RENAL DOPPLER
ANATOMY
• at the level of the superior border of the second lumbar vertebra.
• 1–2 cm below the superior mesenteric artery origin.
• Right artery-originates from the anterolateral aspect of the aorta.
• immediately turns posteriorly to course beneath the inferior vena
cava.
• Right renal artery is not only deep in the abdomen- flank approach is
better.
• Left renal artery originate from the posterolateral surface of the aorta.
• courses posteriorly the surface of the aorta and over the psoas muscle.
• mistaking the origin of the inferior mesenteric artery (IMA) for that
of the left RA.
• the IMA tends to have a high resistance spectral waveform.
• IMA also originates much lower along the aorta than the left RA
“banana peel” view
• the transducer is oriented longitudinally.
• The aorta is located, and the transducer is moved in an anterior-to-
posterior direction until the RA is identified arising from it.
• coursing towards the transducer.
• The main RA divides at the hilum, either within or outside the kidney,
into anterior and posterior branches.
• further divide into segmental and then interlobar arteries.
• The interlobar arteries further divide into a network of arcuate
arteries.
• run at the corticomedullary junction and give off the cortical
(interlobular) branches.
PROTOCOL
• longitudinal survey of the abdominal aorta from the celiac artery to
the iliac bifurcation.
• Gray-scale evaluation is important to assess for irregular plaque and
ostial lesions.
• The presence of significant atherosclerotic plaque should increase the
suspicion for possible ostial renal artery disease.
• begin at the celiac axis or the superior mesenteric artery, move
slightly caudad along the aorta until the origin of each renal artery is
seen
• locate the origin of the renal arteries on transverse images of the aorta
using an anterior transducer approach.
• The right renal artery is often easier to identify than the left with this
approach.
• The left renal artery may be better seen by positioning the patient in a
right lateral decubitus position and scanning from a left posterolateral
transducer approach.
• Each renal artery should be examined with color flow imaging from its
origin to the hilum of the kidney, including the main hilar branches.
• obtain PSV measurements from the origin, proximal, mid, and distal
segments of each renal artery.
• A small sample volume (1.5-2.0mm), and an angle of insonation of 60
degrees or less are used.
• Waveforms are also obtained from the segmental arteries in the
upper, mid, and lower poles of each kidney.
• determine the PSV, acceleration time or index, and the resistivity
index (RI).
NORMAL FINDINGS
• The normal PSV range in adult renal arteries is 60 to 100cm/sec.
• Normal renal artery waveforms demonstrate a rapid systolic upstroke
with persistent forward flow in diastole.
• a complete renal artery Doppler examination can be performed in as
little as 20minutes.
RENAL ARTERY STENOSIS
• It is the most common potentially reversible and curable cause of secondary
hypertension and renal failure.
• most commonly caused by either fibromuscular dysplasia or
atherosclerosis.
• associated with hypertension, renal insufficiency (ischemic nephropathy)
or both.
• arteritis, dissection and neurofibromatosis.
• Arteritis, dissection and neurofibromatosis.
• atherosclerotic disease- mainly affects the orifice and proximal
portion of the RA.
• FMD- involves mid to distal portion.
DOPPLER CRITERIA FOR RENAL ARTERY
STENOSIS
• PROXIMAL CRITERIA-
• direct signs obtained at the site of the stenosis.
• Four criteria are used to diagnose significant proximal stenosis.
• Velocities higher than 180 cm/s suggest the presence of a stenosis of
more than 60% .
• The second criterion is the comparison of PSV values obtained in the
prerenal abdominal aorta with those measured in the Ras.
• renal/aortic ratio (RAR)
• In normal conditions, RAR is lower than 3.5.
• The third criterion is identification of RAs with no detectable Doppler
signal, a finding than indicates occlusion.
• The fourth criterion is the visualization of color artifacts such as
aliasing at the site of the stenosis.
• the presence of turbulence at Doppler evaluation indicating the
presence of a significant stenosis upstream.
DISTAL CRITERIA
• oss of early systolic peak;
• acceleration index (AI) lower than 3 m/s2
;
• acceleration time (AT) < 0.07 s;
• a difference between the kidneys in RI (>0.05–0.07)
Intrarenal Waveform Assessment
• indirect diagnosis of renal artery stenosis through the detection of
damped Doppler waveforms in segmental or interlobar arteries within
the kidney.
• renal artery stenosis can cause pulsus tardus and parvus (“tardus
parvus”) changes in intrarenal arterial flow signals.
• intrarenal waveform findings are more accurate for high-grade renal
artery stenoses exceeding 70% diameter reduction.
• some patients do not have appreciable waveform damping.
