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Gray scale Ultrasound, color Doppler Ultrasound and Contrast- enhanced Ultrasound in Renal Parenchymal Diseases 1 1 2 3 4 5
Transcript of €¦ · Web viewUltrasound (US), which may be combination of gray scale and spectral Doppler US,...
Gray scale Ultrasound, color Doppler Ultrasound and Contrast-enhanced Ultrasound in Renal Parenchymal Diseases
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Abstract
Ultrasound (US), which may be combination of gray scale and spectral Doppler US,
color and power Doppler US, with or without microbubble contrast agents, is usually the first
imaging modality to be employed in renal parenchymal diseases. The most typical
appearance of diffuse renal parenchymal diseases on grayscale US is an increased renal
cortical echogenicity and increased or reduced corticomedullary differentiation. Spectral
Doppler analysis of intrarenal flows may reveal an increase in intrarenal resistive index value
>0.70 in native kidneys, and >0.8 in renal transplants. Gray scale US and spectral Doppler
US do not exhibit high specificity and sensitivity since different renal parenchymal diseases
often display the same US appearance, whereas the same renal parenchymal disease may
present different appearances on US according to disease stage. Consequently, correlation
of the US pattern with patient’s history and clinical background is essential for a correct
characterization.
Key words: Kidney – disease – Ultrasound – Doppler – contrast - microbubbles
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Learning objectives:
Discuss the fundamental US appearance of renal parenchymal diseases
Explain current concepts of gray scale US, Doppler US, and contrast-
enhanced US in the evaluation of renal parenchymal diseases
Identify the current most important indications for gray-scale US of the kidney
and the added value of this technique
Optimize and interpretate color and spectral Doppler information to identify
diffuse renal parenchymal diseases
Define the specific features of each renal parenchymal disease in terms of
gray-scale US, spectral Doppler and color Doppler
Define the role of contrast-enhanced US in renal parenchymal diseases
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US techniques and normal renal anatomy
Gray scale ultrasound (US), with addition of harmonic and compound speckle-
reduction modes and colour Doppler (CD) USmodes, is the first imaging modality for the
study of kidney diseases and for the guidance of interventional procedures including renal
parenchymal biopsy [1, 2]. Convex-array US transducers (broadband frequency probes of 1–
8 MHz in adults, and 3–10 MHz in pediatric patients) are usually employed in the US
scanning of the kidneys.
At gray scale US, the renal cortex – containing renal glomeruli and proximal and distal
tubules - presents a lower echogenicity than the liver, spleen and renal sinus [2], while renal
inner medulla (renal pyramids) - containing vasa rectae, medullary capillary plexus, loops of
Henle, and collecting ducts - may be differentiated from renal cortex in most of adult patients
being hypoechoic in comparison to the renal cortex [2] although the relative hypoechoic
appearance of inner medulla depends on the echogenicity of renal cortext which can be
altered by the fluid status of the patient . Spleen echogenicity is used as a standard
reference to evaluate the echogenicity of the renal cortex in the presence of fatty liver [2].
Furthermore, kidneys may be isoechoic to the liver even when no clinical or laboratory
evidence of renal disease is documented.
Since numerous renal parenchymal diseases may reveal similar appearance on gray
scale US [1, 3], whereas a single renal parenchymal disease may present variable
appearances on gray-scale US according to the stage, the correlation of the US pattern with
patient’s clinical history and background is essential for a correct characterization.
US presents a general sensitivity of 62–77 %, a specificity of 58-73% and a positive
predictive value of 92 % for detecting microscopically confirmed renal parenchymal diseases
[3 – 5]. In early clinical stages of renal parenchymal diseases, kidneys may appear normal
on US, whereas as parenchymal diseases progress hyperechoic renal parenchyma may
reesult also with increased or reduced corticomedullary differentiation. There is a correlation
between cortical echogenicity and focal leukocytic infiltration, severity of global sclerosis,
focal tubular atrophy, and number of hyaline casts per glomerulus [6]. However, lack of
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overlying fat such as in pediatric patients or abundant fat such as in obese patients, may
make corticomedullary differentiation less evident.
Decreased corticomedullary differentitation is observed when inflammatory infiltrates
(glomerulonephritis and acute tubulointerstitial nephritis) and fibrous tissue
(glomerulosclerosis, tubulointerstitial fibrosis) extend to renal medulla or when hyaline casts
are present within collecting ducts. Reversed corticomedullary differentiation is observed in
several specific diseases including medullary nephrocalcinosis [7] due to
hyperparathyroidism, medullary sponge kidney, renal tubular acidosis (type 1), sarcoidosis,
Tamm–Horsfall proteinuria, recessive polycystic disease, and haemoglobinuria.
Renal sinus fat appears hyperechoic if compared with renal parenchyma, in the
presence of hilar adipose tissue with fibrous septae, blood vessels and lymphatics. It may
appear inhomogeneous at US due to septal thickness, fibrosis, atrophy, and loss of adipose
tissue with a progressive lower renal sinus–renal parenchymal differentiation. With increasing
age, amount of renal parenchyma decreases and renal sinus fat increases [1, 2]. Renal
sinus fat may be increased also in renal sinus lipomatosis which can be seen in obesity and
parenchymal atrophy as well as in normal variants [1, 2].
