Antiplatelet therapy for preventing stroke in patients with chronic kidney disease

Chronic kidney disease (CKD), defined as reduced glomerular filtration rate and/or proteinuria, is a serious worldwide health problem. The incidence and prevalence of CKD are increasing with age, and patients with CKD are a population at very high risk for developing stroke. CKD may increase the risk for incident stroke independent of conventional stroke risk factors. A common pathological process including anemia, homocysteine, nitric oxide, oxidative stress, inflammation, and conditions promoting coagulation may be related to the development of stroke in the course of CKD. CKD can also serve as a marker of brain injury, because the cerebral microvascular system has similar hemodynamic features with the vascular beds of the kidney. CKD has been linked with markers of cerebral small artery disease including white matter lesions, lacunar infarctions, and cerebral microbleeds. CKD has been implicated with neurological deterioration during hospitalization, poor functional outcome, and hemorrhagic transformation in patients with acute stroke. Recurrence of stroke may also be higher in CKD patients compared with those having normal kidney function. However, there have been no specific recommendations for antiplatelet therapy in patients with ischemic stroke plus CKD. As CKD patients have distinct characteristics including high bleeding complications and poor response to antiplatelet agents, selecting and adjusting platelet aggregation inhibitors should be individualized. In addition, it should be noted that aspirin may aggravate renal dysfunction. Phosphodiesterase inhibitors restore endothelial dysfunction and may serve as a target for preventing stroke in CKD patients. Aside from antiplatelet therapy, other treatments including lipid control, blood pressure lowering, and renal transplantation are also important. Further studies are warranted for optimal treatment in stroke prevention in CKD patients.