Baseline urinary albumin-to-creatinine ratio was positively associated with the area of novel carotid plaques (P=0.009) and plaque progression (P=0.026) over 7 years.
Cohort (n=4,037)
Does urinary albumin-to-creatinine-ratio predict the initiation and progression of carotid atherosclerosis in non-diabetic persons?
Urinary albumin-to-creatinine ratio is positively associated with the initiation and progression of carotid atherosclerosis in non-diabetic individuals, an effect that is modified by fibrinogen levels.
p-value: p=0.009 for initiation, 0.026 for progression
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 x 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.
Jørgensen et al. (Wed,) conducted a cohort in carotid atherosclerosis (n=4,037). Urinary albumin-to-creatinine-ratio (ACR) vs. Lower ACR quartiles was evaluated on Area of novel plaques and plaque-progression (p=0.009 for initiation, 0.026 for progression). Baseline urinary albumin-to-creatinine ratio was positively associated with the area of novel carotid plaques (P=0.009) and plaque progression (P=0.026) over 7 years.