{"id":"ade7276ae9ff","type":"article","url":"https://hartvaat.nl/2016/08/01/apol1-nierrisicovarianten-en-cerebrale-wittestoflaesies/","title":"APOL1-nierrisicovarianten en cerebrale wittestoflaesies","title_en":"APOL1 renal-risk variants associate with reduced cerebral white matter lesion volume and increased gray matter volume.","category":"preventie","category_label":"Preventie","professions":["internist"],"tags":[],"journal":"Kidney international","doi":"10.1016/j.kint.2016.04.027","source_url":"https://doi.org/10.1016/j.kint.2016.04.027","authors":["Barry I Freedman","Crystal A Gadegbeku","R Nick Bryan","Nicholette D Palmer","Pamela J Hicks","Lijun Ma","Michael V Rocco","S Carrie Smith","Jianzhao Xu","Christopher T Whitlow","Benjamin C Wagner","Carl D Langefeld","Amret T Hawfield","Jeffrey T Bates","Alan J Lerner","Dominic S Raj","Mohammad S Sadaghiani","Robert D Toto","Jackson T Wright","Donald W Bowden","Jeff D Williamson","Kaycee M Sink","Joseph A Maldjian","Nicholas M Pajewski","Jasmin Divers"],"significance":5,"published":"2016-08-01","source_date":"2016-08-01","image":"","kennis":[],"congress":"","summary_en":"This study showed that APOL1 renal risk variants are associated with altered cerebral white and gray matter volumes, suggesting that the genetic risk for kidney disease also affects brain structure through shared vascular mechanisms.","created":"2026-07-03T10:26:15Z","updated":"2026-07-03T13:25:35Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Studie naar het verband tussen APOL1-genrisicovarianten, verminderd cerebaal wittestofvolume en vergroot grijzestofvolume. Onderzoekt de neurovasculaire implicaties van genetisch nierdisease risico.","abstract_original":"To assess apolipoprotein L1 gene (APOL1) renal-risk-variant effects on the brain, magnetic resonance imaging (MRI)-based cerebral volumes and cognitive function were assessed in 517 African American-Diabetes Heart Study (AA-DHS) Memory IN Diabetes (MIND) and 2568 hypertensive African American Systolic Blood Pressure Intervention Trial (SPRINT) participants without diabetes. Within these cohorts, 483 and 197 had cerebral MRI, respectively. AA-DHS participants were characterized as follows: 60.9% female, mean age of 58.6 years, diabetes duration 13.1 years, estimated glomerular filtration rate of 88.2 ml/min/1.73 m(2), and a median spot urine albumin to creatinine ratio of 10.0 mg/g. In additive genetic models adjusting for age, sex, ancestry, scanner, intracranial volume, body mass index, hemoglobin A1c, statins, nephropathy, smoking, hypertension, and cardiovascular disease, APOL1 renal-risk-variants were positively associated with gray matter volume (β = 3.4 × 10(-3)) and negatively associated with white matter lesion volume (β = -0.303) (an indicator of cerebral small vessel disease) and cerebrospinal fluid volume (β= -30707) (all significant), but not with white matter volume or cognitive function. Significant associations corresponding to adjusted effect sizes (β/SE) were observed with gray matter volume (0.16) and white matter lesion volume (-0.208), but not with cerebrospinal fluid volume (-0.251). Meta-analysis results with SPRINT Memory and Cognition in Decreased Hypertension (MIND) participants who had cerebral MRI were confirmatory. Thus, APOL1 renal-risk-variants are associated with larger gray matter volume and lower white matter lesion volume suggesting lower intracranial small vessel disease."}