• This is because the shape of intrarenal arterial waveforms is affected by
multiple factors.
• Patient with generalized arterial stiffness and/or high resistance in the
microvasculature from parenchymal renal disease, the damping effects of
a main renal artery stenosis may be obliterated.
• damped intrarenal waveforms can occasionally be seen in the absence of
significant renal artery stenosis in patients with aortic stenosis or aortic
occlusion
• downstream effects of renal artery stenosis can be diagnosed merely
by visual inspection of the shape of the segmental or interlobar
Doppler waveforms.
• the initial systolic peak is absent
• (OR)
• the systolic peak is grossly rounded in patients with severe ipsilateral
stenosis
• flow at the renal hilum- damped and show a slow rise to the peak
systole.
• This phenomenon has been called the “tardus–parvus” effect.
POST TREATMENT
DOPPLER WAVEFORM ABNORMALITIES IN
NONVASCULAR RENAL DISEASE
• Flow resistance within the renal parenchyma may be increased by a
variety of pathologic processes like
• urinary tract obstruction
• acute and chronic parenchymal disorder
• glomerulosclerosis, acute tubular necrosis, and pyelonephritis.
• All of these conditions are associated with increased flow resistance
in the microvasculature of the kidney.
• causes the Doppler waveforms to exhibit increased pulsatility.
• This may be evident on visual inspection of waveforms or through
pulsatility measures such as the RI.
RI & DIABETIC NEPHROPATHY
• Obtained from the Doppler spectrum of intrarenal segmental and
interlobar arteries.
• Normal RRI values in adults are in the range of 0.47–0.70 with a
difference between two kidneys less than 5–8 % .
• diabetic patients with normal renal function and normo-albuminuria
showed RRI values significantly higher compared to non-diabetic
controls without kidney disease.
• identification of morphologic and hemodynamic changes in the
earlier stages of diabetic nephropathy.
• RI significantly correlates with the degree of proteinuria resulting
higher in patients with macroalbuminuria.
• RI>0.7 is an independent predictor of the risk of worsening renal
function
RI & CKD
• RI has shown to be related with glomerulosclerosis, arteriolosclerosis
and tubulointerstitial lesions more than others morphologic
parameters like renal length and cortex area.
• Patients with High-Normal RRI showed good response to steroid
therapy [high normal RRI (0.65 ≤ RI < 0.7)].
• In mild to moderate renal dysfunction, RRI predicts CKD progression
and poor outcome.
• In vasculitis such LES, Wegener Granulomatosis and PAN, RRI shows
significant correlation with creatinine level and presence of
interstitial disease.
• normal RRI value is considered a good prognostic factor.
• Ultrasound may be a useful tool to identify the degree of disease
progression and secondary response to immunological and
antihypertensive therapy.
RI & AKI
• RI monitors renal perfusion in critically ill patients and vasoactive
agents’ impact on renal circulation.
• In acute renal injury AKIN stage 3 or RIFLE class F, RRI usually
exceed 0.7.
• a threshold of 0.75 is reported as optimal in recognizing between
renal and prerenal disease.
• in prerenal ARF, RRI values lower than 0.7 are related to a good
recovery after fluid rehydration.
• RRI >0.7 suggest a developing ischemic ATN and worse prognosis.
Role of RI in evaluating AKI-
Evaluating renal perfusion
Predicting renal response to vasoactive agents.
Recognize between pre-renal and renal disease.
Predicting AKI onset and recovery in septic shock patients.
Predicting renal obstruction.
RI & RENAL ALLOGRAFT
• Chronic allograft nephropathy (CAN) remains the leading cause of poor
graft outcome.
• interstitial fibrosis and tubular atrophy.
• result of several different immunologic and non-immunologic processes..
• The main clinical aspects of CAN include slow but variable loss of
function, often in combination with proteinuria and hypertension.
• Color Doppler ultrasonography and RRI are valid tools in evaluating
vascular and not vascular graft compartments and its evolution in the
follow-up.
• a direct correlation between acute tubular necrosis and RRI, when
biopsy was performed because of graft dysfunction.
• RRI >0.75 at the 3 month by the time of transplantation has been
associated with increased risk of new onset diabetes after
transplantation (NODAT).
Renal vein thrombosis
• bland or tumor thrombus.
• Comprises partial occlusion of the vein versus complete obstruction.
• Clinically RVT presents with hematuria or signs of renal failure such
as rising creatinine or anuria.
• an increase in renal size and change in echogenicity is often observed
due to associated venous congestion.
• Spectral Doppler demonstrates a reversal of diastolic flow in the main
renal artery.
