Case Report: Tocilizumab for Acute Kidney Graft Dysfunction in Patient Affected by COVID-19.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was isolated in January 2020 and, on March, the WHO declared the status of a pandemic. It causes a cytokine release syndrome, called "cytokine storm," characterized by systemic inflammation involving elevated levels of cytokines and hyperactivation of immune cell; this profound alteration in the immune system led to an overshooting inflammatory response contributing to morbidity and mortality. Solid organ transplant recipients are at particularly higher risk of developing critical coronavirus disease 2019 (COVID-19) due to chronic immunosuppression; in fact, establishing the balance between infection and rejection in any transplant recipient is the principal aim when prescribing immunosuppression. Tocilizumab, a humanized monoclonal antibody against interleukin-6 (IL-6) receptor widely adopted in adult rheumatoid arthritis, is used as rescue therapy for chronic antibody-mediated rejection in kidney transplantation. Data about the use of tocilizumab for treating acute kidney graft dysfunction in a setting of kidney-transplanted patients affected by COVID-19 are lacking. In this case study, we discuss the case of kidney transplant recipient with proven SARS-CoV-2 infection that develops acute graft dysfunction and the management of immunosuppression with concomitant tocilizumab administration.

Recurrence of immunoglobulin A nephropathy after kidney transplantation: a narrative review of the incidence, risk factors, pathophysiology and management of immunosuppressive therapy.

Glomerulonephritis (GN) is the underlying cause of end-stage renal failure in 30-50% of kidney transplant recipients. It represents the primary cause of end-stage renal disease for 25% of the dialysis population and 45% of the transplant population. For patients with GN requiring renal replacement therapy, kidney transplantation is associated with superior outcomes compared with dialysis. Recurrent GN was previously considered to be a minor contributor to graft loss, but with the prolongation of graft survival, the effect of recurrent disease on graft outcome assumes increasing importance. Thus the extent of recurrence of original kidney disease after kidney transplantation has been underestimated for several reasons. This review aims to provide updated knowledge on one particular recurrent renal disease after kidney transplantation, immunoglobulin A nephropathy (IgAN). IgAN is one of the most common GNs worldwide. The pathogenesis of IgAN is complex and remains incompletely understood. Evidence to date is most supportive of a several hit hypothesis. Biopsy is mandatory not only to diagnose the disease in the native kidney, but also to identify and characterize graft recurrence of IgAN in the kidney graft. The optimal therapy for IgAN recurrence in the renal graft is unknown. Supportive therapy aiming to reduce proteinuria and control hypertension is the mainstream, with corticosteroids and immunosuppressive treatment tailored for certain subgroups of patients experiencing a rapidly progressive course of the disease with active lesions on renal biopsy and considering safety issues related to infectious complications.