Intrarenal oxygen homeostasis in diabetic kidney disease

Kidney disease is a major cause for premature mortality in diabetic patients.

The focus has shifted from a glomerulocentric to a predominantly tubulocentric view of mechanisms initiating the development of diabetic kidney disease (DKD).

We, and others, have previously reported intrarenal hypoxia in diabetic kidneys, caused by increased oxygen consumption, in both experimental models and patients.This five-year research program focuses on the role of a deranged renal oxygen metabolism as a central mechanism for the development of DKD, with special emphasis on mitochondrial function, tubular sodium transport efficiency and renal oxygen delivery.

Interventions will be directed to key components in order to validate the proposed hypothesis.The clinical significance is derived from a novel hypothesis that could provide a mechanistic explanation for DKD.

The results from the proposed research program may also provide insight into the pathogenesis of chronic kidney disease in hypertension, acute kidney injury and ischemia-reperfusion injury.Once diagnosed with chronic kidney disease, these patients are left with current treatments that at best delay disease progression, irrespectively of etiology.

Results from our research can result in earlier identification of patients that require intensive monitoring and early treatment, so as to prevent disease progression.