Oxidative stress is a key component in the pathogenesis of a broad number of renal disorders, including acute kidney injury, chronic kidney disease, and various types of nephropathies. Moreover, oxidative stress seems to at least partly explain the intricate relationship the kidney has with other pathological entities, for instance with cardiovascular comorbidities. Renal replacement therapies give end-stage renal disease patients a fighting chance; however, even these interventions may carry the risk of enhancing existing oxidative stress. Even if nutritional components are not currently routinely used, many have shown promise in preclinical or even clinical studies and could counter some of the deleterious pathways that oxidative stress sets in place. This narrative review provides an update on how these natural nutrients could be beneficial to renal disease patients, and it also aims to give an incentive to future research in the field.

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.