Mortality After Home Hemodialysis Treatment Failure and Return to In-Center Hemodialysis.

RATIONALE & OBJECTIVE: Patients on home hemodialysis (HHD) may eventually return to in-center hemodialysis (ICHD) for clinical, technical, or psychosocial reasons. We studied the mortality of patients returning to ICHD after HHD, comparing it with the mortality experience among patients receiving HHD and patients receiving ICHD without prior treatment with HHD. STUDY DESIGN: Retrospective cohort study. SETTING & PARTICIPANTS: All patients represented in the Australia and New Zealand Dialysis and Transplant Registry (ANZDATA) who commenced HD during 2005-2015 and were treated for >90 days. EXPOSURE: ICHD and/or HHD, and clinical characteristics at study entry. OUTCOME: Mortality and cause of death. ANALYTICAL APPROACH: A time-varying multivariate Cox proportional hazards analysis with shared frailty was implemented to explore the association between patient treatment states and mortality. Patients were censored at the time of transplantation or change in treatment modality to peritoneal dialysis. RESULTS: A total of 19,306 patients initiated HD and were treated for >90 days. The mean age of patients was 60.8 ± 15.4 (SD) years, 62% were male, and 49% had diabetes. After HHD treatment failure, adjusted mortality was increased compared with continued HHD at 0-30 days (HR, 3.93 [95% CI, 2.09-7.40]; P < 0.001), 30-90 days (HR, 3.34 [95% CI, 1.98-5.62]; P < 0.001), and >90 days (HR, 2.29 [95% CI, 1.84-2.85]; P < 0.001). LIMITATIONS: Covariates recorded at dialysis initiation, residual confounding underlying successful initiation of HHD treatment, and observational data lacking detail on cause of HHD treatment failure. CONCLUSIONS: HHD treatment failure is associated with a significant increase in mortality compared with continued HHD. This risk was present in both the early (first 30 days and 30-90 days) and late (>90 days) periods after HHD treatment failure. Further investigation into the specific causes of treatment failure and death may highlight specific high-risk patients.

Effect of Low-Sodium versus Conventional Sodium Dialysate on Left Ventricular Mass in Home and Self-Care Satellite Facility Hemodialysis Patients: A Randomized Clinical Trial.

BACKGROUND: Fluid overload in patients undergoing hemodialysis contributes to cardiovascular morbidity and mortality. There is a global trend to lower dialysate sodium with the goal of reducing fluid overload. METHODS: To investigate whether lower dialysate sodium during hemodialysis reduces left ventricular mass, we conducted a randomized trial in which patients received either low-sodium dialysate (135 mM) or conventional dialysate (140 mM) for 12 months. We included participants who were aged >18 years old, had a predialysis serum sodium ≥135 mM, and were receiving hemodialysis at home or a self-care satellite facility. Exclusion criteria included hemodialysis frequency >3.5 times per week and use of sodium profiling or hemodiafiltration. The main outcome was left ventricular mass index by cardiac magnetic resonance imaging. RESULTS: The 99 participants had a median age of 51 years old; 67 were men, 31 had diabetes mellitus, and 59 had left ventricular hypertrophy. Over 12 months of follow-up, relative to control, a dialysate sodium concentration of 135 mmol/L did not change the left ventricular mass index, despite significant reductions at 6 and 12 months in interdialytic weight gain, in extracellular fluid volume, and in plasma B-type natriuretic peptide concentration (ratio of intervention to control). The intervention increased intradialytic hypotension (odds ratio [OR], 7.5; 95% confidence interval [95% CI], 1.1 to 49.8 at 6 months and OR, 3.6; 95% CI, 0.5 to 28.8 at 12 months). Five participants in the intervention arm could not complete the trial because of hypotension. We found no effect on health-related quality of life measures, perceived thirst or xerostomia, or dietary sodium intake. CONCLUSIONS: Dialysate sodium of 135 mmol/L did not reduce left ventricular mass relative to control, despite improving fluid status. CLINICAL TRIAL REGISTRY NAME AND REGISTRATION NUMBER: The Australian New Zealand Clinical Trials Registry, ACTRN12611000975998.

Changing ethnic and clinical trends and factors associated with successful home haemodialysis at Auckland District Health Board.

