Structured handoff to improve communication from inpatient to outpatient dialysis units: A quality improvement project.

BACKGROUND: Patients with end-stage kidney disease requiring dialysis encounter high hospital readmission rates. One contributor is poor communication between hospitals and outpatient dialysis facilities. We hypothesized that improved communication may reduce 30-day hospital readmissions for patients on dialysis at an urban, safety net hospital. METHODS: We created a standardized discharge handoff tool that is easy to use and provides concise data for dialysis centers. The handoff tool is a novel, electronic MACRO template (called a "dot-phrase") to be included in discharge documentation. Instructions for the dot-phrase and electronic facsimile (e-faxing) were sent to Internal Medicine residents immediately prior to their rotation on an inpatient Renal service. We then measured the intervention implementation rate and its impact on hospital readmission metrics. RESULTS: We compared 3 months of preintervention and 6 months of postintervention data, identifying 82 and 135 index discharges in each respective study period. Patients were predominantly male (56.2%) and receiving hemodialysis (89.8%); a minority (9.2%) were undomiciled at the time of discharge. Mean age was 60.5 years (SD 14.0). Renal discharges followed by 30-day Renal readmission were not statistically lower in the postintervention group for the index discharge alone (26.8% vs. 20.0%, p = 0.12), but were for overall discharges (51.2% vs. 25.7%, p < 0.0001). The dot-phrase was used in 95.4% of discharge summaries, and 74.7% of discharge summaries were e-faxed within 24 h of discharge. CONCLUSION: There was high uptake of a standardized discharge handoff tool among Internal Medicine residents on a Renal inpatient service. Using a handoff tool and e-faxing may improve communication with outpatient dialysis centers and may reduce readmissions among some patients but is likely insufficient to fully address high readmission rates. Subsequent intervention iterations would benefit from further collaboration with outpatient dialysis units for customization of the handoff tool to meet local communication needs.

Tryptophan metabolites suppress the Wnt pathway and promote adverse limb events in chronic kidney disease.

Chronic kidney disease (CKD) imposes a strong and independent risk for peripheral artery disease (PAD). While solutes retained in CKD patients (uremic solutes) inflict vascular damage, their role in PAD remains elusive. Here, we show that the dietary tryptophan-derived uremic solutes including indoxyl sulfate (IS) and kynurenine (Kyn) at concentrations corresponding to those in CKD patients suppress ß-catenin in several cell types, including microvascular endothelial cells (ECs), inhibiting Wnt activity and proangiogenic Wnt targets in ECs. Mechanistic probing revealed that these uremic solutes downregulated ß-catenin in a manner dependent on serine 33 in its degron motif and through the aryl hydrocarbon receptor (AHR). Hindlimb ischemia in adenine-induced CKD and IS solute-specific mouse models showed diminished ß-catenin and VEGF-A in the capillaries and reduced capillary density, which correlated inversely with blood levels of IS and Kyn and AHR activity in ECs. An AHR inhibitor treatment normalized postischemic angiogenic response in CKD mice to a non-CKD level. In a prospective cohort of PAD patients, plasma levels of tryptophan metabolites and plasma's AHR-inducing activity in ECs significantly increased the risk of future adverse limb events. This work uncovers the tryptophan metabolite/AHR/ß-catenin axis as a mediator of microvascular rarefaction in CKD patients and demonstrates its targetability for PAD in CKD models.