Assessment of renal size is important in the diagnosis, treatment and determination of
prognosis in diffuse renal diseases even though renal volume correlates better with total
body area and renal function [8, 9]. especially if the volume is obtained by using 3D
ultrasound system instead of being length-based [10]. The length of both kidneys is
considered normal between 10 and 12 cm with a kidney length <10 cm unusual in people
younger than age 60 years [2]. Reduced kidney dimensions are typically found in chronic
kidney disease, while increased renal dimensions may result from infiltrative diseases (e.g.,
multiple myeloma, amyloidosis, lymphoma), acute glomerulonephritis or tubulointerstitial
nephritis due to edema and inflammation, and renal vein thrombosis due to obstruction of
blood flow and subsequent edema. Normally, renal margins are smooth, except in some
normal anatomical variants such as functional parenchymal defects and renal fetal
lobulations. Mean normal value of renal cortical thickness, measured from the base of the
medullary pyramid to the edge of the kidney, ranges from 7mm to 10 mm (being thicker at 5
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the renal poles), while renal parenchyma thickness including renal medulla ranges from
15mm to 20 mm [2].
Renal parenchymal arterial and venous vessels have to be evaluated by flow
optimization for slow flows with low pulse repetition frequency, low wall filter, and by
appropriate gain setting with the lowest possible level of noise [1, 2]. Increased sensitivity of
color and power Doppler and ultrasensitive Doppler techniques (also called micro-Doppler
imaging), based on ultrafast plane wave imaging, in which Doppler signals corresponding to
all pixels are acquired at the same time continuously and simultaneously across the full
image, and advanced clutter suppression algorithms [11] provided by the latest digital US
equipments allows depiction and spectral Doppler interrogation of the renal parenchymal
vessels up to the interlobular arteries [11] (Figure 1). Assessment of renal vascular
resistances is obtained by spectral Doppler trace analysis and measurement of angle-
corrected (<60°) peak systolic and diastolic velocities with calculation of the intrarenal
resistive indices (RIs): (peak systolic velocity minus the end-diastolic velocity) divided by the
peak systolic velocity).
The mean reference value for normal renal RI in adults is 0.60 ± 0.10, with 0.70 as
the upper limit of normal [2, 7, 12]. The RIs measured on segmental, interlobar and arcuate
renal parenchymal arteries are normally below 0.70, and decrease progressively from
segmental to interlobular vessels [2, 7, 12]. Intrarenal RIs do not reliably distinguish the
different types of renal medical disorders [12]. While it has been shown that intrarenal RIs
are related not only to intrarenal vascular resistance but also to vascular compliance,
intersitial and venous pressure, heart rate, aortic stiffness, and pulse pressure [13 – 15].
However, RIs maintain an important diagnostic role and may increase in several many
causes of acute renal diseases, including acute urinary tract obstruction, acute tubular
necrosis, acute rejection, hepatorenal syndrome, and sepsis due to increases in down-
stream resistance, while RIs remain normal in prerenal azotemia and glomerular diseases.
Contrast-ehanced US (CEUS) with microbubble – based contrast agents is the
method of choice for identification of parenchymal perfusion defects, such as renal infarction,
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cortical necrosis, and ischemia, with a sensitivity of over 90% [11, 16] but it is not frequently
used for diffuse renal disease.
Shear – wave US elastography (transient eleastography, acoustic radiation force
impulse - ARFI -, or Supersonic shearwave imaging) generates an US force that propagates
a shear wave through tissue to assess quantitatively the elastic properties of tissues. Shear –
wave US elastography ARFI quantifies shearwave velocities which are related to renal tissue
stiffness in kPa while normal renal cortical stiffness ranges from 2.15 to 2.54 m/s (13.9–19.3
kPak) and increases in chronic kidney disease or chronic renal allograft nephropathy due to
renal interstitial fibrosis [2, 11, 17 – 19] even though poor correlation was found [20].
Unfortunately, ARFI is not standardized for kidneys and ARFI would be difficult to be
employed in kidneys with thin renal cortex due to difficult ROI placement. Moreover, chronic
kidney diseases are often present in obese patients and US elastrography doesn’t provide
reliable results after 6cm depth.
The appearance of renal parenchymal diseases on gray scale and Doppler US, with
some reference to CEUS and US elastography, will be described. Bibliographic search was
conducted on PubMed, Scopus, and Web of Science medical databases by using the terms
“kidney”, “disease”, “ultrasound”, “Doppler”, and “contrast agents” as search criteria. Each
cited study had IRB or IACUC approval. All ultrasound US images are original and not
previoulsly published, and no permission to reprint was necessary.
Renal Infections
In acute renal infections bacteria may reach the kidney principally through the
ascending route, while the haematogenous route represents a less common alternative
pathway of infection. Acute renal infections correspond to active interstitial nephritis
characterized by the presence of polymorphonuclear leukocytes within the lumen of the
tubules. The most prevalent agents include E. Coli, Proteus Mirabilis, Klebsiella
Pneumoniae, Staphilococcus Aureus, Pseudomonas Aeruginosa [21]. Renal involvment may
also be observed in Even disseminated fungal infection, infective endocarditis, tuberculosis,
and filariasis may affect the kidney. Predisponing Predisposing factors include vesicoureteral 7
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reflux, pre-existing urinary tract diseases, diabetes mellitus, stones, immunodeficiency,
neurogenic bladder, and surgical complications. The diagnosis of acute pyelonephritis is
based on clinical symptoms and laboratory findings. Classic symptoms include an abrupt
onset of chills, fever, and unilateral or bilateral flank pain. Histologically, there is extensive
focal destruction by inflammation, with relative preservation of vessels and glomeruli.
Infiltrates mainly contain neutrophils , which are which even fill filling tubules and collecting
ducts. Papillary necrosis may be present.