• Changes in echogenicity may include the following:
• (1) hypoechoic cortex with decreased corticomedullary
differentiation,
• (2) hyperechoic cortex with preservation of corticomedullary
differentiation
• (3) mottled heterogeneity accompanied by the loss of normal
intrarenal architecture
• the conclusive diagnosis of renal vein thrombosis depends on the
direct identification of thrombus in the renal vein.
• With acute thrombosis, the renal vein is invariably enlarged, and
Doppler signals are absent.
• A small trickle of flow may be present around the clot, and this may
produce low velocity, continuous Doppler signals.
RENAL ARTERY ANEURYSM
• mean of 4.5 to 5mm at the ostium.
• Most renal artery aneurysms do not exceed 2cm in diameter and are usually
discovered incidentally.
• Most are saccular and noncalcified and tend to occur at the bifurcation of
the main renal artery.
• Renal artery aneurysms are subdivided into two categories: extrarenal and
intrarenal.
EXTRA RENAL
• caused by atherosclerosis and
FMD.
• the main renal artery may
demonstrate a “string of beads”
appearance on power Doppler.
• may show long segmental
narrowing of the proximal, mid
or distal aspects of the main
renal artery.
INTRARENAL
• generally very small and
multiple.
• Seen in pts with PAN.
• Microaneurysms range in size
from 1 to 12mm.
CONCLUSION
• Ultrasound imaging and Color Doppler permit to define
morphological and functional parameters to reach a better prognostic
evaluation among kidney diseases.
• the usefulness of RRI as a prognostic marker has been clearly and
successful highlighted in the follow-up of diabetic and non-diabetic
nephropathies, acute kidney injury and kidney transplantation.
THANK YOU

RENAL DOPPLER ON USG WITH RELEVANT ANATOMY

  • 1.
  • 2.
    ANATOMY • at thelevel of the superior border of the second lumbar vertebra. • 1–2 cm below the superior mesenteric artery origin. • Right artery-originates from the anterolateral aspect of the aorta. • immediately turns posteriorly to course beneath the inferior vena cava. • Right renal artery is not only deep in the abdomen- flank approach is better.
  • 3.
    • Left renalartery originate from the posterolateral surface of the aorta. • courses posteriorly the surface of the aorta and over the psoas muscle. • mistaking the origin of the inferior mesenteric artery (IMA) for that of the left RA. • the IMA tends to have a high resistance spectral waveform. • IMA also originates much lower along the aorta than the left RA
  • 4.
    “banana peel” view •the transducer is oriented longitudinally. • The aorta is located, and the transducer is moved in an anterior-to- posterior direction until the RA is identified arising from it. • coursing towards the transducer.
  • 6.
    • The mainRA divides at the hilum, either within or outside the kidney, into anterior and posterior branches. • further divide into segmental and then interlobar arteries. • The interlobar arteries further divide into a network of arcuate arteries. • run at the corticomedullary junction and give off the cortical (interlobular) branches.
  • 8.
    PROTOCOL • longitudinal surveyof the abdominal aorta from the celiac artery to the iliac bifurcation. • Gray-scale evaluation is important to assess for irregular plaque and ostial lesions. • The presence of significant atherosclerotic plaque should increase the suspicion for possible ostial renal artery disease. • begin at the celiac axis or the superior mesenteric artery, move slightly caudad along the aorta until the origin of each renal artery is seen
  • 9.
    • locate theorigin of the renal arteries on transverse images of the aorta using an anterior transducer approach. • The right renal artery is often easier to identify than the left with this approach. • The left renal artery may be better seen by positioning the patient in a right lateral decubitus position and scanning from a left posterolateral transducer approach. • Each renal artery should be examined with color flow imaging from its origin to the hilum of the kidney, including the main hilar branches.
  • 10.
    • obtain PSVmeasurements from the origin, proximal, mid, and distal segments of each renal artery. • A small sample volume (1.5-2.0mm), and an angle of insonation of 60 degrees or less are used. • Waveforms are also obtained from the segmental arteries in the upper, mid, and lower poles of each kidney. • determine the PSV, acceleration time or index, and the resistivity index (RI).
  • 11.
    NORMAL FINDINGS • Thenormal PSV range in adult renal arteries is 60 to 100cm/sec. • Normal renal artery waveforms demonstrate a rapid systolic upstroke with persistent forward flow in diastole. • a complete renal artery Doppler examination can be performed in as little as 20minutes.
  • 12.
    RENAL ARTERY STENOSIS •It is the most common potentially reversible and curable cause of secondary hypertension and renal failure. • most commonly caused by either fibromuscular dysplasia or atherosclerosis. • associated with hypertension, renal insufficiency (ischemic nephropathy) or both. • arteritis, dissection and neurofibromatosis.
