Albuminuria as risk factor for initiation and progression of carotid atherosclerosis in non-diabetic persons: the Tromso Study

• Published in: European Heart Journal
• Main Authors: Jørgensen, Lone, Jenssen, Trond, Johnsen, Stein Harald, Mathiesen, Ellisiv B., Heuch, Ivar, Joakimsen, Oddmund, Fosse, Einar, Jacobsen, Bjarne K.
• Format: Text
• Language: English
• Published: Oxford University Press 2007
• Subjects: Vascular medicine; Tromso
• Online Access: http://eurheartj.oxfordjournals.org/cgi/content/short/28/3/363; https://doi.org/10.1093/eurheartj/ehl394

Aims High levels of microalbuminuria have been associated with severe atherosclerosis. In this prospective, population-based study, we examined whether urinary albumin-to-creatinine-ratios (ACR) in the lower range were associated with the initiation and progression of atherosclerosis. Methods and results Carotid ultrasonography and measurements of ACR, fibrinogen, monocytes, white cell count, and well-established cardiovascular risk factors were performed in 4037 non-diabetic subjects, 2203 without, and 1834 with pre-existing plaques at baseline. After 7 years new ultrasound measurements were performed. In subjects without pre-existing plaques, 884 had developed at least one plaque during follow-up. Baseline ACR was significantly related to the area of the novel plaques ( P for linear trend = 0.009 over the baseline ACR quartiles, after multiple adjustments). The relationship with ACR was clearly modified by fibrinogen ( P = 0.001, for the interaction ACR × fibrinogen). Subjects with high levels of both ACR and fibrinogen developed plaques with the largest area. In subjects with pre-existing plaques, ACR was related to plaque-progression ( P for linear trend = 0.026, after multiple adjustments). In these individuals, the interaction between fibrinogen and ACR on plaque-growth appeared only in those with minimal atherosclerosis at baseline. Conclusion ACR is positively related to plaque-initiation and plaque-growth. This relationship is substantially modified by fibrinogen in previously plaque-free subjects.