Cerebrorenal interaction and stroke

Beyond the original meaning of chronic kidney disease (CKD) as high-risk state for future dialysis, CKD is now known as an established risk factor for cardiovascular diseases. Stroke is a major player of cardiovascular disease and has deep two-way relationships with CKD. CKD is an evident risk factor for stroke. Meta-analyses of cohort studies and trials indicate that proteinuria/albuminuria increases the risk of stroke by 71-92%, and reduced glomerular filtration rate increases the risk by 43%. In addition, CKD has a strong relationship with subclinical brain damage including white matter changes, microbleeds, cognitive impairment, and carotid atherosclerosis. CKD is prevalent in acute stroke patients; patients with estimated glomerular filtration rate <60 ml/min/1.73 m(2) or proteinuria amounted to 46% of total ischemic stroke patients and 39% of total intracerebral hemorrhage patients in our institute. Acute and chronic management of stroke are influenced by CKD. Therapeutic effects of several antithrombotic and thrombolytic agents, including recently-developed novel oral anticoagulants, are affected by renal function. Moreover, reduced glomerular filtration rate is independently associated with increased 1- and 10-year mortalities in the end. Stroke also has deep relationships with end-stage kidney disease. Stroke occurs much more commonly in dialysis patients than general population or CKD patients without need for dialysis. The triggers of ischemic and hemorrhagic stroke in patients with end-stage kidney disease include special characteristics unique to dialysis, such as drastic hemodynamic change, dialysate and anticoagulants, and vascular calcification. As cohorts of dialysis patients become older, more hypertensive, and more diabetic than before, stroke become more prevalent and more serious events in dialysis clinics. Now, clinicians should have much interest in the association between CKD and cerebrovascular diseases, so-called the cerebro-renal interaction.