pH, Hypoxia and Haemodialysis
pH, Hypoxia and Haemodialysis
End-stage renal disease typically requires haemodialysis to help replace kidney function.
 However, changes in oxygen uptake during haemodialysis have been linked to increased
 all-cause mortality. This complication of haemodialysis is linked to decreasing fluid volume,
 compromising blood flow to tissue and leukostasis within pulmonary tissue. However, an
 alternative cause of reduced oxygen availability (hypoxia) during haemodialysis is acute
 alkalosis. Alkalosis during haemodialysis can cause hypoxia via dysregulated ventilation and
 impaired ability for tissue to extract oxygen. Despite strong rationale for these mechanisms,
 few studies have fully explored causes of hypoxia during haemodialysis. Greater understanding
 may help to mitigate the risk associated with this vital treatment option.

 The study will comprise of end-stage renal disease patients who regularly undergo
 haemodialysis. Three blood samples will be attained before, during and after haemodialysis to
 assess arterial blood gases. In a small subset of patients, white blood cell (WBC) count and
 cardiac output will be assessed via a non-invasive cardiac output monitor during treatment.
 Regression analysis will be performed to help identify predictors of hypoxia during
 haemodialysis. Patient burden is negligible, with blood samples attained from the dialyser as
 part of routine treatment. In the patients who agree for cardiac output assessment, the
 patient will be required to have four small noninvasive sensor pads placed on the chest.
 Patients will be assessed over 3 consecutive treatments during a single week.
Alkalosis may explain multiple complications of HD treatment, most notably hypoxemia. Despite
 a strong rationale for these mechanisms, current consensus suggests ischaemia as the
 predominant catalyst for hypoxia with HD. However, few studies have characterised pH changes
 during HD with many using serum bicarbonate as a proxy of pH status. Nevertheless, these
 studies predominantly indicate acute alkalosis occurrence with HD. Despite these findings,
 few HD units individualise their bicarbonate prescription or assess pH prior to treatment. Of
 554 dialysis facilities worldwide, 49% did not individualise bicarbonate prescriptions.
 Non-individualised bicarbonate prescription risks sub-therapeutic serum bicarbonate levels
 and sub-clinical hypoxemia during HD. Assumption of acidosis and consistent baseline pH prior
 to each HD session may further risk acute alkalosis with HD. Indeed, a normal pH was
 identified in 26 ESRD patients on commencing HD whilst prescribed dialysate bicarbonate of 32
 mmol/L (7.38 ± 0.06) or 26 mmol/L (7.35 ± 0.06). However, pH increased throughout HD with
 acute alkalosis within the 32 mmol/L group (7.48 ± 0.05). These data, suggest individualised
 assessment of pH prior to HD could mitigate alkalosis and subsequent hypoxemia. However,
 small cohorts, limited studies of pH changes over consecutive HD treatments, and few studies
 of links between hypoxemia and pH limit current understanding. This study therefore aims to
 explore pH changes and occurrence of hypoxia with HD.

 Adult patients (18+) will be recruited irrespective of age, gender, or ethnicity. Due to the
 observational nature of the study, no personal benefits will be expressed to the patient.
 Signed consent will be attained from a patient after a minimum of 24hrs has been provided on
 receipt of the participation information sheet. Any questions will be clearly answered prior
 to obtaining consent from the patient. Only patients who have full capacity to give consent
 and full understanding of the purpose and procedures of the study will be recruited.

 There is no foreseen risk to the patient from the study. All blood samples are attained via
 arterial-venous catheter which is inserted prior to treatment as part of the patient's
 routine haemodialysis. In the small subset of patients who have their cardiac output
 assessed, the use of four small non-invasive sensors poses no additional discomfort, risk or
 restriction throughout routine haemodialysis treatment. In a previous project using the
 noninvasive cardiac output monitor (NICOM), no patient expressed any discomfort whilst using
 the device during haemodialysis.

 All patients involved in the project will be anonymised with a study number for data
 collection purposes. No identifiable information will be used during post-hoc analysis.
 Signed consent forms or any other identifiable data will be securely logged within the study
 site file and secured within the renal research office. Only the chief investigator and renal
 research nurses will be aware of patient involvement in the study. Access to identifiable
 data will be strictly limited to the chief investigator.

 There is no conflict of interest from the chief investigator or other members of the research
 team that may influence the study. After completion of the study, data will be compiled and
 drafted for scientific publication with all data securely archived within the study site file
 at the renal research department. Any patient expressing interest in the study findings will
 be provided with the appropriate information verbally or by a written summary of findings.

 All blood samples will consist of ~1.5ml which will be analysed immediately after sampling.
 Samples will subsequently be disposed of immediately after analysis and not be used for any
 subsequent studies.
Inclusion Criteria:

 -  On haemodialysis for at least 3 months.

 -  Haemodialysis 3 times per week.

 -  Age 18 years or older.

 Exclusion Criteria:

 -  Central venous catheter.

 -  Planned kidney transplant during the duration of study.