US is frequently used as a first-line imaging tool to evaluate the urinary tract in
patients with symptoms of pyelonephritis. Unfortunately, gray-scale US presents a sensitivity
of only 20% in patients with pyelonephritis [21, 22] which can rise up to 70 - 90% with the
use of power Doppler [23, 24] and to 80% with the additional application of tissue harmonic
imaging and microbubble contrast agents [25]. At US and tissue harmonic imaging kidneys
appear enlarged with increased parenchymal thickness, loss of renal sinus fat due to diffuse
parenchymal edema, and changes in renal parenchymal echogenicity due to edema
(hypoechoic) or hemorrhage (hyperechoic). The corticomedullary differentiation can also be
reduced [21, 22]. Color and power Doppler and CEUS may reveal focal absence of renal
parenchyma vascularity due to reactive vasoconstriction (Figure 2). Haematogenous
abscesses are usually found in immunodepressed patients, in diabetic patients or in patients
with i.v. drug abuse or with infection foci. At gray-scale US, the typical abscess appears as a
wall thickenedthick-walled hypoechoic mass with through transmission, hypervascular wall
and internal debris that lacks internal flow on color Doppler US [21 – 24]. The role of CEUS
is limited in noncomplicated acute pyelonephritis due to the poor contrast ratio between the
infected and noninfected parenchyma, but the detection of abscesses and even
microabscesses can be easily achieved [11].
Chronic recurrent pyelonephritis corresponds to a chronic interstitial nephritis with
long-standing, recurrent infection and ongoing renal destruction and not to the residuum of
inactive disease (reflux nephropathy). Chronic pyelonephritis is more frequent in diabetics,
with an incidence of 20–40% compared to 2–6% in the normal population according to
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autopsy series [21]. The imaging findings are characterized by renal scarring, atrophy and
cortical thinning, hypertrophy of residual normal tissue (which may mimic a mass lesion),
calyceal clubbing secondary to retraction of the papilla from overlying scar, thickening and
dilatation of the caliceal system, and overall renal asymmetry.
Primary diffuse renal parenchymal diseases
Primary diffuse renal parenchyma diseases (Figure 2) may be due to glomerual
diseases [26] (Table 1) or tubulointerstitial diseases [27] (Table 2) even though primary
glomerular diseases are often associated with prominent tubulointerstitial changes.
Acute glomerulonephritis may manifest as acute nephritic syndrome (hematuria,
proteinuria <3.5 g/dayie, red cell casts and decreased glomerular filtration rate [GFR])
(Figure 23) or as nephrotic syndrome (proteinuria ≥3 grams per day, low serum albumin
level and edema) or as.
Glomerulonephritis is often caused by antibody-induced inflammation through in situ
immune complex formation due to anti-glomerular basement membrane (GBM)
autoantibodies, deposition of circulating immune complexes, and antineutrophil
cytoplasmatic autoantibodies (ANCA). Histologically, the main feature is cellular proliferation
of mesangial or endothelial cells, leukocyte infiltration and GBM thickening due to
subendothelial (e.g. membranoproliferative glomerulonephritis) or subepithelial immune
complex deposition (e.g. postinfectious glomerulonephritis or membranous
glomerulonephritis) or also immune complex deposition within GBM itself often with
components of complement or within the mesangium (e.g. systemic lupus erythematosus or
IgA nephropathy), and hyalinosis and sclerosis of the glomerulus. Those immune complexes
activate complement and recruit inflammatory cells resulting in inflammatory injury. Rapidly
progressive glomerulonephritis is a variant of the acute nephritic syndrome associated with a
rapid loss of renal function and with capillary thrombosis and necrosis and/or capillary
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hypercellularity, mesangial hypercellularity, and subendothelial immune complex deposits
characterized by extensive crescents (usually >50%).
Nephrotic syndrome is also a rare manifestation of malignancy associated with
paraneoplastic syndrome. It has been reported in various malignancies including malignant
lymphoma, colon cancer, lung cancer and prostate cancer. Membranous glomerulonephritis
represents the main cause of paraneoplastic nephrotic syndrome.
In glomerulonephritis with a prevalent mesangial matrix and GBM involvement -
minimal-change glomerulonephritis, IgA nephropathy, focal glomerulosclerosis, and
membranous glomerulonephritis - cortical echogenicity is usually normal or slightly increased
since glomerular component accounts only for 8% of renal parenchyma [6]. Increased
echogenicity is more common in crescentic (Figure 4, Figure 5) and membranoproliferative
glomerulonephritis (Figure 3), in diabetic glomerulosclerosis and tubulointerstitial renal
diseases (Figure 46, Figure 57) which present glomerular, interstitial, and vascular
involvement [6]. The renal parenchymal vascularity is reduced on color and power Doppler
US while intrarenal RI values are significantly correlated to the amount of arteriolosclerosis,
glomerular sclerosis, edema, and interstitial fibrosis. Frequently Doppler US reveals elevated
RIs (>0.70) in kidneys with active disease involving the tubulointerstitial (Figure 46) or
vascular compartment, whereas kidneys with glomerular diseases present more often normal
RI values [1] except in crescentic and membranoproliferative glomerulonephritis where RI
values are frequently increased. Doppler US is useful in the follow-up of renal parenchymal
diseases to predict noninvasively the improvement or worsening of renal function according
to progressive decrease or increase (>0.70 – 0.75) of RI values.
Renal allograft
The most common complications in renal allografts include renal vein thrombosis,
arterial occlusion, acute tubular necrosis (ATN), interstitial fibrosis and tubular atrophy
(previously called chronic allograft nephropathy), and acute or chronic allograft rejection.
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Acute renal allograft rejection (1 - 3 weeks after transplantation) consists of intimal
arteritis (subendothelial infiltration by mononuclear cells) and tubulitis (renal intersitium
infiltration by > 4 mononuclear cells / tubular cross-section). Histological specimen of the
transplanted kidney is required to differentiate acute rejection from ATN since gray-scale US
and Doppler US may reveal only aspecific non specific findings like increase in renal length,
increased cortical echogenicity, reduction in corticomedullary differentiation, and increase in
intrarenal RIs [28] (Figure 86). However, the evidence of lack of flow during diastole on
Doppler US was found described as typical for ATN [29] and even for renal vein thrombosis.
