Since March 2022, donors with detectable SARS-CoV-2 RNA have been accepted for extrapulmonary organ transplants in Brazil. In this report, we described 11 successful organ transplants (6 kidney, 5 liver) from 5 asymptomatic infected donors.
Background: Over the last decade, there has been a steady increase in the number of patients diagnosed with end stage renal failure (ESRF). Renal transplant remains the best available treatment for ESRF. The aim of this study is to assess the surgical outcomes following renal transplantation in a single tertiary centre in Aotearoa New Zealand.
Sterile inflammation has been increasingly recognized as a hallmark of non-infectious kidney diseases. Induction of pro-inflammatory cytokines in injured kidney tissue promotes infiltration of immune cells serving to clear cell debris and facilitate tissue repair. However, excessive or prolonged inflammatory response has been associated with immune-mediated tissue damage, nephron loss, and development of renal fibrosis.
While the Banff classification dichotomizes kidney allograft rejection based on the localization of the cells in the different compartments of the cortical kidney tissue [schematically interstitium for T cell mediated rejection (TCMR) and glomerular and peritubular capillaries for antibody-mediated rejection (AMR)], there is a growing evidences that subtyping the immune cells can help refine prognosis prediction and treatment tailoring, based on a better understanding of the pathophysiology of kidney allograft rejection. In the last few years, multiplex IF techniques and automatic counting systems as well as transcriptomics studies (bulk, single-cell and spatial techniques) have provided invaluable clues to further decipher the complex puzzle of rejection. In this review, we aim to better describe the inflammatory infiltrates that occur during the course of kidney transplant rejection (active AMR, chronic active AMR and acute and chronic active TCMR).
Small-for-size syndrome is a clinical syndrome of early allograft dysfunction usually following living donor liver transplantation due to a mismatch between recipient metabolic and functional requirements and the graft's functional capacity. While graft size relative to the recipient size is the most commonly used parameter to predict risk, small-for-size syndrome is multifactorial and its development depends on a number of inter-dependant factors only some of which are modifiable. Intra-operative monitoring of portal haemodynamics and portal flow modulation is widely recommended though there is wide variation in clinical practice.
