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Purpose of program: This article will provide guidance on how to best manage patients with glomerulonephritis (GN) during the COVID-19 pandemic. Sources of information: We reviewed relevant published literature, program-specific documents, and guidance documents from international societies. An informal survey of Canadian nephrologists was conducted to identify practice patterns and expert opinions. We hosted a national webinar with invited input and feedback after webinar. Methods: The Canadian Society of Nephrology (CSN) Board of Directors invited physicians with expertise in GN to contribute. Specific COVID-19-related themes in GN were identified, and consensus-based recommendations were made by this group of nephrologists. The recommendations received further peer input and review by Canadian nephrologists via a CSN-sponsored webinar. This was attended by 150 kidney health care professionals. The final consensus recommendations also incorporated review by Editors of the Canadian Journal of Kidney Health and Disease. Key findings: We identified 9 areas of GN management that may be affected by the COVID-19 pandemic: (1) clinic visit scheduling, (2) clinic visit type, (3) provision of multidisciplinary care, (4) blood and urine testing, (5) home-based monitoring essentials, (6) immunosuppression, (7) other medications, (8) patient education and support, and (9) employment. Limitations: These recommendations are expert opinion, and are subject to the biases associated with this level of evidence. To expedite the publication of this work, a parallel review process was created that may not be as robust as standard arm’s length peer review processes. Implications: These recommendations are intended to provide optimal care during the COVID-19 pandemic. Our recommendations may change based on the evolving evidence.

Purpose of program: To provide guidance on the management of patients with advanced chronic kidney disease (CKD) not requiring kidney replacement therapy during the COVID-19 pandemic. Sources of information: Program-specific documents, pre-existing, and related to COVID-19; documents from national and international kidney agencies; national and international webinars, including webinars that we hosted for input and feedback; with additional information from formal and informal review of published academic literature. Methods: Challenges in the care of patients with advanced CKD during the COVID-19 pandemic were highlighted within the Canadian Senior Renal Leaders Forum discussion group. The Canadian Society of Nephrology (CSN) developed the COVID-19 rapid response team (RRT) to address these challenges. They identified a lead with expertise in advanced CKD who identified further nephrologists and administrators to form the workgroup. A nation-wide survey of advanced CKD clinics was conducted. The initial guidance document was drafted and members of the workgroup reviewed and discussed all suggestions in detail via email and a virtual meeting. Disagreements were resolved by consensus. The document was reviewed by the CSN COVID-19 RRT, an ethicist and an infection control expert. The suggestions were presented at a CSN-sponsored interactive webinar, attended by 150 kidney health care professionals, for further peer input. The document was also sent for further feedback to experts who had participated in the initial survey. Final revisions were made based on feedback received until April 28, 2020. Canadian Journal of Kidney Health and Disease (CJKHD) editors reviewed the parallel process peer review and edited the manuscript for clarity. Key findings: We identified 11 broad areas of advanced CKD care management that may be affected by the COVID-19 pandemic: (1) clinic visit scheduling, (2) clinic visit type, (3) provision of multidisciplinary care, (4) bloodwork, (5) patient education/support, (6) home-based monitoring essentials, (7) new referrals to multidisciplinary care clinic, (8) kidney replacement therapy, (9) medications, (10) personal protective equipment, and (11) COVID-19 risk in CKD. We make specific suggestions for each of these areas. Limitations: The suggestions in this paper are expert opinion, and subject to the biases associated with this level of evidence. To expedite the publication of this work, a parallel review process was created that may not be as robust as standard arms’ length peer-review processes. Implications: These suggestions are intended to provide guidance for advanced CKD directors, clinicians, and administrators on how to provide the best care possible during a time of altered priorities and reduced resources.

Background. Previously, we identified an antimitogenic IgG antibody separated from sera of patients with known kidney transplant chronic rejection. This antibody inhibits individual patients' own unprimed T helper cell responses to alloantigens as well as a third-party mixed lymphocyte response, but does not inhibit autologous unprimed T helper cell proliferation to adherent anti-CD3 antibody. We suggest that the mechanism of inhibitory action is allogeneic-dependent. Methods. We used a series of similar experimental designs to test the presence of this antibody in uremic, sensitized patients and have studied its relationship to sensitization as defined by the presence of lymphocytotoxins in four uremic groups: highly sensitized with or without previous graft loss, moderately sensitized with or without graft loss, nonsensitized without previous graft loss, and nonsensitized with graft loss. Results. (1) Sensitization is associated with the presence of a potent antibody that blocks primary mixed lymphocyte response. Primed cells are less susceptible to its antimitogenic action. (2) The blocking antibody activity is present only in sensitized patients who have IgG lymphocytotoxic activity against the same HLA class I antigens. (3) The blocking activity is unequal in the following order: IgG 3 > IgG 1 > IgG 2. (4) Although IgG 1 and 2 fractions contain lymphocytotoxic activity against HLA class I antigens, the IgG 3 fraction does not. Conclusions. The differential effect of IgG antibodies on naive and memory T cells may explain why humoral responses to alloantigens can be maintained in the presence of blocking antibodies.