graduated six fellows. His scholarly activities include investigator-initiated research on neurocognitive impairments associated with tacrolimus, an immunosuppressant used in transplant recipients. His research has demonstrated the feasibility of high-level cognitive assessments in clinical settings and expanded into multicenter trials such as the ABCs Trial. He is also the Principal Investigator for clinical trials on immune tolerance, BK viremia, and diabetic kidney disease progression. His work contributes significantly to advancing understanding and treatment in transplant immunology and nephrology.

Research topics

• Internal medicine
• Medicine
• Virology
• Environmental health
• Demography
• Gerontology
• Immunology
• Family medicine

Selected publications

• Potravitug for Treatment of BK Polyomavirus Infection in Kidney Transplant Recipients: SAFE KIDNEY II, a Randomised, Double-Blind, Placebo-Controlled Phase 2 Trial

  SSRN Electronic Journal · 2026-01-01

  preprintOpen access
  PublisherDOI

• Durable Salvage of a Renal Transplant with Perioperative Endovascular Thrombectomy of Iliofemoral Venous Thrombosis

  Journal of Vascular Surgery Venous and Lymphatic Disorders · 2025-02-13

  articleOpen access

  Objectives: Nutcracker syndrome (NCS) is a vascular compression syndrome resulting in left flank pain, abdominal pain, and possibly hematuria, which occurs when the left renal vein is compressed typically between the aorta and the superior mesenteric artery.This can occur with rapid weight loss, resulting in a narrowed aortomesenteric angle.The association with bariatric surgery and left renal vein compression is poorly understood, and the development of NCS after weight loss surgery is not well-represented in the literature.Herein, we present a series of patients who developed NCS following bariatric surgery.Methods: A single-center, retrospective chart review evaluating development of NCS after bariatric surgery between April 2020 and March 2023.Results: We identified six patients who underwent bariatric surgery and subsequently developed symptomatic left renal vein compression necessitating surgery.100% of patients were female, and age ranged from 32 to 68 years old.Gastric bypass accounted for 50% of bariatric procedures, and gastric sleeve was performed in 33% of patients.All patients suffered from left flank pain, and 33% developed hematuria.A dilated left ovarian vein was present in 66% of patients, and dilated lumbar vein was present in 50% of patients.All patients underwent a venous decompression surgery, either left renal vein transposition (33%), left renal artery denervation and left renal vein decompression surgery (50%), or left renal autotransplant (17%).All patients had continued resolution of NCS symptoms at minimum 1 year follow-up.Conclusions: Bariatric surgery and rapid weight loss can lead to a narrowed aortomesenteric angle, loss of visceral fat pad, and compression of the left renal vein.Left-sided abdominal or flank pain or hematuria after bariatric surgery and weight loss may be a sign of developing NCS and should be evaluated.Patients who undergo surgery for NCS after bariatric surgery have excellent symptom relief at follow-up.

  PublisherOA PDFDOI

• Sequential Measurement of Donor Derived cfDNA and Correlation with Patient Outcomes Post Kidney Transplant