Micro-Doppler techniquesColor Doppler may depict a reduced parenchymal perfusion in
acute renal transplant rejection [30]. Microbubble contrast agent arrival time after i.v.
injection is increased in acute allograft rejection [31] while CEUS can identify improved
parenchymal perfusion due to change in immunosuppressive therapy [32].
The features suggestive of chronic allograft rejection consist in of GBM duplication
and interstitial fibrosis and tubular atrophy, vascular changes, and glomerulosclerosis.
Doppler US reveals an increase in the intrarenal RI values (>0.8) while real-time
elastography can suggest the presence of progressive renal graft scarring [8, 11, 20, 33, 34,
35]. CEUS can monitor microvascular changes expressed by reduced parenchymal
perfusion in the early diagnosis of chronic allograft nephropathy [32, 36] and may detect
transplant renal artery stenosis with higher diagnostic accuracy than Doppler US [37]. Similar
findings are described in renal transplant interstitial fibrosis and tubular atrophy also with
evidence of increased renal tissue stiffness on US elastography [11].
Acute kidney injury
Acute kidney injury (AKI) represents an abrupt (within 48 hours) decrease in kidney
function and is defined as any of the following: increase in serum creatinine by ≥ 0.3mg/dl (≥
26.5 s defined as any of the following: increase in serum creatinine to ≥ 1.5 - 2 times
baseline; or urine volume < 0.5 ml/kg/h for 6 hours (oliguria) according to Kidney Disease
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Improving Global Outcomes (KDIGO) [38, 39, 40, 41]. Kidney failure is a stage of AKI and it
is defined as a GFR < 15ml/min per 1.73 m2 [40]. AKI is classified as prerenal if caused by
reduced blood flow to kidneys, intrarenal if due to conditions that injure the glomerular
capillaries (e.g. acute glomerulonephritis), vessels (e.g. vasculitides), renal tubular epithelium
(e.g. ischemic or toxic ATN due to carbon tetrachloride, mercury, lead, ethylene glycol,
tetracyclines, or cis-platinum), or renal interstitium (acute tubulointerstitial nephritis) - and
postrenal if caused by urinary tract obstruction. The two leading causes of AKI that occur in
the hospitals are prerenal and intrarenal due to ischemic or toxic ATN.
Acute tubular necrosis (ATN). It can be due to ischemia or nephrotoxicity. Despite the
intrinsic ability of the kidney to regulate renal blood flow and glomerular filtration rate,
prerenal AKI can lead to ischemic ATN when renal blood flow falls below 20 - 25% of normal
as in cardiocirculatory shock. Histologically, ATN consists in of destruction of tubular cells
with rupture of GBM and tubular occlusion by casts. Although kidneys with ATN may appear
normal on gray-scale US [42], usually kidneys appear enlarged with increased cortical
echogenicity with decreased corticomedullary differentiation and with increased RI values
(Figure 97). Proteinaceous casts are thought to cause the increased echogenicity
associated with ATN [38, 43]. ATN may also occur in extremely ill individuals, often as a
result of obstetric complications, hemorrhagic or septic shock, disseminated intravascular
coagulation, severe trauma, sepsis, malaria or burns. Necrosis results from constriction of
small intracortical blood vessels with preferential flow of blood away from the renal cortex.
Usually, the involved kidney becomes shrunken and scarred and cortical nephrocalcinosis
may then develop. ATN is not completely reversible in up to 25% of patients [28].
Differential diagnosis between different AKI forms. In patients with renal impairment
gray-scale and color-Doppler US are the first imaging modalities to differentiate postrenal
AKI due to urinary tract obstruction from prerenal and renal AKI and to assess renal vessels
and parenchymal abnormalities without the use of nephrotoxic agents. The renal size is
usually normal in prerenal AKI, while in renal AKI both kidneys may appear normal although
they frequently appear enlarged and with increased cortical echogenicity and
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corticomedullary differentiation especially when related to tubulointerstitial nephritis, and
acute glomerulonephritis. The finding of large, smooth kidneys with nondilated calyces
should indicate that AKI is probably due to primary acute kidney disease and that the
process is potentially reversible. On the other hand, detection of kidneys of reduced size
suggests a complicated underlying chronic nephropathy and worse prognosis. In prerenal
AKI RIs < 0.7 are related to complete recovery after fluid restoration, whereas in renal AKI
RIs are often >0.7. The threshold values of renal RI for renal impairment and/or prognostic
values of poor renal outcome range from 0.70 to 0.79 [44]. The clinical course of renal AKI
may be monitored with Doppler US by using serial measurements of intrarenal RIs with a
progressive decrease of RIs, which can precede the recovery of renal function, or with an
increase of RIs in case of complications [45 - 48]. In patients with AKI CEUS can reflect renal
perfusion reduction [49 – 52] and may detect renal parenchymal perfusion defects as non-
enhancing areas even in globally hypoperfused kidneys [16, 53, 54].
In postrenal AKI, accounting for 5-25% of AKIs, gray-scale US is accurate in detecting
hydronephrosis, consisting in a dilation of the urinary collecting system (renal calyces,
infundibula, and pelvis), even though it may reveal false-negative results, such as obstructive
AKI with nondilated urinary tract (due to dehydration or renal parenchyma tissue stiffness
such as in chronic kidney diseases), or false-positive results such as dilation of the urinary
tract in nonobstructed patients. Doppler US may provide unique data not available from gray-
scale US in postrenal AKI. A mean RI >0.7 is considered a significant diagnostic clue for
postrenal AKI [55 – 57].
