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Basic science research remains fundamental to progress in clinical care, understanding of disease pathophysiology and underpinning the evolution of personalised medicine. Exposure to research is pivotal to educating students, but a declining profile of basic science research has the potential to erode research capacity further. The capacity for women to engage in research and remain in academia long term is continually challenged by negative gender‐based experiences and institutional barriers. The authors explored themes and authorship of abstracts presented at Australia and New Zealand–‐based nephrology conferences, as a surrogate marker of trends in research activity and gender engagement. Basic science research and female senior authorship declined during the study period, which has serious implications for the future of nephrology. [ABSTRACT FROM AUTHOR]

Background: This study aimed to describe the clinical outcomes of total pancreatectomy with islet autotransplantation (TP‐IAT) in Australia. Methods: Individuals selected for TP‐IAT surgery according to the Minnesota Criteria (Appendix) without evidence of diabetes were evaluated including time to transplantation from pancreatectomy, islet numbers infused and post‐transplantation HbA1c, C‐peptide, total daily insulin and analgesic requirement. Results: Sixteen individuals underwent TP‐IAT from Australia and New Zealand between 2010 and 2020. Two recipients are deceased. The median islet equivalents/kg infused was 4244 (interquartile range (IQR) 2290–7300). The median C‐peptide 1 month post‐TP‐IAT was 384 (IQR 210–579) pmol/L and at median 29.5 (IQR 14.5–46.5) months from transplant was 395 (IQR 139–862) pmol/L. Insulin independence was achieved in eight of 15 (53.3%) surviving recipients. A higher islet equivalents transplanted was most strongly associated with the likelihood of insulin independence (P < 0.05). Of the 15 surviving recipients, 14 demonstrated substantial reduction in analgesic requirement. Conclusion: The TP‐IAT programme in Australia has been a successful new therapy for the management of individuals with chronic pancreatitis including hereditary forms refractory to medical treatment to improve pain management with 50% insulin independence rates. This study describes the Australian experience of total pancreatectomy with islet autotransplantation. Sixteen individuals underwent total pancreatectomy with islet autotransplantation in Australia from 2010 to 2020. [ABSTRACT FROM AUTHOR]

Background Common marmosets are known to develop an IgM glomerulopathy, which has been linked with 'wasting marmoset' syndrome. This study investigated renal pathology in a colony of marmosets, with and without weight loss. Methods Renal histology, immunofluorescence, and electron microscopy were performed on marmosets euthanized for research or for weight loss. Serum and urine biochemistry were measured during life and at euthanasia. Results Histology from 25 adult marmosets (19 research and 6 weight loss) showed mesangial expansion in the majority of glomeruli. Mesangial changes correlated with electron-dense deposits and IgM deposition by immunofluorescence; negligible other pathology was seen. Glomerular basement membrane thickness appeared increased compared to reported human measurements. Low-grade proteinuria was present in all animals, but did not progress. Renal function was normal in all animals. Conclusions Marmosets develop a glomerulopathy characterized by mesangial expansion, IgM deposition, and proteinuria. This is a benign occurrence and not specifically associated with weight loss. [ABSTRACT FROM AUTHOR]

ABSTRACT: Introduction: Plasma cell-rich rejection is a distinct histological phenomenon associated with poor renal allograft outcomes. Aboriginal and Torres Straight Islander (ATSI) transplant recipients have poorer allograft survival and higher rates of acute rejection. We sought to determine whether a higher incidence of plasma cell-rich infiltrates (PCIR) could account for poorer survival. Methods: Renal transplant biopsies performed in recipients from the Northern Territory of Australia between 1985 and 2007 were reviewed and correlated with outcome. Biopsies were designated PCIR positive when plasma cells constituted >10% of the interstitial infiltrate. Results: Four hundred and seventy-seven biopsies from 177 recipients (108 ATSI) were performed. Median graft survival was shorter for recipients with PCIR: 4.0 years (interquartile range 2.18-6.41) versus 5.4 years (2.0-9.99) ( P = 0.013). ATSI recipients had higher rates of plasma cell-rich rejection (RR 1.76, 95% CI 1.43-2.17, P < 0.0001), which occurred earlier (251 vs 869 days, P = 0.03) compared with non-indigenous recipients. On multivariate analysis, PCIR did not independently influence allograft survival. There was a correlation between PCIR and panel reactive antibody peak >20% (RR 1.29, 95% CI 1.03-1.56, P = 0.025), ≥5 human leukocyte antigen mismatches (RR 1.91, 1.41-2.58, p < 0.0001), increasing post-transplant infection rate (>10 infections RR 5.11, 1.69-15.5, P = 0.004), and subsequent death from septicaemia (RR 1.6, 1.17-2.18, P = 0.003). Conclusion: PCIR is associated with infection and markers of chronic immunological stimulation but does not independently contribute to inferior renal allograft outcomes, even in ATSI recipients. [ABSTRACT FROM AUTHOR]

Calcific uremic arteriolopathy (CUA) is a rare event primarily in patients with end-stage kidney disease which is charaterized by small vessel media calcification, panniculitis, dermal necrosis producing exquisitely painful difficult to heal wounds. Mortality rates may be as high as 80%, predominantly due to intervening sepsis. This clinical phenomenon is being increasingly reported and treated with a widening number of agents. Recent case reports highlight the benefit of two modalities that have been employed as adjuvant therapy with significant success in the treatment of CUA. Hyperbaric oxygen (HBO) is capable of enhancing oxygen delivery to the ulcerating lesions that characterize CUA. Chronic hypoxia can be reversed using HBO to facilitate growth factor production, neoangiogenesis, fibroblast proliferation, and collagen synthesis that may facilitate all aspects of wound healing. Sodium thiosulfate appears to chelate and solubilize calcium ions, reducing the calcium vascular load that appears to participate in the obliterative small vessel disease. There is a rapid analgesic effect and slower regression of cutaneous calcific nodules. The authors advocate for aggressive treatment of CUA, using all available therapies. [ABSTRACT FROM AUTHOR]

