Acute Kidney Injury Secondary to Trauma Brain Injury (TBI) and the Role of Angiotensin-1-7

Acute kidney injury (AKI) following traumatic brain injury (TBI) can highly influence the patient's outcomes. The involvement of the renin-angiotensin system (RAS) and Angiotensin II (Ang-II) in inducing renal injury after stroke has been reported in different studies. This study evaluated, TBI's impact on kidney function/structure and the therapeutic potential of Angiotensin-1-7 (Ang-1-7).

Thirty-two male Wistar rats were randomly assigned to four experimental groups including: Vehicle, TBI, Ang-1-7, and TBI+ Ang-1-7. Then blood urea nitrogen (BUN), creatinine (Cr), malondialdehyde (MDA), nitrite, and renal damage, based on the kidney tissue damage score (KTDS), were evaluated.

Traumatic brain injury induced significant renal dysfunction, evidenced by elevation in serum Cr levels in TBI group compared to vehicle group, P<0.05. Notably, this functional impairment occurred without observable histopathological damage in renal tissue sections stained with H&E. Therapeutic administration of Ang-1-7 post-TBI attenuated these effects in TBI+Ang-1-7 group, reducing Cr levels P<0.05. The treatment concurrently decreased oxidative stress, with (MDA) concentrations in TBI+Ang-1-7 group compared to TBI group. However, no significant differences were detected in serum BUN levels across experimental groups.

TBI causes functional but not structural renal impairment, reversible with Ang-1-7 via Mas receptor activation.