  • 13.
    • Arteritis, dissectionand neurofibromatosis. • atherosclerotic disease- mainly affects the orifice and proximal portion of the RA. • FMD- involves mid to distal portion.
  • 14.
    DOPPLER CRITERIA FORRENAL ARTERY STENOSIS • PROXIMAL CRITERIA- • direct signs obtained at the site of the stenosis. • Four criteria are used to diagnose significant proximal stenosis. • Velocities higher than 180 cm/s suggest the presence of a stenosis of more than 60% .
  • 15.
    • The secondcriterion is the comparison of PSV values obtained in the prerenal abdominal aorta with those measured in the Ras. • renal/aortic ratio (RAR) • In normal conditions, RAR is lower than 3.5. • The third criterion is identification of RAs with no detectable Doppler signal, a finding than indicates occlusion.
  • 18.
    • The fourthcriterion is the visualization of color artifacts such as aliasing at the site of the stenosis. • the presence of turbulence at Doppler evaluation indicating the presence of a significant stenosis upstream.
  • 19.
    DISTAL CRITERIA • ossof early systolic peak; • acceleration index (AI) lower than 3 m/s2 ; • acceleration time (AT) < 0.07 s; • a difference between the kidneys in RI (>0.05–0.07)
  • 20.
    Intrarenal Waveform Assessment •indirect diagnosis of renal artery stenosis through the detection of damped Doppler waveforms in segmental or interlobar arteries within the kidney. • renal artery stenosis can cause pulsus tardus and parvus (“tardus parvus”) changes in intrarenal arterial flow signals. • intrarenal waveform findings are more accurate for high-grade renal artery stenoses exceeding 70% diameter reduction.
  • 21.
    • some patientsdo not have appreciable waveform damping. • This is because the shape of intrarenal arterial waveforms is affected by multiple factors. • Patient with generalized arterial stiffness and/or high resistance in the microvasculature from parenchymal renal disease, the damping effects of a main renal artery stenosis may be obliterated. • damped intrarenal waveforms can occasionally be seen in the absence of significant renal artery stenosis in patients with aortic stenosis or aortic occlusion
  • 22.
    • downstream effectsof renal artery stenosis can be diagnosed merely by visual inspection of the shape of the segmental or interlobar Doppler waveforms. • the initial systolic peak is absent • (OR) • the systolic peak is grossly rounded in patients with severe ipsilateral stenosis
  • 23.
    • flow atthe renal hilum- damped and show a slow rise to the peak systole. • This phenomenon has been called the “tardus–parvus” effect.
  • 25.
  • 27.
    DOPPLER WAVEFORM ABNORMALITIESIN NONVASCULAR RENAL DISEASE • Flow resistance within the renal parenchyma may be increased by a variety of pathologic processes like • urinary tract obstruction • acute and chronic parenchymal disorder • glomerulosclerosis, acute tubular necrosis, and pyelonephritis.
  • 28.
    • All ofthese conditions are associated with increased flow resistance in the microvasculature of the kidney. • causes the Doppler waveforms to exhibit increased pulsatility. • This may be evident on visual inspection of waveforms or through pulsatility measures such as the RI.
  • 29.
    RI & DIABETICNEPHROPATHY • Obtained from the Doppler spectrum of intrarenal segmental and interlobar arteries. • Normal RRI values in adults are in the range of 0.47–0.70 with a difference between two kidneys less than 5–8 % . • diabetic patients with normal renal function and normo-albuminuria showed RRI values significantly higher compared to non-diabetic controls without kidney disease.
  • 30.
    • identification ofmorphologic and hemodynamic changes in the earlier stages of diabetic nephropathy. • RI significantly correlates with the degree of proteinuria resulting higher in patients with macroalbuminuria. • RI>0.7 is an independent predictor of the risk of worsening renal function
  • 31.
    RI & CKD •RI has shown to be related with glomerulosclerosis, arteriolosclerosis and tubulointerstitial lesions more than others morphologic parameters like renal length and cortex area. • Patients with High-Normal RRI showed good response to steroid therapy [high normal RRI (0.65 ≤ RI < 0.7)]. • In mild to moderate renal dysfunction, RRI predicts CKD progression and poor outcome.
  • 32.
    • In vasculitissuch LES, Wegener Granulomatosis and PAN, RRI shows significant correlation with creatinine level and presence of interstitial disease. • normal RRI value is considered a good prognostic factor. • Ultrasound may be a useful tool to identify the degree of disease progression and secondary response to immunological and antihypertensive therapy.
  • 33.
