Acute kidney injury (AKI) is frequent after cerebral insults, with an incidence close to 10% in both traumatic brain injury (TBI) and cerebrovascular disease. AKI in this context has substantial impact on mortality and neurological outcome. Numerous factors may play a role in the development of AKI after brain injury: intravascular volume depletion, raised-intra-abdominal pressure, rhabdomyolysis or sepsis in TBI; age, ischemic heart disease or arteriosclerotic disease in stroke. However, brain-kidney crosstalk mechanisms are complex and there remains a strong rationale for a causal relationship between brain and kidney injury. Cerebral lesions might alter renal function through a neuro-endocrine pathway combining sympathetic system, renin-angiotensin-aldosterone and glucocorticoid activation. Altogether these systems impair renal autoregulation ultimately leading to AKI. In addition, cerebral lesions might lead to a systemic inflammatory response making the kidney vulnerable for dysfunction. Indeed, inflammation and immune system activation are core mechanisms for the development of AKI. Last, direct lesions of specific area of the brain might lead to vasomotor changes and AKI. In this work, we reviewed the epidemiology of AKI after brain injury and examine potential mechanisms suggesting a causal relationship between these two entities.