Cerebral microbleeds and renal dysfunction: Degenerative neurobiological shared mechanisms within intracerebral hemorrhage

Abstract

Intracerebral hemorrhage (ICH) is a significant global source of morbidity and mortality, with a frequently grim prognosis. Microvascular dysfunction in the form of small vessel disease appears to cause the vast majority of spontaneous cerebral hemorrhages. Cerebral microbleeds, hemorrhagic markers of small vessel disease, seem prevalent in ICH patients. The cerebral microvasculature resembles the renal microvasculature and therefore, the two may share common, complex degenerative mechanisms of frailty, and renal impairment appears to be an additional burden on ICH cases. There could be a potential neurobiological interplay between cerebral microbleeds and renal dysfunction in the context of ICH, with possible bidirectional influences on a molecular and cellular level. Separately, the two entities appear to influence ICH occurrence, recurrence and prognosis. Our review sheds light on the fact that when cerebral microbleeds and renal impairment are brought together, there is potential for clinically relevant pathophysiological feedback mechanisms.