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BackgroundResearch on factors associated with dialysis withdrawal is scarce. This study examined the predictors that might influence rate of dialysis withdrawal. Existing literature is summarized, analyzed and synthesized to identify gaps in the literature with regard to the factors associated with dialysis withdrawal.MethodsThis scoping review used a systematic search to synthesize research findings related to dialysis withdrawal and identified gaps in the literature. The search strategy was developed and applied using PubMed, EMBASE and CINHAL databases. The selection criteria included articles written in English and published between 1997 and 2016 that examined dialysis withdrawal and associated factors in patients with any modality of renal dialysis.. Case reports and studies only including renal transplant patients were excluded. Fifteen articles were selected in accordance with these selection criteria.ResultsThe literature review revealed a scarcity of research on dialysis withdrawal and associated factors. Furthermore, the study findings were inconsistent and inconclusive. Authors have defined dialysis withdrawal in terms of dialysis discontinuation, withholding, death, withdrawal, treatment refusal/cessation, or technique failure. Authors have selected homogeneous patient population on either hemodialysis (HD) or peritoneal dialysis (PD) patients, thus making comparisons of studies and generalization of findings difficult.ConclusionFuture studies should explore the influence of both HD and PD on patient-elected dialysis withdrawal using a large a priori calculated sample size.Electronic supplementary materialThe online version of this article (10.1186/s12882-018-0894-5) contains supplementary material, which is available to authorized users.

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It has been demonstrated that MEK1, one of the two MEK isoforms in Raf-MEK-ERK1/2 pathway, is essential for successful EV71 propagation. However, the distinct function of ERK1 and ERK2 isoforms, the downstream kinases of MEKs, remains unclear in EV71 replication. In this study, specific ERK siRNAs and selective inhibitor U0126 were applied. Silencing specific ERK did not significantly impact on the EV71-caused biphasic activation of the other ERK isoform, suggesting the EV71-induced activations of ERK1 and ERK2 were non-discriminative and independent to one another. Knockdown of either ERK1 or ERK2 markedly impaired progeny EV71 propagation (both by more than 90%), progeny viral RNA amplification (either by about 30% to 40%) and protein synthesis (both by around 70%), indicating both ERK1 and ERK2 were critical and not interchangeable to EV71 propagation. Moreover, suppression of EV71 replication by inhibiting both early and late phases of ERK1/2 activation showed no significant difference from that of only blocking the late phase, supporting the late phase activation was more importantly responsible for EV71 life cycle. Taken together, this study for the first time identified both ERK1 and ERK2 were required for EV71 efficient replication and further verified the important role of MEK1-ERK1/2 in EV71 replication.

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