Nephrology training in Australia and New Zealand: a survey of outcomes and adequacy

Advanced training programmes in nephrology should provide broad exposure to all aspects of nephrology. In Australia and New Zealand (ANZ), the Advanced Training Committee in Nephrology oversees training, and recent increases in trainee numbers have led to concern about dilution of experience.To investigate early career paths of nephrologists in ANZ and determine the adequacy of training by comparing self-determined competency and skill relevance among recently graduated nephrologists.In 2015, the Advanced Training Committee in Nephrology administered an online survey during the annual subscription for members of the Australian and New Zealand Society of Nephrology. Nephrologists who were awarded Fellowship after 2002 were invited to participate.The survey was completed by 113 Fellows with 8 respondents excluded (response rate 44.1%). Initial post-Fellowship work included full-time public hospital appointments (34.3%) or undertaking full-time higher research degrees (41.9%). The majority reported securing their desired employment. Respondents indicated adequate training in most clinical skills; however, responses of 'well trained' in home haemodialysis (41.8%), conservative care (42.9%), automated peritoneal dialysis (38.8%), and assessment of kidney transplant recipients (48%) and living kidney donors (34.7%) were less adequate. Although considered highly relevant to current practice, responses of 'well trained' were low for management and research skills, including complaint management (16.3%), private practice management (2%), health system knowledge (14.3%) and regulations (6.1%), ethics approval (23.5%), research funding (11.2%) and quality assurance (26.5%).Nephrology training in ANZ generally meets clinical needs and most secure their desired employment. Training in management and research are areas for improvement

Evaluation of Fetuses in the Preventive IVIG Therapy for Congenital Heart Block (PITCH) study

The recurrence rate of anti-SSA/Ro associated congenital heart block (CHB) is 17%. Reversal of 3rd degree block has never been achieved. Based on potential reduction of maternal autoantibody titers as well as fetal inflammatory responses, IVIG was evaluated as a preventative therapy for CHB

IL-23, not IL-12, Directs Autoimmunity to the Goodpasture Antigen

The autoantigen in Goodpasture disease is the noncollagenous domain of α3 type IV collagen [α3(IV)NC1]. We previously demonstrated that IL-12p40−/− mice are protected from experimental autoimmune anti–glomerular basement membrane (anti-GBM) glomerulonephritis, seemingly defining a role for IL-12 in this disease; however, the recent identification of IL-23, a heterodimer composed of IL-12p40 and IL-23p19 subunits, raises the possibility that IL-23, rather than IL-12, may modulate this disease instead. We immunized wild-type, IL-12p35−/− (IL-12 deficient, IL-23 intact), IL-12p40−/− (deficient in both IL-12 and IL-23), and IL-23p19−/− (IL-12 intact, IL-23 deficient) mice with recombinant mouse α3(IV)NC1. Wild-type mice developed autoreactivity to α3(IV)NC1: Humoral responses, cellular responses, renal histologic abnormalities, leukocyte accumulation, autoantibody deposition, and IL-17A mRNA expression (a cytokine produced by the IL-23–maintained Th17 subset). IL-23 but not IL-12 was detected in the immune system. Regardless of the presence of IL-12, mice deficient in IL-23 were protected, but mice with IL-23 were not. Both IL-23–deficient strains exhibited lower autoantibody titers, reduced cellular reactivity, diminished cytokine production (IFN-γ [Th1], IL-17A [Th17], TNF, and monocyte chemoattractant protein 1), and less renal disease and glomerular IgG deposition. The deficient responses in the absence of IL-23 were not due to increased regulatory T cells; IL-12p40−/− and IL-23p19−/− mice did not show increased proportions of CD4+CD25+FoxP3+ cells or IL-10 levels early in the immune response. In conclusion, autoreactivity to the Goodpasture antigen is directed primarily by IL-23, absence of which results in hyporeactivity including but extending beyond a deficient Th17 response

T-bet Deficiency Attenuates Renal Injury in Experimental Crescentic Glomerulonephritis

T-bet is a transcription factor that is essential for T helper (Th)1 lineage commitment and optimal IFN-γ production by CD4+ T cells. We examined the role of T-bet in the development of experimental crescentic glomerulonephritis, which is induced by Th1-predominant, delayed-type hypersensitivity-like responses directed against a nephritogenic antigen. Anti-glomerular basement membrane (GBM) glomerulonephritis was induced in T-bet−/− and wild-type C57BL/6 mice. Compared with wild-type controls, renal injury was attenuated in T-bet−/− mice with glomerulonephritis, evidenced by less proteinuria, glomerular crescents, and tubulointerstitial inflammation. Accumulation of glomerular CD4+ T cells and macrophages was decreased, and was associated with reduced intrarenal expression of the potent Th1 chemoattractants CCL5/RANTES and CXCL9/Mig. Supporting the pro-inflammatory nature of T-bet signaling, assessment of systemic immunity confirmed that T-bet−/− mice had a reduction in Th1 immunity. The kinetic profile of T-bet mRNA in wild-type mice supported the hypothesis that T-bet deficiency attenuates renal injury in part by shifting the Th1/Th2 balance away from a Th1 phenotype. Expression of renal and splenic IL-17A, characteristically expressed by the Th17 subset of effector T cells, which have been implicated in the pathogenesis of autoimmune disease, was increased in T-bet−/− mice. We conclude that T-bet directs Th1 responses that induce renal injury in experimental crescentic glomerulonephritis

Consumer involvement in topic and outcome selection in the development of clinical practice guidelines

Background Consumer involvement in guideline development is advocated, but minimal participation, such as a nominated consumer representative on a guideline working group, can inhibit their decision-making power and contribution. Little is known about how to involve consumers more effectively in guideline development. Objective To describe a targeted approach for involving consumers actively in guideline development, by focusing on topic and outcome selection, and to discuss the impact on content and structure of the final guideline. Design Descriptive study. Setting and participants Patients and carers (n=24) from a tertiary hospital in Sydney attended three structured peer-facilitated workshops to complete group-based exercises on topic and outcome selection for guidelines for early stage chronic kidney disease. These workshops were run in parallel with the guideline-writing group. For each exercise, participants formed small groups and facilitated their own discussion, recorded their responses and presented them to the wider group. The topics and outcomes identified were fed back to the guideline writers. Results The participants actively engaged in the workshop discussions and articulated topics and outcomes they perceived should be included in clinical guidelines. Four main changes to guideline-related outputs were observed. A new guideline subtopic was introduced, guidelines were consumer-endorsed, guideline recommendations and suggestions for clinical care were augmented with consumer-focused issues, and plain English guidelines were developed. Conclusions Consumer workshops in parallel and feeding into guideline development can be a feasible and effective approach for active consumer contribution. This process can inform the development of both consumer-focused guidelines for clinicians and specific versions for consumers