Study finds high rates of AKI in patients with diabetes
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A study comparing patients with and those without type 2 diabetes found patients with diabetes had significantly higher rates of AKI than those without the condition.
According to Simona Hapca, PhD, of the University of Dundee in the United Kingdom, and colleagues, this finding remained true for patients whether they also had preexisting chronic kidney disease.
“Type 2 diabetes is one of the leading causes of CKD and [end-stage kidney disease] ESKD worldwide,” the researchers wrote. “A large proportion of patients who develop CKD experience prior episodes of AKI, with evidence suggesting that kidney function does not fully recover after the AKI event. Moreover, CKD is a well-known risk factor for AKI, with recent studies suggesting there is a considerable overlap between the pathophysiology underlying the two conditions.”
Arguing that “the relationship is likely to be complex and remains poorly understood,” Hapca and colleagues retrospectively followed a cohort of 9,417 patients with type 2 diabetes and 7,283 without the condition for a median of 8.2 years. Researchers noted 26.6% of patients with diabetes had CKD at recruitment vs. 9.1% for those without diabetes (serving as controls). In addition, patients with type 2 diabetes were older and had lower eGFR at baseline than controls.
Results showed patients with diabetes were more likely than those without to develop AKI during the follow-up (48.6% vs 17.2%) and were also more likely than controls to develop CKD.
For patients without CKD, researchers determined the AKI rate among those with diabetes was approximately five times greater than those without diabetes (121.5 vs. 24.6 per 1,000 person-years).
For patients who had CKD at recruitment or developed the condition during the follow-up, the AKI rate in those with diabetes was more than double that of controls (384.8 vs. 180 per 1,000 person-years after CKD diagnostic date; 109.3 vs. 47.4 per 1,000 person-years before CKD onset in those developing CKD after recruitment).
Additional findings suggested that while decline in eGFR slope was steeper before AKI in patients with diabetes than in those without diabetes, loss of eGFR became steeper in patients without diabetes after AKI episodes.
Hapca and colleagues elaborated on the results, suggesting there remains uncertainty in the area.
“We found that those who develop AKI with diabetes have a greater decline in eGFR slope before developing AKI than those who do not,” they wrote. “These findings are expected because a declining kidney would be more susceptible to episodes of AKI. However, it is surprising that there is less additional decline in eGFR in those with diabetes, compared with those without, after an episode of AKI compared with before an AKI episode. It remains unclear what the mechanism underlying AKI is in patients with diabetes.”
Therefore, they contended that further work must be done to evaluate the pathogenesis for AKI and the associated risk factors in this patient population.
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