Abstract

Although α-glucosidase inhibitors (AGIs) are commonly used for controlling postprandial blood glucose, AGIs-induced liver injuries have been reported. However, the relationship between AGIs and liver injuries in advanced chronic kidney disease (CKD) patients remains unexplored. In this nationwide case-control study, we recruited 1765 advanced diabetic CKD patients, who received AGIs therapy from January 1, 2000 to December 31, 2010 as the study sample and 5295 matched controls. Recent and former AGIs users were defined as patients who received the AGIs prescription for 30–60 d and 30–210 d before the event of liver injury. The risk of AGIs-induced liver injury was examined using time-dependent Cox proportional hazards model. Liver injury occurred in 3.9% of patients in the study group and 3.3% of patients in the control group. AGIs use did not increase the risk of liver injury in advanced CKD patients (P = 0.19). The stratified analysis indicated no increased risk of liver injury in all AGIs-using subgroups (all P > 0.05). The available evidence supports extending the use of AGIs without increasing the risk of liver injury in patients with advanced CKD. Additional randomized controlled trials are warranted to confirm our results.

Highlights

  • The liver is the most vital organ for the metabolic disposition of all drugs, and drug-related liver injury is a potential complication of nearly every medication[1]

  • We examined the relationship between the use of Alpha-glucosidase inhibitors (AGIs) and liver injury in advanced chronic kidney disease (CKD) patients in a Taiwanese population-based cohort

  • AGIs are not recommended for patients with creatinine clearance < 25 mL/min/1.73 m2 because studies examining the safety of AGIs use in patients with advanced CKD are limited

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Summary

Results

This study included 1765 diabetic patients with advanced CKD who received AGIs therapy and 5295 diabetic patients with advanced CKD who did not receive AGIs therapy as matched controls. The models revealed an increased risk of liver injury in men, and baseline liver disease patients. The sensitivity analysis, which excluding baseline liver disease proved that AGIs was not associated with increased risk of liver injury (supplement table 2). The mean DDD within 30–210 d (< 0.4, which was equal to 120 mg of acarbose) was associated with a non-significant increased risk of liver injury, as indicated by the turning point. The multivariate stratified analysis revealed no increased risk of liver injury across all examined subgroups, including the presence or absence of liver cirrhosis, viral hepatitis, chronic hepatitis, subsequent ESRD, or each OHAs use, including metformin, DPP4-inhibitors, thiazolidinedione, or sulfonylurea (Fig. 2). A high or low DCSI score based on diabetes-related organ damage was not associated with an increased risk of liver injury after AGIs use

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