Carotid vascular remodelling in patients with autosomal dominant polycystic kidney disease.

Aim: To study carotid vascular wall remodelling in patients with autosomal dominant polycystic kidney disease (ADPKD) using integrated backscatter signal (IBS) analysis. Methods: 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. Results: 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). Conclusion: Carotid remodelling occurs in the early stage of ADPKD and can be aggravated by hypertension. Fibrosis contributes to the vascular rearrangement. [ABSTRACT FROM AUTHOR]