Chronic kidney disease
Chronic kidney disease is defined as GFR <60 ml/min per 1.73 m2 for > 3 months. In
chronic kidney disease gray-scale US reveals reduced renal length and cortical thickness, an
hyperechoic renal parenchyma with a poor visibility of renal pyramids, and an increased
evidence amount of renal sinus fat (Figure 810). Renal length does not correlate with renal
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reduced function, whereas it correlates, as does cortical echogenicity, with severity of
pathological changes, including global sclerosis, focal tubular atrophy and hyaline cast
number per glomerulus [6, 58, 59]. In patients with chronic kidney disease increased renal
RIs (≥0.8) [58 – 60] and the mean splenic RI subtracted from the mean renal RI [61] are
related toindicate progression towards AKI. Disease progression with reduced renal
parenchyma perfusion and increased stiffness in renal parenchyma can be assessed by
CEUS [62] and real-time US elastography [63]. Patientswith chronic kidney disease treated
with dialysis or renal transplantation oftendevelop acquired cystic kidney disease in end-
stage renal disease with a significantly increased risk of solid and cystic malignancies [64].
Systemic vasculitides
In systemic vasculitides glomerulonephritis represent a local form of vasculitis that
involves glomerular capillaries. On histology the major finding consists in of inflammation with
leucocyte infiltration within and around vessel walls. Systemic vasculitides affecting the
kidney comprise Antineutrophil Cytoplasmic Antibody (ANCA) positive vasculitides,
rheumatoid vasculitis, cryoglobulinemia-related vasculitis, hypersensitivity vasculitides
(leukocytoclastic vasculitis angiitis), Behçet's disease, and IgA vasculitis (Henoch–Schönlein
purpura).
ANCA-associated vasculitides are a group of small and medium sized vessel
vasculitides which are characterized by the presence of ANCA in the peripheral circulation
directed against leukocyte myeloperoxidase or proteinase-3 and causing inflammation by
activating leukocytes by direct binding [Table 3] [21, 65]. ANCA-associated vasculitides are
characterized by glomerular necrosis with crescents accompanied by extracapillary
proliferation, inflammatory cell infiltration, and often rupture of the Bowman’s capsule [66].
US may reveal early involvement in renal vasculitis since vascular and interstitial
components are both involved in renal vasculitides. On gray-scale US renal vasculitides
manifest as an increased cortical echogenicity with reduced corticomedullary differentiation
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(Figure 911). US may reveal also multiple cortical hypoechoic areas of variable size and
shapes with cortical distortion, expressing regions of parenchymal edema [2, 6]. The
intrarenal RI values are significantly correlated with creatinine level and presence of
interstitial disease. Multiple intra-renal arterial aneurysms may be identified (Figure 120).
Vascular diseases
This category includes all those pathologies which may affect the large and/or small
renal arteries [Table 4].
Renal artery stenosis. Atherosclerotic renal artery disease can lead to renovascular
hypertension and ischemic renal disease with progressive decreased inof renal size and
function up to end-stage renal disease. In haemodynamically significant renal artery stenosis
accelerated flow is detected at the site of stenosis with high systolic peak velocity (>200
cm/s), renal-aortic ratio greater than 3.5, and post-stenotic turbulent flow with spectral
broadening and reversed flow. A decreased RIs with increased side-by-side difference higher
than 5%, prolonged acceleration time (higher than 0.05–0.08 secs) with loss of early systolic
peak and decreased acceleration (lower than 370–470 cm/sec2) may be observed in
interlobar–arcuate renal cortical arteries in severe significant renal artery stenosis (>70%)
(Figure 13). In stenosis higher than 70% of renal artery branches or of accessory renal
arteries, a similar pattern may be observed in a portion of the kidney [67].
Renal cortical necrosis. Renal cortical necrosis can complicate any condition
associated with hypovolemic or endotoxic shock as in premature placental separation late in
pregnancy. The most typical finding corresponds tois an hypoechoic band, corresponding to
the renal cortex, which surrounds the kidney. CEUS shows no enhancement within the renal
cortex due to tissue necrosis with homogenous enhancement of the renal medullary tissue
and adjacent renal parenchyma [68] (Figure 141).
Atheroembolic renal disease. Renal cholesterol microembolization may be caused by
renal angioplasty, atrial fibrillation and cardiac valvular defects. In patients with severe aortic 15
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atherosclerosis, atheromatous debris may embolize into the renal arteries up to glomerular
capillaries causing AKI. Even though large renal infarcts may be hypoechoic in comparison
with the viable renal parenchyma segmental renal infarcts are usually isoechoic or rarely
hyperechoic if haemorrhagic component is present [68 – 70]. Both color and power Doppler
US may increase diagnostic capabilities of US, especially in elderly or obese patients and in
patients with renal diseases, by depting depicting renal infarcts as avascular regions.
Howerver, CEUS is more sensitive than color or power Doppler US for the identification of
the non-enhancing parenchyma [69].
Renal vein thrombosis. Diagnosis of renal vein thrombosis relies on visualization of
an echogenica thrombus within a dilated renal vein devoid of flow signals on color Doppler
evaluation. Both kidneys areThe affected kidney is usually enlarged with reduced cortical–
medullary differentiation since even the renal cortex becomes hypoechoic. Doppler spectral
analysis of renal arteries may reveal slightly increased RIs with absent or reversed holo-
diastolic flow in renal interlobar–arcuate arteries and normal parenchymal venous flows,
since collateral venous supplies open after renal vein thrombosis. However, even though
absent or reversed diastolic signals on Doppler US could be suggestive of renal vein
thrombosis,their absence should not prevent further diagnostic work-up [68].
