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Introduction:Obesity at the initiation of dialysis was reported to adversely affect the clinical outcome of peritoneal dialysis (PD) patients, and weight gain is common after started on PD. However, there are few studies on the prognostic implications of weight gain after PD. Methods:We reviewed the change in body weight of 954 consecutive patients during the first 2 years of PD in a single Hong Kong center. Their subsequent clinical outcomes, including patient and technique survival rates, hospitalization, and peritonitis rates, were analyzed. Results:The mean age was 60.3 ± 12.2 years; 535 patients (56.1%) were men, and 504 (52.8%) had diabetes. From 1995–1999 to 2015–2019, the percentage of body weight gain during the first 2 years of PD was 1.0 ± 7.9%, 1.6 ± 7.1%, 1.6 ± 7.2%, 3.9 ± 9.5%, and 4.0 ± 10.3% for each 5-year period, respectively (pfor linearity <0.0001). The subsequent 5-year patient survival rates were 29.9%, 43.3%, 40.5%, 43.6%, and 43.3% for patients with weight loss >5%, weight loss 2–5%, weight change with ±2%, weight gain 2–5%, and weight gain >5% during the first 2 years on PD, respectively (log-rank test, p= 0.035). With multivariable Cox regression model to adjust for clinical confounders, weight loss >5% during the first 2 years of PD was associated with a worse patient survival rate subsequently (adjusted hazard ratio 4.118, 95% confidence interval 1.040–16.313, p= 0.044), while weight gain was not associated with subsequent patient survival. Weight change during the first 2 years of PD does not appear to affect subsequent technique survival, hospitalization, decline in residual renal function, or peritonitis rate. Discussion and Conclusions:Weight gain is common during the first 2 years of PD, but weight gain does not appear to have any significant impact on the subsequent outcome. In contrast, weight loss >5% was significantly associated with worse patient survival subsequently.

ABSTRACTWe investigate a new variation of a token reconfiguration problem on graphs using the cyclic shift operation. A coloured or labelled token is placed on each vertex of a given graph, and a ‘move’ consists in choosing a cycle in the graph and shifting tokens by one position along its edges. Given a target arrangement of tokens on the graph, our goal is to find a shortest sequence of moves that will re-arrange the tokens as in the target arrangement. The novelty of our model is that tokens are allowed to shift along any cycle in the graph, as opposed to a given subset of its cycles. We first discuss the problem on special graph classes: we give efficient algorithms for optimally solving the 2-Coloured Token Shifting Problem on complete graphs and block graphs, as well as the Labelled Token Shifting Problem on complete graphs and variants of barbell graphs. We then show that, in the 2-Coloured Token Shifting Problem, the shortest sequence of moves is NP-hard to approximate within a factor of , even for grid graphs. The latter result settles an open problem posed by Sai et al.

The complex links between obesity, chronic kidney disease (CKD) and cardiovascular disease (CVD) are not completely understood. The objective of this review is to describe and discuss the anatomy, physiology, and biochemistry of the adipose tissue, as well as its involvement in the pathophysiology of CVD and CKD. We searched for original articles in PubMed. The search terms used were “obesity”, “CKD”, and “CVD”. In addition, we also identified publications from our personal databases of literature about obesity, CKD and CVD to identify any important studies that might have been missing from the PubMed search. We further searched the reference lists of identified articles for further relevant papers. Epidemiological studies show that obesity is associated with obesity-related glomerulopathy (ORG) as well as an increase in the risk of CKD in the general population. A number of pathophysiological mechanisms, including renal hemodynamic changes, neurohumoral pathways that activate the sympathetic and renin-angiotensin-aldosterone systems, proinflammatory and profibrotic effects of various adipokines, and insulin resistance may explain the excessive risk of CKD development and progression in obese patients. In patients with mild to moderate CKD, obesity per secontributes a modest increase in cardiovascular risk, while the effect of obesity on the cardiovascular risk of patients with advanced CKD is probably due to the concurrent metabolic syndrome and coexisting cardiovascular risk factors, but the effect of obesity on the cardiovascular risk of patients with advanced CKD is probably the result of the concomitant metabolic syndrome and coexisting cardiovascular risk factors. There are recent data suggesting that subcutaneous and visceral adipose tissue have different and probably opposite effects on the CVD risk in CKD. Further studies are necessary to distinguish the specific clinical implication of different adipose tissue compartments, and to determine the principal mediators that connect obesity, CKD and CVD.

Drug-eluting balloon percutaneous transluminal angioplasty significantly prolonged 6-month and 1-year lesion primary patency and 6-month circuit primary patency in patients with hemodialysis access stenosis when compared those in patients who underwent conventional balloon percutaneous transluminal angioplasty.