Thrombotic microangiopathy (TMA) is a clinicopathological entity characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ injury, occurring due to endothelial damage and microthrombi formation in small vessels (1, 2). It can affect up to 15% of transplanted patients and is associated with significant morbidity and mortality (3).
TMA is primary when a genetic or acquired defect is identified (as in atypical hemolytic uremic syndrome [aHUS] and thrombotic thrombocytopenic purpura) or secondary when occurring in the context of another disease process, such as infection, autoimmune disease, malignancy, or drugs (4) (Table 1
Belatacept is a soluble recombinant fusion protein composed of the constant fragment of human immunoglobulin G1 and modified extracellular domain of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). It inhibits T-lymphocyte activation by blocking costimulation, the requisite signal that T-lymphocytes must receive through interactions between proteins expressed on antigen-presenting cells and T-lymphocytes in addition to signal from engagement of the antigen receptor (Figure 1).
Belatacept mechanism of action
In 2011, the US Food and Drug Administration (FDA) approved belatacept for prophylaxis against acute rejection in de novo adult kidney transplant recipients based on randomized trials that showed better
Barry I. Freedman, Lijun Ma, and Marva M. Moxey-Mims
Discovery of the genetic association between apolipoprotein L1 (APOL1) gene kidney-risk variants and chronic kidney disease in individuals with recent African ancestry dramatically altered the landscape in nephrology (1). This observation accounted for much of the threefold higher incidence rate of end stage kidney disease (ESKD) in African Americans (AAs) compared with other populations. APOL1 genotypes also underlie a portion of the disparity in outcomes after deceased donor kidney transplantation (DDKT). Kidneys transplanted from deceased donors with African ancestry fail more rapidly than those from non-African ancestry donors (2). A
The short period of 2020 to 2022 has felt like its own era in the field of kidney transplantation, with significant advances in the field on various fronts. The next two editions of Kidney News will highlight some of these advances in kidney transplantation, which push the barriers of science and society. This first and current edition will focus on racial inequities in transplantation and measures to address them, the new kidney transplant allocation system, updates from the Apolipoprotein L1 (APOL1) Long-term Kidney Transplantation Outcomes (APOLLO) study, and groundbreaking advances in xenotransplantation and finally,
The kidney allocation policy within the United States was initially established in 1987 to promote the equitable and utilitarian distribution of deceased donor kidneys (1). The policy, managed by the United Network for Organ Sharing (UNOS)/Organ Procurement and Transplantation Network (OPTN), was extensively revised in 2014 to increase the utilization of available kidneys, reduce regional variability in access to transplantation, and improve posttransplant outcomes. Major changes at the time included the introduction of the Kidney Donor Profile Index (KDPI) and Estimated Post Transplant Survival (EPTS) scores as estimates of kidney quality and projected recipient survival, respectively, and also
Oxalate or oxalic acid is a dicarboxylic acid formed in the human body from exogenous dietary sources and endogenous metabolism of ascorbic acid and some amino acids. It is essentially a terminal metabolic product that is produced by the liver, absorbed by the intestine from dietary sources, and freely filtered by the kidneys (Figure 1) (1). There is no human enzyme that can degrade it further.
Regional disparity in deceased donor kidney transplant rates
Hepatic metabolism and dietary oxalate absorption generate plasma oxalate, which is then primarily excreted by kidneys into urine.
During the past few months, I have participated in several meetings that included in-depth discussions about the future of the health care workforce in the United States. Each time, the discussion started with predictions about shortages of every kind of health professional—from physicians to nurses to physician assistants/associates to other clinicians—and then shifted to concerns about the ability to provide high-quality patient care in the future as a result.
Although this editorial will focus on the future of nephrologists in the United States, I recognize that the situation is dire throughout the world, particularly for nurses. Earlier this year, the
Structural racism is a root cause of health inequities. The term structural racism refers to differential access by racial group to opportunities, resources, and societal well-being and is mediated through complex health care systems (1). To undergo kidney transplant, patients must navigate a multistep, conditional process that requires multiple health system and clinician interactions. This process exerts a differential burden on patients from marginalized groups. Studies in recent decades have demonstrated that racial minority groups experience lower rates of kidney transplant listing and transplant compared with patients of White race (2, 3). Patients of
A. Cozette Killian, Paige M. Porrett, Jayme E. Locke, and Vineeta Kumar
In 1964, the first kidney xenotransplant from a chimpanzee to human was performed successfully (1). Although the recipient survived 9 months, subsequent animal-to-human transplants were limited by immunologic barriers and the need for a sustainable organ source (2). Pigs soon became the ideal organ source because they produce large litters and mature rapidly, and availability is virtually unlimited (2, 3). Pigs have organs comparable in size and function with humans and lower risk of zoonoses, and their hormones and tissues are already used, suggesting positive public opinion (2, 3
Over the past 10 to 20 years, there has been a revolution in the care of patients with cancer. In addition to classic chemotherapy agents, anti-cancer agents now include targeted therapies and immunotherapies, which harness the power of the immune system. These new therapies have transformed cancer into a chronic disease for many patients. Importantly, acute and chronic kidney diseases, electrolyte and acid-base disorders, and hypertension have become highly prevalent complications in this group of patients. This is particularly true for those with liver cancer, multiple myeloma, renal cell carcinoma, leukemias and lymphomas, and cancer patients treated with potentially nephrotoxic