Nephrology (Carlton, Vic.) · 2009
Carotid vascular remodelling in patients with autosomal dominant polycystic kidney disease.
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Rong Shu, Jin Xiucai, Ye Chaoyang, Chen Jiabin, Mei Changlin
Аннотация
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.
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.