Evaluating the clinical experience of a regional in-center nocturnal hemodialysis program: The patient and staff perspective.

INTRODUCTION: End-stage kidney disease causes significant morbidity, mortality, and reduced quality of life. Despite improvements in conventional hemodialysis, these problems persist. In-center nocturnal hemodialysis (INHD) has been shown to be beneficial in observational studies. This report outlines a 4-year renal network experience of INHD from the patient and frontline staff perspective. METHODS: Staff and patients' experiences of INHD were evaluated through two work streams. Work stream one: 12 patients who chose to stop INHD and 24 patients who chose to continue with INHD completed an anonymous survey. Work stream two: one-to-one interviews with 20 patients receiving INHD and seven staff working INHD shifts were conducted. Clinical incident reporting for conventional hemodialysis and INHD from April 2014 to December 2018 was reviewed. FINDINGS: Work stream one: Five themes were identified; facilities, time, health and well-being, sleep, and transport. A patient "starter pack" was developed and improvements to the dialysis unit were completed. Work stream two: Patient interviews demonstrated starter packs to aid sleep were well received; sleep itself was not a single reason to discontinue INHD. Staff indicated that their greatest concern was staffing levels; although staff-to-patient ratio remains unchanged, total numbers on INHD shifts were fewer, causing concern around less colleague availability for support during an emergency. SAFETY: 363 clinical incidents were reported across all dialysis shifts; for conventional hemodialysis, a larger proportion were due to medical interventions, infection control, and transport; for INHD, most incidents centered around communication with patients and relatives, delays in patient transfer, and issues with medical equipment or facilities. DISCUSSION: Patients continue with INHD due to increased social time and perceived health benefits. Patient starter packs and adjustments to the dialysis unit may enhance sleep. This experience has optimized the design of the NightLife study; a randomized controlled trial evaluated the effect of INHD on quality of life.

Cardiac Remodelling in Patients Undergoing in-Centre Nocturnal Haemodialysis: Results from the MIDNIGHT Study, a Non-Randomized Controlled Trial.

Evidence suggests extended-hours haemodialysis (HD) may improve cardiovascular, medical and quality-of-life outcomes. In-centre nocturnal haemodialysis (INHD) is an established but underutilized method of providing extended-hours treatment. This 6-month, non-randomized controlled trial (ISRCTN16672784) recruited 13 INHD patients and 12 control patients on conventional HD. The effects of treatment on left ventricular (LV) structure, function and myocardial fibrosis were assessed using cardiac magnetic resonance imaging and native T1 mapping. Quality-of-life and clinical measures were also collected. INHD led to significant reductions in LV mass (-14.75 vs. +6.54 g; p = 0.02), global T1 (-30.62 vs. 0.4 ms; p = 0.05) and non-septal native T1 values (-30.93 vs. 8.96 ms; p = 0.02) over time. There were also significant improvements in serum phosphate (-0.39 vs. +0.02 mmol/L; p = 0.03) and reductions in ultrafiltration rates (-2.32 vs. +0.70 mL/h/kg p = 0.05) between INHD and controls. Six-months of INHD was associated with favourable LV remodelling and reduced myocardial fibrosis compared to patients on conventional haemodialysis.

Structural basis of hypoxic pulmonary hypertension: the modifying effect of chronic hypercapnia.

Exposure to chronic hypoxia causes pulmonary hypertension and pulmonary vascular remodelling. In chronic lung disease, chronic hypercapnia frequently coexists with hypoxia and is associated with worsening of pulmonary hypertension. It is generally stated that pulmonary hypertension in these conditions is secondary to hypoxic vascular remodelling and that hypercapnia augments this remodelling thus worsening the hypertension. We review recent evidence which shows that although chronic hypoxia causes thickening of the walls of pulmonary arterioles, these changes do not lead to structural narrowing of the lumen by encroachment. Moreover, hypoxia leads to new vessel formation within the pulmonary vasculature and not loss of vessels as formerly thought. Such neovascularization may provide a beneficial adaptation by increasing the area of the gas exchange membrane. These novel structural findings are supported by recent reports that inhibitors of the RhoA pathway can acutely reduce pulmonary vascular resistance in chronically hypoxic lungs to near normal values, demonstrating that structural changes are not the dominant mechanisms underling hypoxic pulmonary hypertension. Chronic hypercapnia inhibits the development of hypoxic pulmonary hypertension, pulmonary vascular remodelling and hypoxia-induced angiogenesis. This last effect might be maladaptive, as it would prevent the potentially beneficial increase in gas exchange membrane area. These findings suggest that structural narrowing of the vascular lumen of resistance vessels is not the mechanism by which hypoxia and hypercapnia cause pulmonary hypertension in chronic lung disease.