There is definitive experimental proof that a lattice of dendritic cells (DC) exist within the renal parenchyma. Kidney-resident DC (KDC) are an important constituent of passenger leucocytes that initiate the direct component of allograft rejection in transplantation and form a central element of the innate immune response following injurious stimuli to the kidney. DC are recruited to the kidney in pathophysiological states such as glomerulonephritis and ischaemia–reperfusion injury. However, the exact mechanism for engaging and attracting DC to infectious and transplant antigens, and whether specific DC subsets are involved remains unresolved. In addition, the extent to which resident and infiltrating DC contribute to the propagation of injury or rejection is also unclear. Despite consistently expanding published work regarding DC location, phenotype and function, there are a number of deficiencies in our knowledge base, particularly in relation to KDC. [ABSTRACT FROM AUTHOR]

Introduction: BK virus nephropathy (BKVN) is a significant cause of late renal allograft loss. It is characterized histologically by an interstitial nephritis that can be difficult to distinguish from acute cellular rejection (ACR). We investigated whether immunophenotyping of the infiltrate would aid this distinction. Methods: Ten cases of biopsy-proven BKVN, following renal transplantation, were identified from a single transplant centre. The infection was confirmed by renal biopsy and staining for SV-40 T-antigen. Biopsies from 20 consecutive patients with ACR were identified and used as controls. There was no evidence of BK infection serologically or histologically in these patients. Immunohistochemical staining with anti-CD20, perforin and granzyme B was performed on remaining tissue samples. Results: Clustered B cells were demonstrated in both BKVN and ACR. Hence, the CD20-stained component within the interstitial infiltrate was not useful in distinguishing these biopsies. Perforin-stained slides demonstrated fewer cytotoxic T cells in the biopsies with BK virus (average 2.4 ± 1.4 cells per 100 lymphocytes per field) compared with those samples with acute rejection (8.6 ± 5.7 cells per 100 lymphocytes, P < 0.0001). No significant difference in granzyme B staining was detected between ACR and BKVN. Conclusion: Clustered B cells and granzyme B staining did not differentiate between ACR and BKVN. However, ACR cellular infiltrate was rich in perforin positive cells suggesting that perforin staining may be a useful marker to discriminate between these conditions. [ABSTRACT FROM AUTHOR]

Aims: Kidney transplant units in Australia are confined to large hospitals in major metropolitan areas, yet this may limit access and diminish outcomes in people who do not live in these large centres. The authors examined the viability of a kidney transplant unit located in northern Australia (NA), with particular emphasis on recipient outcomes and the number of donors. Methods: ‘Northern Australia’ was arbitrarily defined as ‘north of the tropic of Capricorn’ for Queensland and Western Australia and included the entire Northern Territory. Data on donors and transplant recipients were provided by ANZDATA and ANZOD registries, identified by postcode. Results: Between 1998 and 2004 in NA there were 163 deceased donor kidneys and 97.5% of available organs were transplanted. There were no Aboriginal/Torres Strait Islander (ATSI) donors from NA. Recipients from NA in this time included 55 patients receiving living grafts and 156 receiving deceased donor grafts, of whom 36% were ATSI, making up half of the total ATSI transplanted in Australia during this time period. Compared with the rest of Australia, NA recipients were older, waited longer on dialysis, had longer ischaemic times and a greater number of human leucocyte antigen mismatches, and were more likely to be diabetic and obese. Despite the longer cold ischaemic time in NA recipients, no difference in immediate graft function was seen. ATSI recipients in NA, when compared with their southern Australian counterparts, had poorer patient survival (HR = 3.19, 95% CI 1.44–7.08, P < 0.001), but equivalent graft survival (HR = 1.67, 95% CI 0.95–2.95, P = not significant) on multivariate analysis. Key factors that would influence feasibility of a Northern Australian transplant unit include adequate staffing, and support services in addition to currently available resources. Conclusion: Current donor numbers in NA are adequate for past recipients of kidney transplant, but may not cover future needs without a significant increase in donor rate. A transplant unit situated in northern Australian would require significant resources to ensure long-term viability and its effect on outcomes is uncertain. [ABSTRACT FROM AUTHOR]

Calcific uremic arteriolopathy (CUA) is a rare but serious life-threatening complication of CRF that manifests as painful nonhealing eschars in association with panniculitis and dermal necrosis. This condition is being increasingly recognized and reported as a contributing factor to death in dialysis patients. The pathognomic lesion is vascular calcification with intimal arterial hypertrophy and superimposed small vessel thrombosis. Hyperparathyroidism and elevated concentrations of serum phosphate remain consistent clinical features of most cases reported. Controversy still exists regarding the role of parathyroidectomy in this condition with some studies suggesting improved outcome with surgical intervention. A number of potential new etiological factors have been identified including reduced serum levels of a calcification inhibitory protein α,2-Heremans–Schmid glycoprotein (Fetuin-A) and abnormalities in smooth muscle cell biology in uremia. Promising new treatment options including hyperbaric oxygen therapy and sodium thiosulfate infusion have been reported in case series. Benefits from biphosphonates and tissue plasminogen activator have also been reported. Overall these new treatment approaches and understanding of potential mechanisms underlying this important severe clinical condition offer new hope in the diagnosis and management of this severely morbid and often fatal condition. [ABSTRACT FROM AUTHOR]