Diabetic Nephropathy. Diabetic nephropathy is the leading cause of kidney disease in
patients starting renal replacement therapy and affects roughly 40% of type 1 and type 2
diabetic patients [71 – 74]. Diabetic nephropathy typically manifests with gradual progression
of disease from microalbuminuria to proteinuria, usually about 15 years after onset of
diabetes. The diabetic patient is also prone to pyelonephritis, papillary necrosis, and
obstructive nephropathy which lead to renal failure. At histologic analysis diabetic
nephropathy presents diffuse expansion of collagenous component of the glomerulus with
accumulation of extracellular matrix, progressive thickening of GBM (diffuse intercapillary
glomerulosclerosis) and expansion of mesangium up to nodular glomerulosclerosis with
associated hyaline in arterioles and occasionally in Bowman’s capsule (Kimmelstiel–Wilson
nodules). On gray-scale US diabetic nephropathy manifests with enlarged kidneys due to
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hyperfiltration and hypertrophy, increased parenchymal thickness, and increase of the renal
parenchymal echogenicity with increased visibility of renal pyramids and corticomedullary
differentiation (Figure 152). In advanced diabetic nephropathy, kidneys become smaller,
renal parenchymal echogenicity may appear increased or normal according to vascular and
interstitial compartment involvement, whereas renal margins are usually diffusely irregular
[75]. The RIs are typically elevated in advanced diabetic nephropathy, whereas RIs are often
normal in the early stage of disease [76]. The RIs are highly correlated with serum creatinine
concentration and creatinine clearance rate, whereas an elevated RI (≥0.70) is associated
with impaired renal function, increased proteinuria, and poor prognosis [77]. CEUS can be
used for the diagnosis of the renal cortical perfusion reduction in early and late stage diabetic
patients expressed by a reduced area under time-intensity curve obtained after microbubble
injection [78, 79].
Hypertensive nephrosclerosis. Sustained Systemic hypertension causes hypertensive
nephrosclerosis (benign nephrosclerosis) which represents the second most common
diseases that result in chronic kindey disease and patient referral for transplantation.
Hypertensive nephrosclerosis corresponds to the macroscopic renal change related to
hypertension and consists in the granularity of renal cortical surfaces with evidence of coarse
scars due to arteriolosclerosis of the interlobar, arcuate and interlobular renal arteries with
thickening and collapse of GBM. Glomerular tufts are obliterated by scar and collagen and
matrix material are deposited within the Bowman space with tubular atrophy and interstitial
fibrosis with chronic inflammation. Malignant hypertensive nephrosclerosis is often
superimposed on hypertensive nephrosclerosis with intimal thickening in arteries and
fibrinoid necrosis and hyaline sclerosis of arterioles. On gray-scale US both kidneys are
usually symmetrically reduced in their diameters with cortical scars, irregularities of renal
margins and reduction in renal parenchymal thickness in most of patients [75] although these
findings are not specific. Color and power Doppler US reveal nonspecific reduction of
vascularization while renal RIs are typicallycan be increased (>0.7 and frequently around
0.8).
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Antiphospholipid syndrome is a common autoimmune disease caused by pathogenic
antiphospholipid antibodies causing recurrent vascular thrombosis in arterial, venous or small
vessels and pregnancy complications. It is classified as primitive when antiphospholipid
syndrome occurs in the absence of other autoimmune diseases or a secondary when it
occurs in association with a number of autoimmune disorders and mostly systemic lupus
erytematosus. Antiphospholipid antibodies are associated with various renal manifestations
including large renal vessel thrombosis, renal artery stenosis, and antiphospholipid
nephropathy consisting in acute thrombotic microangiopathy, proliferative and fibrotic lesions
of the intrarenal vessels, and ischemic lesions of the renal parenchyma which can lead to
AKI and manifest with increased RIs (>0.7) on Doppler US [80] (Figure 1316)
Hepatorenal syndrome represents a functional renal impairment which occurs in 20%
- 40% of patients with advanced liver disease. The pathophysiological hallmark is portal
hypertension leading to splanchnic arterial vasodilation, which leads to vasoconstriction of
the renal renal arteries, and reduced renal perfusion and GFR [81]. At Doppler US RI values
are markedly elevated in patients with clinically overt hepatorenal failure and represent
independent predictors of kidney dysfunction [81]. CEUS may detect improvement in renal
parenchyma perfusion in response to pharmacologic treatment in patients with hepatorenal
syndrome [82].
Thrombotic microangiopathy with thrombocytopenia and microangiopathic hemolytic
anemia represents the most severe form of vascular endothelial cell injury leading to AKI and
it may be caused by hemolytic uremic syndrome and thrombotic thrombocytopenic purpura
or also it may be drug-induced [Table 4]. Thrombotic thrombocytopenic purpura is caused by
a genetic or acquired deficiency of a protease creating microvascular thrombosis. Renal
involvement is often absent. Hemolytic uremic syndrome is a microangiopathic hemolytic
anemia that causes thrombocytopenia, renal failure, and hypertension and occurs principally
in children about 3–10 days following episodes of gastroenteritis due to enterohemorrhagic
E. Coli or viral upper respiratory tract infections.It is A similar syndrome occurs less
frequently in adults, often associated with complications of pregnancy or during the
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postpartum period but can be associated with the use of oral contraceptives or may occur
following treatment with antineoplastic agents. Histologically there is a wide band of
subendothelial expansion due to insudation of plasma protein and endothelial cell swelling
with narrowing of the capillary lumen promoting thrombosis and ischemic necrosis.
Thrombotic microangiopathy determinesClinically manifests with microangiopathic hemolytic
anemia, thrombocytopenia, and, in certain conditions, AKI due toplatelet or platelet-fibrin
thrombi in the interlobular renal arteries, arterioles, and glomeruli. Gray-scale US reveals
enlarged kidneys, enhanced echogenicity of the renal cortex and increased corticomedullary
differentiation with sharp delineation of swollen hypoechoic pyramids [83 – 85]. RIs are
markedly increased, often over 0.9.
