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Background: The current literature recognises that left ventricular hypertrophy makes a key contribution to the high rate of premature cardiovascular mortality in dialysis patients. Determining how we might intervene to ameliorate left ventricular hypertrophy in dialysis populations has become a research priority. Reducing sodium exposure through lower dialysate sodium may be a promising intervention in this regard. However there is clinical equipoise around this intervention because the benefit has not yet been demonstrated in a robust prospective clinical trial, and several observational studies have suggested sodium lowering interventions may be deleterious in some dialysis patients. Methods/design: The Sodium Lowering in Dialysate (SoLID) study is funded by the Health Research Council of New Zealand. It is a multi-centre, prospective, randomised, single-blind (outcomes assessor), controlled parallel assignment 3-year clinical trial. The SoLID study is designed to study what impact low dialysate sodium has upon cardiovascular risk in dialysis patients. The study intends to enrol 118 home hemodialysis patients from 6 sites in New Zealand over 24 months and follow up each participant over 12 months. Key exclusion criteria are: patients who dialyse more frequently than 3.5 times per week, pre-dialysis serum sodium of <135 mM, and maintenance hemodiafiltration. In addition, some medical conditions, treatments or participation in other dialysis trials, which contraindicate the SoLID study intervention or confound its effects, will be exclusion criteria. The intervention and control groups will be dialysed using dialysate sodium 135 mM and 140 mM respectively, for 12 months. The primary outcome measure is left ventricular mass index, as measured by cardiac magnetic resonance imaging, after 12 months of intervention. Eleven or more secondary outcomes will be studied in an attempt to better understand the physiologic and clinical mechanisms by which lower dialysate sodium alters the primary end point. Discussion: The SoLID study is designed to clarify the effect of low dialysate sodium upon the cardiovascular outcomes of dialysis patients. The study results will provide much needed information about the efficacy of a cost effective, economically sustainable solution to a condition which is curtailing the lives of so many dialysis patients. Trial registration: Australian and New Zealand Clinical Trials Registry number: ACTRN12611000975998 [ABSTRACT FROM AUTHOR]

Henoch–Schönlein purpura (HSP) is a systemic small-vessel leucocytoclastic vasculitis with deposition of immune complexes containing Immunoglobulin A (IgA). IgA Nephropathy (IgAN) is a glomerulonephritis caused by mesangial deposition of IgA. The onset of HSP, but not IgAN, has been linked to influenza vaccination.We report the first case of HSP with glomerular involvement, in a renal transplant recipient following influenza vaccination. The patient had prior end-stage renal failure (ESRF) secondary to IgAN, without clinical evidence of IgAN recurrence after transplantation. This is of clinical relevance as influenza vaccination is regarded safe, effective, and recommended after renal transplantation.Nephrologists should be aware of the potential for influenza vaccination to have adverse effects in renal transplant recipients, especially if the primary renal disease is HSP or IgAN. [ABSTRACT FROM PUBLISHER]

Presents letters to the editor relating to nephrology. Serum magnesium and parathyroid hormone levels in dialysis patients; Rarity of home hemodialysis; Rate of allograft failure with increase level of blood pressure.

The present investigation aims to examine the role of α-synuclein seed amplification assays for screening Parkinson's disease. Parkinson's disease (PD) is a debilitating neurodegenerative disorder caused by the loss of dopaminergic neurons in the midbrain, leading to symptoms such as tremors, bradykinesia, postural instability, dementia, and depression. It is classified as an α-synucleinopathy related to the role of α-synuclein aggregates in neuron degeneration. Diagnosis relies on clinical assessment without premortem diagnostic tests or imaging, often resulting in delayed detection and impaired symptom management. In this regard, our study explores a screening technique using an amplification assay to measure α-synuclein levels in cerebrospinal fluid, which could potentially identify early pathological changes and improve diagnostic accuracy and patient outcomes. While preliminary results are promising, further studies are needed to evaluate this approach's accuracy and clinical feasibility. A review of numerous trials demonstrates that α-synuclein seeding amplification assays (SAA) are a highly reliable, sensitive, and specific diagnostic tool for PD. This assay offers a promising opportunity to improve early diagnosis and quantify severity, especially for asymptomatic individuals or those with a family history of PD, allowing for earlier intervention and more effective disease management. In summary, the emerging body of evidence supporting α-synuclein as a biomarker should allow patients with PD to be detected and treated sooner, enhancing patients' quality of life and potentially changing the disease trajectory.

Duchenne muscular dystrophy (DMD) is one of the most prevalent X-linked inherited neuromuscular disorders, with an estimated incidence between 1 in 3500 and 5000 live male births. The median life expectancy at birth is around 30 years due to a rapid and severe disease progression. Currently, there is no cure for DMD, and the standard of care is mainly palliative therapy and glucocorticoids to mitigate symptoms and improve quality of life. Recent advances in phosphorodiamidate morpholino antisense oligonucleotide (PMO) technology has proven optimistic in providing a disease-modifying therapy rather than a palliative treatment option through correcting the primary genetic defect of DMD by exon skipping. However, as a result of the high variance in mutations of the dystrophin gene causing DMD, it has been challenging to tailor an effective therapy in most patients. Viltolarsen is effective in 8% of patients and accurately skips exon 53, reestablishing the reading frame and producing a functional form of dystrophin and milder disease phenotype. Results of recently concluded preclinical and clinical trials show significantly increased dystrophin protein expression, no severe adverse effects, and stabilization of motor function. In summary, viltolarsen has provided hope for those working toward giving patients a safe and viable treatment option for managing DMD. This review summarizes an overview of the presentation, pathophysiology, genetics, and current treatment guidelines of DMD, pharmacological profile of viltolarsen, and a summary of the safety and efficacy with additional insights using recent clinical trial data., (© 2024. The Author(s), under exclusive licence to Springer Healthcare Ltd., part of Springer Nature.)

Background: CT pulmonary angiography (CTPA), D-dimer testing, and pre-test probability scoring have greatly improved the ability to manage patients with suspected pulmonary embolism. International guidelines suggest combining these investigations for the best yield. We have been investigating the use of CTPA in patients with suspected pulmonary embolism (PE) admitted to the Department of General Medicine at Christchurch Hospital, New Zealand., Methods: A retrospective audit of 100 patients with suspected pulmonary embolism who had a CTPA performed between October 2003 and April 2004., Results: CTPA was positive for PE in 31% of admissions. The pre-test probability was documented in only 4% of admissions. All patients with PE had a significantly elevated D-dimer (> 499 ng/mL). Wells score calculated by the investigators showed 59 (59%) to have a low, 33 (33%) a moderate, and 8 (8%) a high risk for PE. Of these, PE was diagnosed in 9 (15%), 15 (45%), and 7 (88%) respectively; 93% of patients had a blood gas performed, yet only 77% had the D-dimer measured. No patient with a measured and negative D-dimer had a diagnosis of a PE; 32 CTPAs were performed on 32 patients out of hours., Conclusion: There was a very low uptake of the formal use of pre-test probability scores by medical registrars. This audit confirms that, in patients with low or moderate risk of PE and a negative D-dimer, an alternative diagnosis should be considered. The management of suspected venous thromboembolism (VTE) could be improved; it is likely that after hours CTPA could be reduced.