Renal dysfunction as a complication of acute brain damage

Abstract

The development of internal disease as a result of the brain damage was first described more than one hundred years ago, but the role of acute stroke and traumatic brain injury (TBI) in the progression of renal dysfunction has not been studied enough. Within the first 7 days after onset of subarachnoid hemorrhage or TBI, up to 25 % patients develop acute kidney injury (AKI). Other important manifestations of cerebro-renal disorders include central salt-wasting syndrome and syndrome of inappropriate antidiuretic hormone secretion, that both manifest by hyponatremia, but differ in pathogenesis and clinical tactics. In addition, patients with extensive brain lesions are characterized by excessive sympathetic activation with the release of proinflammatory cytokines, such as tumor necrosis factor α (TNFα), interleukin-6 (IL-6) and interferon γ (IFNγ), which also contributes to the development of AKI. Investigation of the main features of cerebro-renal syndrome will contribute to the early diagnostics, choice of the appropriate management strategy (careful and limited use of nephrotoxic antimicrobial drugs, osmotic diuretics and intravenous contrasting in neuroimaging) and to the improvement of the prognosis.