Device-assisted continuous ambulatory peritoneal dialysis: A single-centre experience.

BACKGROUND: Peritoneal dialysis (PD) patients with impaired hand-eye function require helper assistance. Our centre developed a connection device that assists patients with impaired hand-eye function to perform PD exchange themselves, but the clinical outcomes in these patients have not been investigated. METHODS: We retrospectively reviewed patients who had device-assisted continuous ambulatory peritoneal dialysis (CAPD) during 2007-2016 and compared their clinical outcomes with age- and sex-matched patients receiving helper-assisted CAPD. RESULTS: One hundred seventy-two patients (86 each in the device- and helper-assisted CAPD groups) were followed for 29.9 (19.4-43.3) months. The device- and helper-assisted groups had comparable peritonitis rates (0.489 and 0.504 episode per patient-year, respectively, p = 0.814), with no difference in the distribution of causative organisms and the organism-specific peritonitis rates. The device-assisted group showed similar peritonitis-free survival compared with the helper-assisted group (2.58 (1.85-3.31) vs. 1.78 (0.68-2.88) years, p = 0.363) and time-to-PD discontinuation (6.27 (3.65-8.90) vs. 4.35 (3.48-5.22) years, p = 0.677). The median patient survival was similar between the two groups (3.89 (2.22-5.55) vs. 3.81 (3.27-4.36) years in the device- and helper-assisted groups, respectively, p = 0.505). CONCLUSION: Device-assisted CAPD confers comparable outcomes as helper-assisted CAPD and is a viable option in PD patients with impaired hand-eye function.

Update on diagnosis, pathophysiology, and management of diabetic kidney disease.

Diabetic kidney disease (DKD) is a chronic complication of diabetes mellitus which may eventually lead to end-stage kidney disease (ESKD). Despite improvements in glycaemic control and blood pressure management with renin-angiotensin-aldosterone system (RAAS) blockade, the current therapy cannot completely halt DKD progression to ESKD in some patients. DKD is a heterogeneous disease entity in terms of its clinical manifestations, histopathology and the rate of progression, which makes it difficult to develop effective therapeutics. It was formerly considered that albuminuria preceded kidney function decline in DKD, but recent epidemiological studies revealed that a distinct group of patients presented kidney dysfunction without developing albuminuria. Other comorbidities, such as hypertension, obesity and gout, also affect the clinical course of DKD. The pathophysiology of DKD is complex and multifactorial, involving both metabolic and haemodynamic factors. These induce activation of intracellular signalling pathways, oxidative stress, hypoxia, dysregulated autophagy and epigenetic changes, which result in kidney inflammation and fibrosis. Recently, two groups of antidiabetic drugs, sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists, were demonstrated to provide renoprotection on top of their glucose-lowering effects. Several other therapeutic agents are also being developed and evaluated in clinical trials.