![]() ![]() ![]() AKI is associated with up to an eight-fold increase risk in mortality 3, 4 and ischaemia is one of the most common causes of AKI accounting for 50% of all cases. ![]() This study demonstrates a role for fructokinase and endogenous fructose as mediators of acute renal disease.Īcute kidney injury (AKI) is a common clinical syndrome that complicates up to −20% of hospital admissions and 30–50% of intensive care unit admissions 1, 2. Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI is significantly ameliorated when exposed to luteolin, a recently discovered fructokinase inhibitor. Wild type but not fructokinase knockout animals demonstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation. Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex characterized by high levels of aldose reductase, sorbitol and endogenous fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fructokinase in the pathogenesis of ischaemic acute kidney injury (iAKI). The polyol pathway is a metabolic route able to convert glucose into fructose. Acute kidney injury is associated with high mortality, especially in intensive care unit patients. ![]()
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