Improving the Detection and Management of Kidney Health in Primary Care.

Chronic kidney disease (CKD) is a major cause of morbidity and mortality, contributing to approximately 20 000 deaths in 2021 in Australia. Importantly, progression of CKD can be substantially reduced if it is detected and treated early. Here we present the perspectives of a general practitioner (primary care physician), a nephrologist and a patient advocate on how the diagnosis and management of CKD in primary care could be improved.

Patient awareness and beliefs about the risk factors and comorbidities associated with chronic kidney disease : A mixed-methods study.

Aim: Diabetes, hypertension and smoking may contribute to the development and progression of chronic kidney disease (CKD) and its complications. The aim of this study was to assess patients' awareness and beliefs about these and other risk factors associated with CKD.

Methods: Participants with CKD Stages 1-5 were purposively sampled for participation in a mixed methods study.

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

Background: 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.

Aim: 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.

Knowledge deficit of patients with stage 1-4 CKD: a focus group study.

Background: Patients with early-stage chronic kidney disease (CKD) must make lifestyle modifications and adhere to treatment regimens to prevent their progression to end-stage kidney disease. The aim of this study was to elicit the perspectives of patients with stage 1-4 CKD about their disease, with a specific focus on their information needs in managing and living with CKD and its sequelae.

Methods: Patients with CKD stages 1-4 were purposively sampled from three major hospitals in Sydney, Australia to participate in focus groups.

Chronic kidney disease in the elderly - assessment and management.

Background: A reduction in estimated glomerular filtration rate (eGFR), and/or the presence of proteinuria, are the predominant manifestations of chronic kidney disease (CKD), which is common in the elderly population.

Objective: This article outlines the clinical significance of CKD in the elderly and summarises recently updated recommendations for its assessment, staging and management.

Discussion: Most elderly patients with CKD present asymptomatically.

DEC205-DC targeted DNA vaccines to CX3CR1 and CCL2 are potent and limit macrophage migration.

Monocytes utilise a variety of chemokines to traffic to atherosclerotic plaques. CX3C chemokine ligand 1 (CX3CL1 & Fractalkine) and its receptor CX3CR1 and monocyte chemoattractant protein 1 (CCL2) have been identified as chemokines/receptors that have an important role in the migration and recruitment of monocytes during the pathogenesis of several inflammatory diseases including atherosclerosis. DNA vectors containing single chain variable region fragment (scFv) for DC-targeted receptor DEC205 were cloned with mouse CX3CR1 and CCL2 genes respectively, and vaccinated into C57/BL6 mice weekly for 3 weeks.

The IL-27 receptor has biphasic effects in crescentic glomerulonephritis mediated through Th1 responses.

Despite its initially defined role as a T-helper type 1 cell (Th1)-inducing cytokine, interleukin-27 (IL-27) has complex roles in vivo. The role of IL-27 receptor (IL-27R) was defined in experimental crescentic glomerulonephritis induced by a foreign antigen, sheep globulin, which is planted in glomeruli. This lesion is dependent on a Th1 effector cellular response.

Atorvastatin enhances humoral immune responses but does not alter renal injury in experimental crescentic glomerulonephritis.

Aim: Statins are widely used for their cholesterol-lowering effects and for prevention of cardiovascular disease. Evidence indicates that these drugs also have immunomodulatory and other non-lipid lowering effects, with studies suggesting benefit in some animal models of immune (particularly T helper (Th)1)-mediated inflammatory disease and their corresponding human disease counterparts. We sought to evaluate the immunomodulatory effects and therapeutic potential of atorvastatin in experimental crescentic glomerulonephritis, a Th1-predominant animal model of glomerulonephritis.

Development of anti-glomerular basement membrane disease after remission from perinuclear ANCA-associated glomerulonephritis in a patient with HLA susceptibility.

A 62-year-old woman presented with acute renal failure, hematuria, proteinuria, and increased C-reactive protein level. She was positive for antineutrophil cytoplasmic antibodies (ANCAs) directed against myeloperoxidase (MPO) and negative for anti-glomerular basement membrane antibody. Kidney biopsy confirmed a diagnosis of pauci-immune crescentic glomerulonephritis with no immunoglobulin G staining.

IL-23, not IL-12, directs autoimmunity to the Goodpasture antigen.

The autoantigen in Goodpasture disease is the noncollagenous domain of alpha3 type IV collagen [alpha3(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 alpha3(IV)NC1.

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-gamma 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.

Ischaemia induces paradoxical changes in axonal excitability in end-stage kidney disease.

Peripheral neuropathy is present in 65% of patients with end-stage kidney disease (ESKD). No cause is yet established: nerve excitability studies have shown that axons are chronically depolarized, primarily owing to hyperkalaemia, but in vitro studies have suggested a role for axonal Na+/K+ pump dysfunction. To investigate Na+/K+ pump activity in vivo, lower limb ischaemia was induced in five ESKD patients and six healthy controls by a sphygmomanometer cuff, inflated to 200 mm Hg and maintained for 13 min.

Neuropathy, axonal Na+/K+ pump function and activity-dependent excitability changes in end-stage kidney disease.

Objective: To investigate the mechanisms underlying peripheral neuropathy and to provide insights into axonal Na(+)/K(+) pump function in patients with end-stage kidney disease (ESKD).

Methods: Nerve excitability was assessed in 10 ESKD patients before and after a single session of haemodialysis and in 29 age-matched control subjects. Changes in excitability were recorded at baseline and following maximal voluntary contraction (MVC) of abductor pollicis brevis (APB) for 60s.

Altered motor nerve excitability in end-stage kidney disease.

Although multiple toxins have been implicated in the development of uraemic neuropathy, no causative agent has been identified. In the present study, the excitability properties of lower limb motor nerves in patients with end-stage kidney disease treated with haemodialysis were measured before, during and after a standard 5 h haemodialysis session, in an attempt to explore the pathophysiology of uraemic neuropathy. Compound muscle action potentials were recorded from tibialis anterior and extensor digitorum brevis, following stimulation of the common peroneal nerve in 14 patients.