    RI & AKI •RI monitors renal perfusion in critically ill patients and vasoactive agents’ impact on renal circulation. • In acute renal injury AKIN stage 3 or RIFLE class F, RRI usually exceed 0.7. • a threshold of 0.75 is reported as optimal in recognizing between renal and prerenal disease.
  • 34.
    • in prerenalARF, RRI values lower than 0.7 are related to a good recovery after fluid rehydration. • RRI >0.7 suggest a developing ischemic ATN and worse prognosis.
  • 35.
    Role of RIin evaluating AKI- Evaluating renal perfusion Predicting renal response to vasoactive agents. Recognize between pre-renal and renal disease. Predicting AKI onset and recovery in septic shock patients. Predicting renal obstruction.
  • 36.
    RI & RENALALLOGRAFT • Chronic allograft nephropathy (CAN) remains the leading cause of poor graft outcome. • interstitial fibrosis and tubular atrophy. • result of several different immunologic and non-immunologic processes.. • The main clinical aspects of CAN include slow but variable loss of function, often in combination with proteinuria and hypertension.
  • 37.
    • Color Dopplerultrasonography and RRI are valid tools in evaluating vascular and not vascular graft compartments and its evolution in the follow-up. • a direct correlation between acute tubular necrosis and RRI, when biopsy was performed because of graft dysfunction. • RRI >0.75 at the 3 month by the time of transplantation has been associated with increased risk of new onset diabetes after transplantation (NODAT).
  • 38.
    Renal vein thrombosis •bland or tumor thrombus. • Comprises partial occlusion of the vein versus complete obstruction. • Clinically RVT presents with hematuria or signs of renal failure such as rising creatinine or anuria. • an increase in renal size and change in echogenicity is often observed due to associated venous congestion. • Spectral Doppler demonstrates a reversal of diastolic flow in the main renal artery.
  • 39.
    • Changes inechogenicity may include the following: • (1) hypoechoic cortex with decreased corticomedullary differentiation, • (2) hyperechoic cortex with preservation of corticomedullary differentiation • (3) mottled heterogeneity accompanied by the loss of normal intrarenal architecture
  • 40.
    • the conclusivediagnosis of renal vein thrombosis depends on the direct identification of thrombus in the renal vein. • With acute thrombosis, the renal vein is invariably enlarged, and Doppler signals are absent. • A small trickle of flow may be present around the clot, and this may produce low velocity, continuous Doppler signals.
  • 43.
    RENAL ARTERY ANEURYSM •mean of 4.5 to 5mm at the ostium. • Most renal artery aneurysms do not exceed 2cm in diameter and are usually discovered incidentally. • Most are saccular and noncalcified and tend to occur at the bifurcation of the main renal artery. • Renal artery aneurysms are subdivided into two categories: extrarenal and intrarenal.
  • 44.
    EXTRA RENAL • causedby atherosclerosis and FMD. • the main renal artery may demonstrate a “string of beads” appearance on power Doppler. • may show long segmental narrowing of the proximal, mid or distal aspects of the main renal artery. INTRARENAL • generally very small and multiple. • Seen in pts with PAN. • Microaneurysms range in size from 1 to 12mm.
  • 47.
    CONCLUSION • Ultrasound imagingand Color Doppler permit to define morphological and functional parameters to reach a better prognostic evaluation among kidney diseases. • the usefulness of RRI as a prognostic marker has been clearly and successful highlighted in the follow-up of diabetic and non-diabetic nephropathies, acute kidney injury and kidney transplantation.
  • 48.

Editor's Notes

  • #7 Color Doppler scan through the left kidney, obtained in the right lateral decubitus position, allows complete visualization of the left renal artery.
  • #16 Renal artery stenosis. Pulsed Doppler interrogation of the right renal artery, at the site of color aliasing, reveals elevated peak systolic velocities (PSVs; 382.3cm/sec.)
  • #17 B, Pulsed Doppler sampling of the aorta, at the level of the renal arteries, reveals a PSV of 88.6cm/ sec. The renal-aortic ratio is 4.3, consistent with significant renal artery stenosis
  • #24  C, Renal hilar sampling reveals characteristic damping (tardus-parvus) of the segmental artery waveform. Note the absence of the early systolic peak, rounded contour, and prolonged systolic acceleration time. LP, lower pole; RK, right kidney; SEG, segmental arter
  • #42 , Gray-scale image of the right kidney shows a loss of corticomedullary differentiation in the upper renal pole (arrow). B, Color Doppler image reveals an enlarged right renal vein filled with a heterogeneous material (arrows) compatible with a tumor thrombus. Note is made of a patent renal artery parallel to the enlarged renal vein (arrowhead).