Carotid vascular remodelling in patients with autosomal dominant polycystic kidney disease

Abstract

To study carotid vascular wall remodelling in patients with autosomal dominant polycystic kidney disease (ADPKD) using integrated backscatter signal (IBS) analysis. Included in the study were: 60 ADPKD patients with preserved renal function, including 32 patient with hypertension and 28 with normotension; 25 patients with essential hypertension; and 30 healthy volunteers. Carotid intima-media thickness (IMT) was measured by 2-D conventional ultrasonography. Acoustic tissue characterization of the carotid wall was assessed by IBS analysis, and the percentage of regions considered as fibromatosis was calculated in all groups. Carotid IMT in hypertensive ADPKD patients (0.8 +/- 0.05 vs 0.68 +/- 0.02 mm, P < 0.01 and 0.8 +/- 0.05 vs 0.56 +/- 0.04 mm, P < 0.01 respectively) and patients with essential hypertension (0.79 +/- 0.03 vs 0.68 +/- 0.02 mm, P < 0.01 and 0.79 +/- 0.03 vs 0.56 +/- 0.0 4 mm, P < 0.01 respectively) was significantly greater than that of normotensive patients and healthy subjects. Carotid IMT in normotensive ADPKD patients was also significantly greater than that in healthy subjects (0.68 +/- 0.02 vs 0.56 +/- 0.04 mm, P < 0.01). Calibrated IBS (C-IBS) in hypertensive ADPKD patients was significantly greater than that in patients with essential hypertension and normotensive ADPKD patients (-21.2 +/- 1.51 dB vs -23.1 +/- 1.61 dB, P < 0.05; -21.2 +/- 1.51 dB vs -24.5 +/- 1.34 dB, P < 0.01). C-IBS in normotensive ADPKD patients was significantly greater than that in healthy subjects (-24.5 +/- 1.34 dB vs -26.2 +/- 1.69 dB, P < 0.01). The percentage of regions that could be considered as fibromatosis in hypertensive ADPKD patients was significantly greater than that in patients with essential hypertension and normotensive ADPKD patients (30.0% vs 22.4%, P < 0.05; 30.0% vs 17.9%, P < 0.01). The percentage of regions that could be considered as fibromatosis in normotensive ADPKD patients was significantly greater than that in healthy subjects (15.2% vs 10.3%, P < 0.01). Carotid remodelling occurs in the early stage of ADPKD and can be aggravated by hypertension. Fibrosis contributes to the vascular rearrangement.