Parvus tardus waveform suggesting renal artery stenosisremember the more proximal stenosis
Donald Richardson1,
Judith Foster2,
Alex M. Davison1 and
Henry C. Irving2
1 Department of Renal Medicine and
2 Department of Clinical Radiology, St James's University Hospital, Leeds, UK
Correspondence and offprint requests to:
D. Richardson, Department of Renal Medicine, St James's University Hospital, Beckett Street, Leeds LS9 7TF, UK.
Keywords: Doppler ultrasound; reno-vascular disease; aortic coarctation; aortic stenosis; renal failure
Introduction
Colour Doppler ultrasound with spectral analysis of waveforms from intra-renal vessels may provide diagnostic information regarding vascular disease in both native and transplant kidneys. The normal spectral waveform from an intra-renal artery has a sharp systolic rise, a gradual reduction in velocity of flow in later systole, and low velocity forward flow throughout diastole (Figure 1
).

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Fig. 1. Normal intra-renal arterial waveform, showing a sharp systolic upstroke peak and forward flow throughout the cardiac cycle.
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In the investigation of intra-renal vessels the `Parvus tardus waveform' has been described, where the presence of a small amplitude waveform with a prolonged systolic rise (slow upstroke) is considered to be indicative of a proximal stenosis such as a renal artery stenosis [1] (Figure 2
).

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Fig. 2. An arterial waveform from an intra-renal interlobar artery. Note the slope of the systolic upstroke, absence of early systolic peak and diminished amplitude of the waveform indicating a typical `parvus tardus' waveform (from patient C).
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We recently encountered three patients where the demonstration of the parvus tardus waveform suggestive of renal artery stenosis was produced by pathology occurring proximal to the renal artery.
Case reports
Patient A
A 21-year-old woman was referred by her general practitioner for investigation of hypertension. Past medical history included pregnancy related hypertension (without proteinuria) 4 years previously for which she was induced at 38 weeks. The hypertension persisted post-partum (160/105 mmHg) and the general practitioner commenced atenolol then captopril. The blood pressure decreased to 120/80 mmHg. Four years later Brevinor (oral contraceptive pill) was changed to depo-provera and the captopril discontinued. The blood pressure increased to 135/95 mmHg at which point the patient was referred for investigation. A mid-systolic murmur was noted. Urinalysis was normal. Biochemically renal function was normal with a urea of 7.1 mmol/l and creatinine 89 µmol/l. ECG was normal. Renal ultrasound was requested along with a chest X-ray. The ultrasound revealed bilateral parvus tardus waveforms in the renal arteries and a damped monophasic waveform from the aorta (Figure 3
). The chest X-ray showed rib notching (Figure 4
). MRI confirmed aortic coarctation distal to the left subclavian artery (Figure 5
). The patient underwent successful graft repair of the coarctation with withdrawal of antihypertensive medication and resolution of the hypertension (110/70 mmHg).

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Fig. 3. Patient A: (a) intra-renal arterial waveform from the right kidney shows a very severe parvus tardus configuration; (b) parvus tardus waveform from left kidney; (c) parvus tardus waveform from supra-renal aorta with damped monophasic waveform indicating a more proximal stenosis.
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Fig. 5. Patient A: (a) spin echo T1 weighted sagittal section showing blood vessels as flow voids with the coarctation seen just distal to the origin of the left subclavian artery; (b) gradient echo T2 weighted MR showing blood flow displayed as high signal with turbulent flow beyond the coarctation giving a lower signal.
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Patient B
A 70-year-old woman with end-stage renal failure on dialysis for 10 years prior to cadaveric renal transplantation. Past medical history of hypertension, hypercholesterolaemia and hypothyroidism and, after transplantation, steroid-induced diabetes mellitus. Patient was known to have an aortic stenosis with a gradient of 46 mmHg assessed by echocardiogram 10 years prior to transplantation. Three years post-transplant the patient developed worsening hypertension (200/120 mmHg) with peripheral oedema and increasing weight. Renal transplant function was sub-optimal but stable with a creatinine of 140 µmol/l. Ultrasound and Doppler of the transplant showed a parvus tardus waveform (Figure 6
). In the absence of significant proteinuria and in a patient with multiple risk factors for atheroma the coexistence of renal transplant artery stenosis and aortic stenosis was considered. A transplant arteriogram showed no stenosis (Figure 6
).

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Fig. 6. Patient B: (a) Parvus tardus waveform from interlobar artery within the transplant kidney; (b) Renal transplant arteriogram showing no evidence of any renal artery stenosis.
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Patient C
A 49-year-old woman with learning difficulties, a past history of hypertension, primary amenorrhoea, and recurrent right-sided sensory disturbance presented with acute renal failure (urea 66 mmol/l and creatinine 513 µmol/l) after commencement of enalapril and a thiazide diuretic for the hypertension. She was a non-smoker, with no history of renal problems. Phenotypically appearances were compatible with Turner's syndrome. An ejection systolic murmur was noted with marked radio-femoral delay and bruits from collateral vessels across the chest wall were audible. Renal ultrasound and Doppler demonstrated the parvus tardus waveform bilaterally. Echocardiogram showed coarctation and bicuspid aortic valve. Magnetic resonance imaging of the coarctation is shown in Figure 7
. Genetic testing confirmed a Turner's mosaic syndrome. Withdrawal of the angiotensin-converting enzyme inhibitor was coincident with a diuresis and a return to normal renal function (urea 6.9 mmol/l, creatinine 103 µmol/l). Management for the coarctation has been conservative with blood pressure controlled at 170/75 mmHg on atenolol, amlodipine and a thiazide diuretic.

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Fig. 7. Patient C: spin echo T1 weighted MR. Oblique sagittal section shows a diaphragm like coarctation distal to the origin of the left subclavian artery.
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Conclusion
Arteriography remains the `gold standard' for the diagnosis of reno-vascular disease but necessitates an arterial puncture with its potential complications, an injection of potentially nephrotoxic contrast, and is expensive. As a non-invasive technique Doppler ultrasound is becoming commonly used and sensitivities of 89% and specificity of 97% for a stenosis greater than 70% have been claimed [1]. Subsequent analysis has suggested that the probability of an individual patient having a significant stenosis depends upon the slope of the systolic upstroke or the prolongation of the acceleration time of the spectral waveform [2]. In addition to recognizing a possible 30% false negative rate it should be noted that a positive scan although correctly demonstrating that a stenosis exists, does not define the location of that stenosis other than as proximal to the artery studied.
Teaching points
The parvus tardus waveform can be produced by a stenosis at any point proximal to the artery studied. A cause more proximal to the renal vessels should be considered when the Doppler examination of the intra-renal arteries suggests bilateral stenoses or a stenosis in a single or transplant kidney. Studies of the aortic waveform are useful in demonstrating a more proximal lesion. However, it should be remembered that both a proximal aortic lesion and a main renal artery stenosis could co-exist.
References
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Stavros AT, Parker SH, Yakes WF et al. Segmental stenosis of the renal artery pattern recognition of tardus and parvus abnormalities with duplex sonography. Radiology 1992; 184: 487492[Abstract]
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Baxter GM, Aitchison F, Sheppard D et al. Colour Doppler ultrasound in renal artery stenosis: intrarenal waveform analysis. Br J Radiol 1996; 69: 810815[Abstract]