Pre-eclamptic nephropathy. In pre-eclamptic nephropathy (pregnancy-induced
nephropathy) glomeruli are uniformly enlarged and endothelial and mesangial cells are
swollen with narrowing of the lumen of glomerular capillaries. Doppler US may reveal
reduced venous flow [86].
Systemic and hematological diseases
Systemic lupus erythematosus is a multisystem autoimmune disease characterized
by the development of autoantibodies to ubiquitous self-antigens (e.g., antinuclear antibodies
and antidouble-stranded DNA antibodies) and widespread deposition of immune complexes
in affected tissues. In 90% of cases patients are women especially in the age range between
20 and 40 years. Commonly affected organs are kidneys, joints, skin, central nervous
system, blood vessels, gastrointestinal tract, lymph nodes, and pleura. The kidneys are the
most commonly affected organs. Lupus nephritis follows the classification proposed by the
International Society of Nephrology/Renal Pathology Society (ISN/RPS) [Table 5] [21, 66,
87]. Gray-scale US has been reported to have a sensitivity of 95 % in lupus nephritis
detection [88]. In lupus nephritis, kidneys may present reduced or increased dimensions and
an increased cortical echogenicity with increased or even reduced corticomedullary
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differentiation. Gray-scale US may also reveal regions of parenchymal edema manifesting as
multiple cortical hypoechoic areas of variable size and shapes with cortical distortion. The
intrarenal RI values are significantly correlated with creatinine level and severity of lupus
nephritis [89, 90] and also with systemic vascular changes [91], whereas normal intrarenal
RI values are considered as a good prognostic factor.
Renal sarcoidosis is characterized by granulomatous interstitial nephritis with
randomly distributed, distinct granulomas or infiltrative pattern with or without areas of central
necrosis [27]. Renal involvement is seen in 7-22% of patients [92]. Clinical manifestations
include nephrolithiasis and nephrocalcinosis [93] due to the increased absorption of calcium,
nephrogenic diabetes insipidus, renal insufficiency, and acute tubulointerstitial nephritis with
or without granuloma. Kidneys may appear increased in dimensions or atrophic depending
on the extent and duration ofinvolvement. On gray scale US kidneys may appear normal or,
rarely, may manifest multiple tumorlike nodules that can mimic lymphoma or metastatic
tumors [94].
In gout nephropathy hyperechoic papillary foci or a diffuse hyperechoic medulla may
be observed [93]. Renal stones are usually present, while kidneys present normal or reduced
dimensions with smooth margins. In hyperoxaluria, and particularly in enteric hyperoxaluria
due to enhanced absorption of dietary oxalate in patients with ileal disease, kidneys present
normal or reduced dimensions with smooth margins and a hyperechoic renal cortex and
medulla. Glycogenosis results in liver and kidney involvement, with increased liver and
kidney dimensions owing to massive accumulation of glycogen in these organs,
hypoglycemia, and hyperuricemia.
Kidney manifestations of leukemia and lymphomas encompass a broad spectrum of
disease: prerenal AKI, ATN, renovascular disease, renal parenchyma cell infiltration, urinary
tract obstruction, glomerulopathies, and electrolyte and acid-base abnormalities [95]. In
leukemia one or both kidneys are increased in size due to diffuse leukemic cell infiltration,
with/without single or multiple hypoechoic nodules, wedge-shaped lesions or geographic
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areas. In general, when renal involvement is detected at imaging, there is also evidence of
extramedullary involvement. In lymphoma renal involvement is most often observed in
patients with non-Hodgkin disease, typically, diffuse large B cell lymphoma or Burkitt
lymphoma, who also have evidence of advanced-stage extranodal disease.
Gray-scale US reveals renal enlargement without disruption of the renal contour, a
solitary mass or multiple parenchymal lesions , and/or perirenal or renal sinus lesions [96].
Renal function is usually preserved in patients with renal lymphoma, but it can be affected by
diffuse cell parenchyma infiltration and by obstructive uropathy secondary to infiltration and
obstruction of the renal pelvis and ureters by retroperitoneal lymphadenopathy.
Multiple myeloma is an hematologic malignancy involving the pathologic proliferation
of terminally differentiated plasma cells. Light chain deposition disease, or so-called
myeloma cast nephropathy, consisting of Bence Jones or light chain proteins combined with
Tamm–Horsfall protein, is seen in approximately half of patients with multiple myeloma who
have renal disease. Renal failure is caused either by blockage of the tubules by protein casts
or by hypercalcemia and hyperuricemia. Intratubular obstruction results in interstitial fibrosis
and a lymphocytic infiltration associated with tubular atrophy [27]. When the kidney is
affected by monoclonal immunoglobulin deposition [Table 1] and patients do not meet
criteria for a diagnosis of multiple myeloma, the term monoclonal gammopathy of renal
significance is used including light chain cast nephropathy, amyloid light chain (AL)
amyloidosis, cryoglobulinemia (type I and II) and monoclonal immunoglobulin deposition
diseases with light chain, light and heavy chain or even heavy chain deposition disease. All
these disorders involving the kidneys manifest with nephrotic syndrome.
Amyloid nephropathy - both in the AL (associated with a monoclonal plasma cell
dyscrasia) and AA types (associated with a chronic inflammatory disease[97] - consists in
accumulation of fibrillary deposits in the mesangium extending along the inner surface of
GBM frequently obstructing the capillary lumen occasionally also with tubulointerstitial
amyloid deposition [27].
