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Alexandria, Australia

Henson A.,Princess Alexandria Hospital
Renal Society of Australasia Journal | Year: 2014

Acute kidney injury associated with multiple myeloma does not resolve with traditional haemodialysis, often resulting in stage five chronic kidney disease and permanent dialysis, which is an additional burden for patients with an uncertain future. The porous membrane of the high cut-off (HCO) haemodialysis filter is showing promising results in reducing levels of free light chains in serum and hence reverting acute kidney injury. This article focusses on the HCO haemodialysis treatment from a nursing perspective, outlining treatment frequency, anticoagulant and dialysate changes and the instigation of cytotoxic precautions. Experience gained with HCO filters has resulted in a protocol maximising patient safety and ensuring consistency in practice. Source


Johnston C.I.,The University of Notre Dame Australia | Johnston C.I.,A+ Network | O'Leary M.A.,University of Newcastle | Brown S.G.A.,University of Western Australia | And 61 more authors.
PLoS Neglected Tropical Diseases | Year: 2012

Background: Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment. Methodology/Principal Findings: Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5-74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5-15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5-168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4-245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom. Conclusions/Significance: Death adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom. © 2012 Johnston et al. Source


Campbell K.L.,Princess Alexandria Hospital | Campbell K.L.,University of Queensland | Rossi M.,Princess Alexandria Hospital | Rossi M.,University of Queensland
Renal Society of Australasia Journal | Year: 2014

Dietary modification has long been considered a modifiable risk factor for the progression of chronic kidney disease (CKD) and a key management strategy in end-stage kidney disease. This review will focus on the history of the reoccurring focus on dietary components of salt and protein, as well as the impact of consumer behaviour moving towards convenience foods, on intake of phosphate and sugar in the form of fructose. The latest evidence in CKD supports diets low in sodium, discourages strict diets low in protein and presents a strong case to turn the cycle of eating habits back to basics, in a bid to lower processed food intake and improve the health outcomes of our CKD patients. Source


Gingras M.-C.,Baylor College of Medicine | Covington K.R.,Baylor College of Medicine | Chang D.K.,University of Glasgow | Chang D.K.,Royal Infirmary | And 188 more authors.
Cell Reports | Year: 2016

The ampulla of Vater is a complex cellular environment from which adenocarcinomas arise to form a group of histopathologically heterogenous tumors. To evaluate the molecular features of these tumors, 98 ampullary adenocarcinomas were evaluated and compared to 44 distal bile duct and 18 duodenal adenocarcinomas. Genomic analyses revealed mutations in the WNT signaling pathway among half of the patients and in all three adenocarcinomas irrespective of their origin and histological morphology. These tumors were characterized by a high frequency of inactivating mutations of ELF3, a high rate of microsatellite instability, and common focal deletions and amplifications, suggesting common attributes in the molecular pathogenesis are at play in these tumors. The high frequency of WNT pathway activating mutation, coupled with small-molecule inhibitors of β-catenin in clinical trials, suggests future treatment decisions for these patients may be guided by genomic analysis. © 2016 The Authors. Source

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