  American Journal of Transplantation · 2025-08-01

  article
  PublisherDOI

• Early Steroid Withdrawal in Kidney Transplant Recipients: PRO

  Kidney360 · 2025-02-01 · 1 citations

  articleOpen accessSenior author

  The use of corticosteroids to prevent organ rejection was a pioneering advancement of the 1960s and has remained a deeply rooted approach in kidney transplantation. Yet, patients routinely report their concerns for corticosteroid (hereafter, referred to simply as steroid)-induced side effects and their desire to discontinue use, even preferentially over other arguably more pernicious immunosuppressive (IS) medications. When surveyed and given a risk-free choice, about 65% of kidney transplant recipients (KTR) reported they would discontinue steroid use.1 Previous discussions weigh the projected long-term benefits of steroid elimination against the risk of developing allograft rejection attributed to the withdrawal of steroids.2 In the immunologically high-risk candidates, it is clear that short-term outcomes after kidney transplantation have significantly improved with the combined use of steroids and modern maintenance IS. But despite improvements in rates of acute rejection (AR) and 1-year post transplant allograft and patient survival, the long-term outcomes have either remained unaffected or show only modest improvement, especially in low or standard immunological risk recipients.3 Multiple studies, using different strategies to either eliminate or reduce the KTR's cumulative exposure to steroids, with varying combinations of other IS, have been undertaken to highlight these trends. In this debate, we continue to make the case that steroids can be safely discontinued early after transplantation for appropriate patients without significant detrimental effect on long-term outcomes. While studies have confirmed that use of steroids reduce the risk of AR during the early post-transplant period resulting in a decline in early graft loss, it is less clear whether continued steroid use is necessary to prevent rejection months or years after transplant. It is already established that early rejections, when swiftly managed, do not necessarily affect long-term allograft outcomes.4 Indeed, most of the AR events that occurred did so early after steroid withdrawal, were of low Banff grade, and were easily treated with steroids. There is, in fact, growing evidence that early steroid withdrawal in the appropriate population does not result in an increased risk of long-term allograft loss.5 Most studies investigating the continued necessity of steroids withdraw them at a specified time point. Conventionally, steroid avoidance is defined as use for seven days or less, while protocols investigating steroid withdrawal do so in the 3–6 months after transplantation. Note that in clinical practice, late steroid withdrawal is often a consideration as well. For example, in a recipient with avascular necrosis of the hip who is not a candidate for an operative repair. Few studies have investigated late steroid withdrawals. Unfortunately, the long-term consequences of maintenance steroids are all cumulative and therefore only become evident during longer-term follow-up. Death with a functioning allograft has increased over time, presently seen in approximately 40% of KTR. While long-term studies have been unsuccessful to support the continuing need for steroids, their ongoing use certainly has a detrimental and accruing effect on overall recipient health, especially the cardiovascular and metabolic parameters (Table 1). Table 1 - Detrimental effects of long-term corticosteroid use Impaired glycemic metabolism Weight gain Hypertension Hyperlipidemia Increased appetite Osteopenia/Osteoporosis Osteonecrosis Cataract development Skin fragility Impaired wound healing Gastric ulceration Impaired growth (in children) Cushingoid appearance Increased fat deposition Decreased muscle production Irregular menstrual periods Increased risk for infections Fluctuations in mood disorders It is well established that steroid use results in an increased risk of major adverse cardiovascular events.6 Cardiovascular and cerebrovascular events collectively are the cause of 22% of KTR who die with a functioning allograft. Indeed, this rate of cardiovascular death is an alarming ten-fold that for the general population.7 One may argue that the relative contribution of the low-dose steroid is eclipsed by that of calcineurin inhibitors. But it is also recognized that CNI (tacrolimus, in particular) in interaction with other recipient variables (such as age and body mass index) are a risk factor for post-transplant diabetes mellitus development. Recent studies have shown feasibility of simultaneous CNI avoidance and steroid withdrawal for an improved metabolic profile without excessive AR in the first 12 months after transplant.8 Nonetheless, steroid avoidance, early elimination, and late steroid withdrawal all have the potential to reduce the long-term risk of cardiovascular events and death with a functioning allograft, thereby extending the lifetime of the kidney transplant recipient. Therefore, it may be reasonable to accept a higher risk of early AR (which in fact may help label those recipients who have a proven need for continued steroid use) to identify the larger group of KTR who would see the benefit of a reduced cardiovascular risk by not receiving steroids long term. This magnitude of increased risk has been reported to be low in selected low immunologic risk (panel reactive antibodies ≤ 25%) patients, but it should be noted that borderline findings were not recorded as rejection in all studies investigating steroid avoidance.9 Were we to broadly adopt the strategy of universally attempting steroid avoidance or early withdrawal, or perhaps even late withdrawal, we need to more clearly consider the fraction of recipients who would experience a negative consequence. We must also consider how an AR event early after transplant that receives proper management affects the long-term function of these allografts. Another consideration of how much additional harm comes from a one-time high-dose (1500–2000 mg) bolus steroid use to treat AR and weigh this in comparison to the adverse effects of lifelong low-dose steroid use. Multiple studies and two Cochrane debased reviews have investigated the effect of steroid avoidance on post-transplant outcomes (rejection and post-transplant diabetes mellitus, in particular). Using meta-analysis compared with steroid maintenance, steroid withdrawal was associated with a significantly increased 1-year relative risk of AR (RR=1.77). However, it should be noted that 1-year mortality (RR=0.68) and new-onset diabetes after transplantation (RR=0.77) were both reduced.10 The elderly are more susceptible to steroid-related complications compared with younger KTR, particularly to fractures, myopathy, and age-related immune dysfunction resulting in infection and malignancy.11 However, lower-intensity immunosuppression regimens, including steroid avoidance, are known to have equivalent allograft outcomes in elderly recipients. The effect of low-dose steroids on these negative outcomes should not be discounted, as is often the case when considered relative to higher doses. Notably, there are recommendations to prevent, reduce, or retard the development of premature or exaggerated osteoporosis for patients taking prednisone ≥7.5 mg/d, but no such recommendations have been established for prednisone 5 mg/d, the dose most commonly used as part of maintenance immunosuppression regimens. But experimental data confirm the negative effect of low-dose prednisone on markers of bone formation, which were lower compared with patients receiving placebo.12 We acknowledge the increased risk of rejection when steroid avoidance and steroid withdrawal protocols are used in high-risk KTR. And while 3-year allograft survival seems equivalent, we also recognize the concern for an increased rate of DSA development and the role this may have on very long-term allograft survival. Despite these valid concerns, these risks seem to be worth accepting for a carefully selected subgroup of recipients. An increased risk of early, low-grade, steroid-responsive rejection should not be an absolute contraindication to considering an early steroid avoidance, withdrawal, or minimization protocol. Moreover, given that about 12% of current US transplant waitlist comprises retransplant candidates, the long-term use of steroids should be justified by the cumulative cardiovascular and metabolic risks which unfortunately only become apparent after several years of use.

