Longterm effects of severe infections and sepsis.

Mitochondrial dysfunction plays a central role in the pathophysiology of AKI during sepsis, which is in turn associated with increased in-hospital and long-term mortality, as well as an increased risk of CKD among survivors. In this project, we will analyze whether the induction of damage to renal mitochondria during sepsis is associated with a declining renal function, cardiovascular events, co-morbidity, quality of life, functional status and mortality after sepsis.



Although great interindividual variability in ropivacaine concentration was found, both total and unbound maximum serum concentrations remained below the assumed systemic toxic thresholds in all samples.

Survivors of sepsis are at high risk for the development of chronic kidney disease (CKD), cardiovascular events and mortality. Mitochondrial dysfunction, which mainly results from increased generation of free radicals, plays a key role in the pathogenesis of organ failure during sepsis. While adults are at high risk for acute kidney injury (AKI), elderly are in addition at major risk for acute delirium. Although aging-related damage to mitochondrial DNA (mtDNA) is associated with the development of CKD and (fatal) cardiovascular events, it is not known whether sepsis induces similar changes in mitochondria, which may in turn lead to increased morbidity and mortality after sepsis.

Inclusion, day 4, 3 months, 1 year, 2 years

n/a; observational study