To evaluate the reliability of Doppler ultrasonography (US) in identifying children with renal artery stenosis (RAS) among those with hypertension, we compared Doppler US results in 22 hypertensive children (mean age 8.9 +/- 4.3 years), with (13 cases) and without RAS at angiography, and in 33 normotensive children (mean age 8.8 +/- 4.7 years). We observed 2 false-negatives and 2 false-positives with Doppler US. Of the 2 false-negative diagnoses, I had RAS on an accessory renal artery located behind a normal upper polar artery and the other was observed in a patient with bilateral multiple stenosis of the very distal segments of renal arteries. The 2 false-positive diagnoses were due to sinuous left renal artery and to technical reasons, respectively. In another patient, Doppler US showed a tight RAS, while arteriography was normal. RAS was subsequently confirmed by a second arteriography. Peak systolic velocity values of Doppler US were significantly higher in patients with proven angiographic RAS (3.44 +/- 0.66 m/s) than in hypertensive patients with normal renal arteries at angiography (0.99 +/- 0.35 m/s, P < 0.0001) and normotensive healthy children (1.04 +/- 0.23 m/s, P < 0.0001). With the use of multiple views, and the experience acquired with practice, false-negatives or false-positives due to the geometry of the renal artery can be avoided. Nevertheless, very distal stenosis can be missed by Doppler US.

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This study was performed to assess myocardial involvement in 18 children with severe hypertension (HT), using two dimensional (2D) guided M mode echocardiography, prior and during therapy. All patients but 2 had renal or renovascular disease. Septal diastolic thickness (SDT) was utilized as a serial marker. Except for one case, all patients had increased SDT initially (1.03 +/- .26 cm/m2, p less than .01 vs normal). Evolution under therapy allowed subdivision of patients: Group I: 12 patients showed left ventricular (LV) hypertrophy regression, within a follow-up period of 20 +/- 9 months (final SDT: .78 +/- .12 cm/m2 vs initial 1.09 +/- .28, p less than .01). Blood pressure (BP) was normalized in 9 patients, and borderline in 3. Therapy consisted on acebutolol (n = 10), captopril (n = 1), and renal artery surgery (n = 1). Group II: LV hypertrophy was unchanged (n = 3) or increased (n = 3), within a follow-up period of 19 +/- 8 months, with persistent severe (n = 3) or mild (n = 3) HT, under acebutolol (n = 5). Treatment was changed to captopril with subsequent normal BP and echocardiogram improvement (n = 3). In the overall population, final SDT was significantly correlated to the final BP (r = .69, p less than .01). In conclusion, echocardiographic follow-up allowed serial non invasive assessment of LV hypertrophy in our severely hypertensive pediatric population. At first echocardiogram, LV hypertrophy was present in all patients but one. Antihypertensive therapy allowed simultaneous decrease of BP and LV hypertrophy in 12 patients, 10 under acebutolol.

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