  PublisherDOI

• Induction of immune tolerance in living related human leukocyte antigen–matched kidney transplantation: A phase 3 randomized clinical trial

  American Journal of Transplantation · 2025-02-06 · 12 citations

  article
  PublisherDOI

• Assessing changes in donor-derived cfDNA in post-kidney transplant patients and its correlation with graft survival

  Human Immunology · 2025-09-01

  article
  PublisherDOI

• Potravitug for the Treatment of BK Polyomavirus Infection in Kidney Transplant Recipients: A Phase II, Randomized, Double-Blind, Placebo-Controlled Clinical Trial

  Journal of the American Society of Nephrology · 2025-10-01

  article
  PublisherDOI

• Is PET the Best Screening Tool for Cardiac Assessment Prior to Renal Transplant?

  Circulation Cardiovascular Imaging · 2024-01-01

  editorialOpen accessSenior author
  PublisherOA PDFDOI

• Cryoglobulinemic Glomerulonephritis Masquerading as IgA Nephropathy in a Patient with Crohn Disease

  Journal of the American Society of Nephrology · 2024-10-01

  articleSenior author

  Introduction: We report a case of a patient with long standing history of Crohn’s presenting with anemia, acute renal failure requiring initiation of dialysis and lower extremity painful rash. Renal biopsy initially suggested IgA nephropathy given history of Crohn’s and codominant IgA and IgM, but EM features and serological markers made cryoglobulinemic GN a favorable diagnosis. In this case, we address the diagnostic complexity we came across. Case Description: This is a 48-year-old Caucasian female who was admitted with anemia, acute kidney injury, and purpuric rash of the lower extremities. Urinalysis revealed red blood cells and nephrotic range proteinuria. Urine sediment showed RBC casts. Renal function rapidly deteriorated requiring initiation of dialysis. Physical exam revealed painful LE purpuric rash, levido reticularis and dorsal foot ulcers. Imaging showed ground glass opacities. Given the rapid decline in renal function and findings suggestive of systemic vasculitis, a renal biopsy was expedited. Biopsy showed focal necrotizing and crescentic glomerulonephritis on LM, IF staining with +1 IgA ,IgM and +2 C3 staining. However, there were rare subendothelial and mesangial electron dense deposits with curvilinear substructure on EM suggesting cryoglobulinemic GN. Serological markers came back positive for rheumatoid, borderline low C3 with normal C4 and serum cryoglobulin was positive, with immunofixation showing type 2 mixed cryoglobulins. Broad work up was done to identify an infectious or lymphoproliferative etiology of cryogenesis revealing a positive respiratory culture growing Klebsiella pneumonia on BAL, and pleural nodule biopsy showed organizing pneumonia. The patient was promptly started on pulse steroids, IVIG and PLEX with improvement in skin rash. She continued to require dialysis on discharge, and Rituximab was deferred to the outpatient setting due to active infection. Discussion: Cryoglobulinemic glomerulonephritis (GN) is a disorder characterized by the deposition of cryoglobulins. Cryoglobulinemic and IgA vasculitis can have multiple similarities in clinical and pathological features. In this case we encountered multiple overlapping clinical and histological findings, but ultimate diagnosis was favorable for cryoglobulinemic vasculitis. The positive rheumatoid and EM findings helped in making the distinction.

  PublisherDOI

• Progressive Multifocal Leukoencephalopathy (PML): A Dreaded Complication of Immunosuppression

  Journal of the American Society of Nephrology · 2023-11-01 · 1 citations

  articleSenior author

  Journal of the American Society of Nephrology 34(11S):p 610, November 2023. | DOI: 10.1681/ASN.20233411S1610a

  PublisherDOI

Frequent coauthors

• Nisson Schechter

  21 shared

• Anthony K. Canger

  Memorial Sloan Kettering Cancer Center

  18 shared

• Sanjay Kulkarni

  Yale University

  17 shared

• Marco A. Passini

  Sarepta Therapeutics (United States)

  14 shared

• Eric M. Tichy

  Mayo Clinic in Arizona

  14 shared

• Richard N. Formica

  Yale University

  14 shared

• Devin Leake

  10 shared

• Margaret J. Bia

  Yale University

  10 shared

Education

• M.D., Medicine

  Yale University

  1990

• Ph.D., Immunology

  Yale University

  1985

• B.A., Biology

  Yale University

  1981