title: Cardiovascular manifestations of autosomal dominant polycystic kidney disease in young adults.
abstract: OBJECTIVE
  Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common hereditary renal disorder. In addition to renal structure and function abnormalities, the cardiovascular changes (extra renal manifestations) are the frequent findings observed in these subjects. This pilot study describes the viscoelastic properties of the aorta, a predisposing factor for the genesis of hypertension and left ventricular hypertrophy in young adults diagnosed with ADPKD.
  
  
  METHODS
  Twenty new patients with ADPKD, all the off springs of previously diagnosed patients with ADPKD were recruited to participate in the study. Each patient underwent the measurement of 24-hour creatinine clearance (Ccr), 24-hour Ambulatory Blood Pressure Monitoring (ABPM), and ultrasonographic determination of the aortic dimensions and left ventricular measurements by M-mode echocardiogram and 12-lead electrocardiogram (ECG) in the echo laboratory.
  
  
  RESULTS
  The mean age of our ADPKD subjects was 29.9 +/- 6.5 yr. Five patients had impaired renal functions (Ccr < 1.48 ml/sec). Fourteen patients had hypertension and nine were considered Non-dippers on ABPM. The median value of LVMI and AOD was 84.9 g/m2 and 28.5 x 10(-3)/kPa respectively. Forty five percent of these subjects had non-dipping circadian pattern with smaller nocturnal BP reduction. No relationship between AOD, LVMI and 24-hr ABPM was observed; however, a positive trend towards Ccr and AOD was evident.
  
  
  CONCLUSIONS
  The majority of our ADPKD subjects have an unfavourable cardiovascular risk profile: hypertension and a non-dipping circadian BP rhythm. Subjects with evidence of renal function impairment had reduced aortic distensibility, placing them at an increased risk for cardiovascular morbidity and mortality.
authors.affiliation: Department of Nephrology, Atlantic Health Sciences Corporation, Saint John, New Brunswick, Canada.
authors.forename: S Paul
authors.initials: SP
authors.lastname: Handa
mesh_terms: D000328:Adult; D001011:Aorta / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D018660:Blood Pressure Monitoring, Ambulatory; D002318:Cardiovascular Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D002940:Circadian Rhythm; D003401:Creatine / Q000097:blood; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D005799:Genes, Dominant; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D007677:Kidney Function Tests; D008297:Male; D007690:Polycystic Kidney Diseases / Q000150:complications / Q000235:genetics / Q000503:physiopathology*; D012307:Risk Factors
chemical_list: D003401:Creatine