| Methods |
Study design: open‐label, parallel RCT Study time frame: June 2014 to October 2015 Duration of follow‐up: 24 weeks |
| Participants |
Country: Japan Setting: multicentre (4) Inclusion criteria: HD patients with type 2 DM; aged ≥ 20 years and ≤ 80 years; HD duration > 6 months at enrolment; poor glycaemic control defined as a GA level exceeding 20.0% after 8 consecutive weeks of daily administration of conventional therapy (dietary therapy alone, oral antidiabetic agents and/or insulin) Number: treatment group (42); control group (42) Mean age ± SD (years): treatment group (66.9 ± 9.4); control group (66.3 ± 9.4) Sex (M/F): treatment group (27/14); control group (28/13) Exclusion criteria: history of severe heart failure, angina, MI or stroke within the past 6 months; presence of infectious disease, liver dysfunction, thyroid disease, malignant tumours, or treatment with steroids or immunosuppressants; current hospitalisation; treatment with any DPP‐4 inhibitor within the past 6 months |
| Interventions |
Both groups
Before randomisation, patients received fixed doses of conventional antidiabetic drugs (oral hypoglycaemic agents and/or insulin) for 8 weeks, and these drugs were continued during the 24‐week treatment period. If the GA remained ≥20.0% after 12 weeks of treatment in either group, the dose(s) of other antidiabetic drugs could be increased
Treatment group
Oral saxagliptin: 2.5 mg/d Continued their regular medications, such as antihypertensive drugs, ESA, phosphate binders and lipid lowering agents, during the study period
Control group
Continued their regular medications, such as antihypertensive drugs, ESA, phosphate binders and lipid lowering agents, during the study period.
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| Outcomes |
Change in GA Changes in vital signs and laboratory/biochemical tests during the study, and safety. GA and HbA1c levels were measured as indices of glycaemic control Postprandial plasma glucose levels Vital signs: body weight, interdialytic weight gain, BMI, CTR on chest X‐ray, and predialysis SBP and DBP Hb AST, ALT, lactate dehydrogenase, alkaline phosphatase, c‐glutamyl transpeptidase, total cholesterol, HDL, triglyceride, total protein, and albumin concentrations |
| Notes |
Funding source: "Publication of this report was financially supported by a grant from Kyowa Hakko Kirin Co. Ltd. No financial support was received for implementation of this study.) Medical writing support was provided by Dr. Nicholas D. Smith (Edanz Group Ltd.) and Elsevier/ELMCOMTM. Kyowa Hakko Kirin Co. Ltd. was not involved in the study design; in the collection, analysis and interpretation of data; in the writing of the report; or in the decision to submit the article for publication."
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| Risk of bias |
| Bias |
Authors' judgement |
Support for judgement |
| Random sequence generation (selection bias) |
Unclear risk |
Study was described as randomised, method of randomisation was not reported |
| Allocation concealment (selection bias) |
Low risk |
The randomisation of subjects was monitored by an independent investigator with no previous knowledge of the subjects |
| Blinding of participants and personnel (performance bias)
All outcomes |
High risk |
Open‐label study |
| Blinding of outcome assessment (detection bias)
All outcomes |
High risk |
Open‐label study |
| Incomplete outcome data (attrition bias)
All outcomes |
Low risk |
Low dropout rate with 2.3% of each group dropping out |
| Selective reporting (reporting bias) |
Low risk |
All outcomes reported. The prespecified outcomes were available on a clinical trials database |
| Other bias |
Low risk |
"MA has received honoraria from Kyowa Hakko Kirin Co. Ltd. The other authors have no conflict of interest to declare" |
