Impact of Abdominal Aortic Calcification on Central Haemodynamics and Decline of Glomerular Filtration Rate in Patients with Chronic Kidney Disease Stages 3 and 4

• Main Authors: Hanna Jansson, Aso Saeed, Maria K. Svensson, Kristina Finnved, Mikael Hellström, Gregor Guron
• Format: Article
• Language: English
• Published: Karger Publishers 2019-08-01
• Series: Kidney & Blood Pressure Research
• Subjects: Ankle-brachial index; Pulse pressure; Pulse wave velocity; Sclerostin; Vascular calcification
• Online Access: https://www.karger.com/Article/FullText/501687

Background/Aim: Calcifications of large arteries are frequent in chronic kidney disease (CKD) and may contribute to the high cardiovascular risk in this population. The aim of this study was to examine whether abdominal aortic calcification volume (AACV) was a predictor of the rate of decline in glomerular filtration rate (GFR) in a cohort of patients with CKD stages 3 and 4. Methods: Eighty-four patients with CKD stages 3 and 4 were enrolled in this prospective observational study. At study entry, and annually, GFR was measured by plasma 51Cr-EDTA clearance. At baseline, haemodynamics was assessed and AACV was determined by computer tomography. Results: The mean follow-up time was 3.4 years and mean decline in GFR was –2.69 mL/min/1.73 m2 per year. At baseline, abdominal aortic calcification (AAC) was detected in 66 patients (79%). A binary logistic regression analysis revealed that age was the only statistically significant independent predictor of AAC. In patients with AAC, male gender (B = 0.413, p = 0.030), aortic diastolic blood pressure (B = –0.025, p = 0.001) and ankle-brachial index (B = –1.666, p = 0.002) were independently associated with AACV using a multiple linear regression analysis. Neither the presence nor the extent of AAC was significantly associated with the rate of change in GFR during follow-up. Conclusion: In this cohort of patients with CKD stages 3 and 4, only age was an independent predictor of the presence of AAC. AACV was not associated with the rate of decline in GFR.