BACKGROUND: The health and diversity of the population in New Zealand (NZ) is changing under the influence of many socio-economic factors. This may have shifted the landscape of home haemodialysis (HHD). AIMS: To examine the demographic and clinical changes, determinants of HHD training and technique outcome and mortality between 2008 and 2015 at Auckland District Health Board, NZ. METHODS: We compared three incident cohorts of HHD patients between 2008 and 2015. Relevant factors, including demographic and clinical characteristics, training failure, technique failure and mortality were recorded. Factors associated with training and technique failure were examined by multivariate logistic regression. RESULTS: Of 152 patients, 133 completed training, 13 (10%) experienced technique failure and 15 (11%) died. Significant changes in ethnicity (increased: Maori 1.7-fold, Asian 1.7-fold and Pasifika 1.4-fold; decreased: NZ European 2.7-fold, P = 0.001), and major comorbidities, ≥2 major comorbidities (1.8-fold increase, P = 0.03), diabetes (2.1-fold increase, P = 0.013) and heart failure (P = 0.04) were seen. HHD as first renal replacement therapy modality increased 15-fold (P = 0.0001) and training time increased by 4.5 weeks (P = 0.004). Death and technique failure were unchanged over time. Shorter training time, employment and lower C-reactive protein were associated with 'Successful HHD'. 'Unsuccessful HHD' patient characteristics differed by ethnicity. CONCLUSIONS: The HHD population has become more representative of the NZ population, but significantly more comorbid over time. Patient training time has increased, but mortality and technique failure remain stable. 'Successful HHD' is predicted by social and clinical factors, and 'unsuccessful HHD' may have different mechanisms in different patient groups.

Uremic cardiomyopathy is characterized by loss of the cardioprotective effects of insulin.

Chronic kidney disease is associated with a unique cardiomyopathy, characterized by a combination of structural and cellular remodeling, and an enhanced susceptibility to ischemia-reperfusion injury. This may represent dysfunction of the reperfusion injury salvage kinase pathway due to insulin resistance. The susceptibility of the uremic heart to ischemia-reperfusion injury and the cardioprotective effects of insulin and rosiglitazone were investigated. Uremia was induced in Sprague-Dawley rats by subtotal nephrectomy. Functional recovery from ischemia was investigated in vitro in control and uremic hearts ± insulin ± rosiglitazone. The response of myocardial oxidative metabolism to insulin was determined by (13)C-NMR spectroscopy. Activation of reperfusion injury salvage kinase pathway intermediates (Akt and GSK3ß) were assessed by SDS-PAGE and immunoprecipitation. Insulin improved postischemic rate pressure product in control but not uremic hearts, [recovered rate pressure product (%), control 59.6 ± 10.7 vs. 88.9 ± 8.5, P < 0.05; uremic 19.3 ± 4.6 vs. 28.5 ± 10.4, P = ns]. Rosiglitazone resensitized uremic hearts to insulin-mediated cardioprotection [recovered rate pressure product (%) 12.7 ± 7.0 vs. 61.8 ± 15.9, P < 0.05]. Myocardial carbohydrate metabolism remained responsive to insulin in uremic hearts. Uremia was associated with increased phosphorylation of Akt (1.00 ± 0.08 vs. 1.31 ± 0.11, P < 0.05) in normoxia, but no change in postischemic phosphorylation of Akt or GSK3ß. Akt2 isoform expression was decreased postischemia in uremic hearts (P < 0.05). Uremia is associated with enhanced susceptibility to ischemia-reperfusion injury and a loss of insulin-mediated cardioprotection, which can be restored by administration of rosiglitazone. Altered Akt2 expression in uremic hearts post-ischemia-reperfusion and impaired activation of the reperfusion injury salvage kinase pathway may underlie these findings.

Recently published papers: take your predictions with a drop of saline... and breathe deeply before turning on your phone.

Early recognition of sick patients with a poor prognosis, and the rapid institution of appropriate therapy are tenets of good medical management across all specialties. Here we highlight five recent papers that aid us in achieving such goals in and around the intensive care unit (ICU). Both score-generating clinical tools and clinical acumen are championed for identifying the sick, while appropriate, early intervention in acute deterioration is shown to be beneficial, before and after ICU admission. Saline or albumen for resuscitation? The answer became clearer in May, as did what to do about all those mobile phones...