Part of the book: Technical Problems in Patients on Hemodialysis
Part of the book: Chronic Kidney Disease and Renal Transplantation
Despite widespread use in clinical practice for over 30 years, many questions remain unanswered regarding fluid convection and reinfusion strategies in haemodiafiltration (HDF). Randomised controlled trials have failed to consistently demonstrate improved survival with convective therapies, but a dose-dependent improvement in outcome has been suggested. The ‘minimum’ and ‘ideal’ volumes of convection are undefined. Online generation of ultrapure dialysis fluid has allowed unprecedented convection volumes; however, delivery of fluid directly into the blood circuit requires strict monitoring. The replacement fluid may be reinfused at multiple points in the circuit. Post-dilution HDF is highly efficient in terms of solute clearance but is limited by haemoconcentration. Pre-dilution HDF prolongs filter life but requires significant convection volumes to achieve adequate solute clearance. Mid-dilution HDF utilises a specific dialyser, which is associated with additional cost and escalating transmembrane pressure. Mixed-dilution HDF appears to offer an attractive balance between solute clearance efficiency and haemoconcentration, however these findings need to be confirmed in large studies. The majority of trials comparing fluid reinfusion strategies have enrolled small numbers of patients over brief study periods. It is unclear whether high-quality evidence examining fluid convection and reinfusion will become available and practice may need to rely on observational data.
Part of the book: Advances in Hemodiafiltration
Conventional peritoneal dialysis (PD) solutions are characterized by several undesirable characteristics, including acidic pH (5.2–5.5), high glucose concentrations (13.6–42.5 g/L), hyperosmolarity (360–511 mOsm/kg) and relatively high concentrations of glucose degradation products (GDPs). These characteristics have been shown to result in adverse clinical outcomes, including acute peritoneal membrane toxicity (manifested as inflow pain), chronic peritoneal toxicity (including membrane failure, ultrafiltration failure, peritonitis and encapsulating peritoneal sclerosis) and adverse systemic sequelae (including hyperglycaemia, dyslipidaemia, metabolic syndrome, cardiovascular disease and residual renal function decline). Consequently, there has been a great interest in manufacturing newer solutions with more ‘biocompatible’ features to mitigate these adverse effects. This has led to the development of neutral‐pH, low or ultralow GDP solutions, glucose‐sparing PD solutions (icodextrin and amino acid solutions), solutions using alternative osmotic agents (such as hyperbranched polyglycerol) and low‐sodium PD solutions. The aim of this chapter is to provide an up‐to‐date comprehensive review of all types of PD solutions that are currently available, including their impact on patient‐level outcomes.
Part of the book: Some Special Problems in Peritoneal Dialysis
Indoxyl sulphate (IS) and p-cresyl sulphate (PCS) are products of proteolytic bacterial fermentation by gut microbiota. They accumulate in the sera of patients with chronic kidney disease (CKD) and have been associated with CKD progression and cardiovascular and all-cause mortality. Therapeutic strategies for lowering IS and PCS include increased clearance (enhanced dialysis), gastrointestinal sequestration (oral adsorbents), reduced synthesis (dietary protein restriction, dietary fibre augmentation and pre-, pro- or synbiotics), antioxidants and organic anion transporter modulators. This review will discuss the roles of IS and PCS as therapeutic targets and examine the clinical evidence for different treatment options and their effects on CKD and cardiovascular disease risk. We will include our group’s research with pre-, pro- and synbiotic interventions to mitigate serum uraemic toxin accumulation and modify cardiovascular and renal risk.
Part of the book: Chronic Kidney Disease
Cardiovascular disease (CVD) is highly prevalent in the dialysis population, affecting up to 60% of cohorts. Cardiovascular mortality rates are reported to be ~14 per 100 patient-years, which are 10- to 20-fold greater than those of age- and gender-matched controls. CVD is the primary cause of death in up to 40% of dialysis patients in Australia, New Zealand and the United States. Dialysis patients endure a greater burden of both traditional risk factors for CVD and risk factors related to loss of kidney function that may account for the higher CVD morbidity and mortality. Many cardiology guidelines include chronic kidney disease (CKD) and end-stage kidney disease (ESKD) as coronary heart disease (CHD) risk equivalents. It is therefore important for clinicians to both recognise and optimise the cardiovascular health of patients receiving maintenance dialysis. This chapter will focus on risk factor modification, screening and prevention of CVD in dialysis patients.
Part of the book: Aspects in Dialysis
Chronic kidney disease (CKD) is a major global health burden, with a prevalence of 10–15% and high mortality rates. In particular, CKD portends a disproportionately high risk of cardiovascular disease beyond the traditional cardiovascular risk factors, with pathophysiological factors such as oxidative stress, inflammation and hyperuricaemia considered to exert an additional role in accelerated atherosclerosis. The presence of heightened oxidative stress and systemic inflammation in CKD is associated with increased mortality. The possible underlying mechanisms include gut dysbiosis, dialysis factors, infections, metabolic acidosis and hyperuricaemia. The state of oxidative stress and systemic inflammation are closely linked and perpetuate each other resulting in progression of CKD and cardiovascular disease. Potential interventions to alleviate the oxidative stress and inflammation in CKD include lifestyle modifications including dietary changes and exercise, optimization of dialysis procedure and pharmacotherapeutic agents including antioxidants. They present a potentially highly effective approach to add to the currently available traditional risk-modification strategies. To date, the majority of the published trials have had a small number of participants with a short duration of follow up. Therefore, no robust evidence has been established. Larger trials with meaningful clinical outcomes and longer follow up are required to evaluate such potential therapies.
Part of the book: Novel Prospects in Oxidative and Nitrosative Stress