Kidney-Brain-Axis

Acute kidney injury (AKI) develops in 2-5% of hospitalized patients, in 30-50% of intensive care unit (ICU) patients, and in 20% of patients with acute brain injury. AKI morbidity and mortality mostly occurs due to remote secondary organ complications . These non-traditional AKI complications are largely not correctable by dialysis and thus not predominantly (or not at all) related to uremia. 50% of AKI survivors show neurocognitive impairment including in attention, visuomotor and executive domains at 7 months after AKI resolution. In at least 7% of AKI patients with resolved AKI and without a previous history of cognitive dysfunction or concurrent acute brain injury progressive dementia develops within two years of AKI (hazard ratio: 3.4). Experimental studies in rodents reported acute neuroinflammation in the AKI brain.

We have developed a mouse model that recapitulates acute and chronic neuroinflammation and neurocognitive dysfunction after AKI.

We are currently studying interorgan mediators and mechanisms involved in this kidney-brain crosstalk.