Proteinuria

Outline and Objectives Definition Screening/Measurement Etiology Treatmen

Patient and Renal Outcomes of Posttransplant Lymphoproliferative Disorder Following Solid Organ Transplantations - A Single Center Experience

Introduction: Post-transplant Proliferative Disorder (PTLD) is a significant complication after solid organ transplantation (SOT). Major risk factors that contribute to the development of PTLD include Epstein-Barr Virus (EBV) infection and degree of immunosuppression. Despite novel therapies, the 5-year survival rate of PTLD only improved from 40% to 50% over the years. The reported 5-year survival rate of PTLD also remains significantly lower compared to around 90% in other malignancies such as breast and colon cancer. In our center, we hypothesize better transplant outcomes compared to those reported in preceding literatures. Methods: We retrospectively reviewed the electronic medical records of all patients who had a SOT followed by the diagnosis of PTLD from the last 10 years. We collected donor and recipient characteristics, time interval between SOT and PTLD diagnosis, disease characteristics based on the WHO 2017 classification, response to treatment, and outcomes. We calculated the mortality rate and graft failure rate to evaluate patient survival and allograft survival outcomes. Results: In our center, there were 32 patients that underwent a SOT and were later diagnosed with PTLD. Of them, 12 were female, and 8 were non-Hispanic blacks. PTLD was diagnosed in 18 kidney transplants, 11 liver transplants, 2 simultaneous kidney-pancreas transplants, and one simultaneous liver-kidney transplant. Mean time from SOT to PTLD diagnosis was 63 months, with 13 patients diagnosed in the 1st year post transplant. The main PTLD subtype was monomorphic B-cell lymphoma (20/32 patients) and 16 of them were diffuse large B cell lymphomas (DLBCL). Three patients had graft involvement by PTLD. Mean serum creatinine was 2.29 mg/dL, with mean follow up time of 57.7 months. There were 11 deaths in the cohort (33%), and 5 graft failures (15%) at the five year follow up mark. Discussion: Patient survival and allograft survival in PTLD patients are better in our center than reported in the literature. In our cohort, PTLD was not a significant cause of graft failure after 5 years of follow up. Further studies are needed to look at the disease characteristics that will help determine more specific prognostic factors

Patient and renal allograft outcomes of anticoagulation therapy in kidney transplantation

Introduction: Kidney transplant recipients are often on anticoagulation or antiplatelet therapy, for a variety of indications. These medications are associated with increased risk of bleeding but may reduce risk of thrombosis and possible complications such as allograft loss. The aim of our study is to evaluate the effect of perioperative anticoagulation or antiplatelet therapy on patient and allograft outcomes. Methods: Data collection was done by retrospective chart review of all patients who underwent a kidney or kidney/pancreas transplantation at Thomas Jefferson University Hospital (TJUH) from 2012-2019. We recorded perioperative anticoagulation and antiplatelet therapy, risk factors for bleeding and thrombosis, post-transplant episodes of bleeding or thrombosis, allograft function at multiple timepoints from 30 days to 3 years post-transplant, allograft loss, and mortality. Data analysis will evaluate relative outcomes based on perioperative anticoagulation or antiplatelet status. Results: We have completed collecting data for the 872 kidney or kidney/pancreas transplants done at TJUH from 2012-2019 and are currently working on analyzing the data. The patients will be evaluated in groups based on the presence and type of anticoagulation or antiplatelet therapy. These groups will then be compared based on patient and allograft outcomes. Discussion: We expect to find that patients on perioperative anticoagulation or antiplatelet therapy had higher rates and severity of bleeding, but lower rates of thrombosis and therefore allograft loss and mortality. This study will improve our understanding of perioperative anticoagulation and antiplatelet therapy so we may develop treatment guidelines for the TJUH kidney transplant program

Macrophage and adipocyte interaction as a source of inflammation in kidney disease

In obesity, adipose tissue derived inflammation is associated with unfavorable metabolic consequences. Uremic inflammation is prevalent and contributes to detrimental outcomes. However, the contribution of adipose tissue inflammation in uremia has not been characterized. We studied the contribution of adipose tissue to uremic inflammation in-vitro, in-vivo and in human samples. Exposure to uremic serum resulted in activation of inflammatory pathways including NFκB and HIF1, upregulation of inflammatory cytokines/chemokines and catabolism with lipolysis, and lactate production. Also, co-culture of adipocytes with macrophages primed by uremic serum resulted in higher inflammatory cytokine expression than adipocytes exposed only to uremic serum. Adipose tissue of end stage renal disease subjects revealed increased macrophage infiltration compared to controls after BMI stratification. Similarly, mice with kidney disease recapitulated the inflammatory state observed in uremic patients and additionally demonstrated increased peripheral monocytes and inflammatory polarization of adipose tissue macrophages (ATMS). In contrast, adipose tissue in uremic IL-6 knock out mice showed reduced ATMS density compared to uremic wild-type controls. Differences in ATMS density highlight the necessary role of IL-6 in macrophage infiltration in uremia. Uremia promotes changes in adipocytes and macrophages enhancing production of inflammatory cytokines. We demonstrate an interaction between uremic activated macrophages and adipose tissue that augments inflammation in uremia

Improving Transitions of Care for Inpatients with an eGFR \u3c 20ml/min

In this study we conducted an analysis of 22 inpatients with an eGFR\u3c20 that revealed there was a greater prevalence of patients without permanent AV access for HD initiation when compared to national data. These findings demonstrated the need for improved transitions of care and timely creation of AV access for this patient population, thus we sought to improve this. This is the first inpatient initiative that our group is aware with the aim of improving timely AV access and transitions of care for an inpatient population (Figure 1).https://jdc.jefferson.edu/patientsafetyposters/1090/thumbnail.jp

Obesity, inflammatory and thrombotic markers, and major clinical outcomes in critically ill patients with COVID‐19 in the US

Objective This study aimed to determine whether obesity is independently associated with major adverse clinical outcomes and inflammatory and thrombotic markers in critically ill patients with COVID‐19. Methods The primary outcome was in‐hospital mortality in adults with COVID‐19 admitted to intensive care units across the US. Secondary outcomes were acute respiratory distress syndrome (ARDS), acute kidney injury requiring renal replacement therapy (AKI‐RRT), thrombotic events, and seven blood markers of inflammation and thrombosis. Unadjusted and multivariable‐adjusted models were used. Results Among the 4,908 study patients, mean (SD) age was 60.9 (14.7) years, 3,095 (62.8%) were male, and 2,552 (52.0%) had obesity. In multivariable models, BMI was not associated with mortality. Higher BMI beginning at 25 kg/m2 was associated with a greater risk of ARDS and AKI‐RRT but not thrombosis. There was no clinically significant association between BMI and inflammatory or thrombotic markers. Conclusions In critically ill patients with COVID‐19, higher BMI was not associated with death or thrombotic events but was associated with a greater risk of ARDS and AKI‐RRT. The lack of an association between BMI and circulating biomarkers calls into question the paradigm that obesity contributes to poor outcomes in critically ill patients with COVID‐19 by upregulating systemic inflammatory and prothrombotic pathways