Acute kidney injury significantly worsens glycaemic control in hospitalised patients with type 2 diabetes, with the effect driven primarily by hyperglycaemia rather than hypoglycaemia, Danish researchers have found.
The findings challenge the prevailing clinical focus on hypoglycaemia prevention during AKI and point to the need for proactive hyperglycaemia monitoring in this setting.
The study, published in Diabetic Medicine [link here], included 166 hospitalised patients with T2D whose kidney function was measured daily via plasma creatinine levels, with AKI staged using KDIGO guidelines.
Key findings included:
- AKI was associated with a 7.3% reduction in time-in-range, driven primarily by increased time-above-range
- AKI was linked to a 10-fold increase in in-hospital mortality and ICU admission
- Time-in-range fell by 7.6% for every 100 μmol/L rise in plasma creatinine levels
The impact on glycaemic outcomes was most pronounced at AKI onset, with time-in-range gradually improving for each additional day of AKI, the authors noted.
Lead author Dr Mikkel T Olsen and colleagues said their results aligned with findings from non-ICU cohorts showing AKI predicts dysglycaemia and in-hospital mortality. The use of continuous glucose monitoring (CGM) extended previous work by providing greater temporal resolution than point-of-care testing, and by analysing plasma creatinine as a continuous variable rather than a binary AKI yes/no classification.
Several RCTs have shown tight glycaemic control in outpatients with chronic kidney disease increased hypoglycaemia risk, leading to less stringent targets in that setting. But this study suggested the dominant concern in hospitalised patients with T2D is hyperglycaemia.
Even modest creatinine rises within the range commonly seen during hospitalisation influenced glycaemic status primarily through hyperglycaemia, the authors said, adding that clinical management during AKI should extend beyond hypoglycaemia prevention to include active monitoring and control of hyperglycaemia.