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Both onIn multiple myeloma and renal amyloidosis both kidneys appear enlarged and
hyperechoic with increased, normal or even reduced corticomedullary differentiation on gray
scale US (Figure 174) . Other findings consist in of diffusely infiltrative soft tissue encasing
the kidneys with/without calcifications (acute form), renal atrophy with cortical thinning
(chronic form), or focal renal parenchymal mass or hypoenhancing lesions resulting from
amyloid deposition. The RI values at Doppler US are usually increased.
HIV-associated nephropathy
HIV-associated nephropathy is seen in 12% of AIDS patients at histology,is more
frequent in patients with a CD4 cell count <200 cells/mm3 [98] and consists of a focal
segmental glomerulosclerosis with increased mesangial sclerosis and a proliferative cap of
visceral epithelial cells with dilatation of the Bowman ’s space and interstitial fibrosis and
infiltration by mononuclear leukocytes. Clinically, HIV-associated nephropathy should be
suspected in the HIV patient with AKI in the absence of hypertension (Figure 185). AKI in the
HIV population may be due also to ATN secondary to nephrotoxic agents used to treat
opportunistic infections (pentamidine, amphotericin B, and foscarnet) or to antiretroviral
therapy (tenofovir or didanosine). Nephrolithiasis represents a recognized side effect of
indinavir and nelfinavir. US reveals normal-sized or enlarged kidneys, with increased
parenchymal echogenicity and reduced or loss corticomedullary differentiation on grayscale
US with a reduced visibility of renal pyramids related to focal and segmental
glomerulosclerosis and to dilated renal tubules filled by proteinaceous material [99, 100].
Drug - induced kidney disease
Nephrotoxic drugs contribute towards AKI in 20–30% of patients [101]. Most drug
nephropathies involve mainly the tubulointerstitial compartment by a cell-mediated immune
response.
International Serious Adverse Event Consortium classifies drug-induced kidney
diseases [102] into four clinical phenotypes: AKI (further classified in acute vascular disease, 22
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acute glomerual disease, ATN, acute interstitial nephritis) [103], glomerular disease (mainly
membranous GN), nephrolithiasis/crystalluria, and tubular dysfunction. Beta-lactam
antibiotics, sulfonamides, antituberculous drugs, nonsteroidal anti-inflammatory drugs,
diuretics, anticonvulsants, proton pump inhibitors, allopurinol, captopril, phenytoin,
penicillamin, and interferon are among the most important drugs involved in acute interstitial
nephritis.
Gray-scale US may be completely normal or may show non-specific findings in drug
toxicity. Grayscale US may show renal swelling, increased or decreased renal echogenicity,
renal parenchyma calcifications, effacement of the renal sinus or loss of corticomedullary
differentiation (Figure 1619). In analgesic nephropathy kidneys may reveal hyperechoic foci
on renal pyramids due to papillary calcifications, which can also be observed also in
sarcoidosis, primary hyperparathyroidism, diabetes mellitus, medullary sponge kidney, and
prolonged dialysis treatment. Renal papillary necrosis, appearing as an hyperechoic filling
defect without acoustic shadowing within renal calyx, occurs in 70–80 % of patients with
analgesic nephropathy but may be observed also in diabetes mellitus, obstructive uropathy,
sickle cell disease, acute or chronic pyelonephritis, ATN, and renal vein thrombosis. Diffuse
incrementation of renal RIs may be observed.
Contrast medium–induced nephropathy (accounting for 12% of all cases of hospital-
acquired AKI) originates from the kidney medulla's unique hyperosmolar environment. Highly
concentrated iodinated contrast media in the tubules and vessels increases fluid viscosity
determining a flow reduction through medullary tubules, glomerual capillaries and vessels
and thereby damage cells creating medullary vasoconstriction and then hypoxia [104]. US
reveals normal kidneys with increased RIs at Doppler US which reduce progressively after
medical treatment.
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Pediatric Renal Parenchymal Diseases
Although hyperechogenicity of renal parenchyma is a nonspecific parameter even in pediatric
patients, there is a proven relationship between the degree of cortical echogenicity and
histopathological changes on renal biopsy [105].
The more frequent renal parenchymal disease in children is acute glomerulonephritis, where
kidneys may appear normal or enlarged, with or without hyperechoic renal cortex, with
normal or increased RIs, and with a normal or reduced renal parenchymal perfusion on Color
and power Doppler. Other pediatric renal parenchymal diseases associated with increased
renal echogenicity are type I glycogenosis, glomerulosclerosis, oculocerebral syndrome,
renal dysplasia, oxalosis, renal amyloidosis, acute multifocal pyelonephritis, sickle cell
anemia, primary polycythemia, and acute lymphatic leukemia .
Nephrotic syndrome is uncommon in pediatric patients and may be related to acute
glomerulonephritis, collagen vascular diseases, and amyloidoses. In nephrotic syndrome,
kidneys may appear normal on US or may be enlarged with increased parenchymal
echogenicity.
Hemolytic uremic syndrome is a microangiopathic hemolytic anemia that causes
thrombocytopenia, renal failure, and hypertension and occurs principally in children about 3–
10 days following episodes of gastroenteritis due to enterohemorrhagic E. Coli or viral upper
respiratory tract infections. A similar syndrome (named thrombotic thrombocytopenic
purpura) occurs less frequently in adults (see above). Renal cortex appears typically
hyperechoic with increased corticomedullary differentiation, probably related to platelet
aggregates and fibrin thrombi in the lumen of glomerular capillaries. Markedly elevated RIs
are found.
Nephrocalcinosis is rare in children and associated mainly with hypercalcemic status, renal
tubular diseases, enzymatic disorders, prolonged furosemide therapy, and Tamm–Horsfall
proteinuria.
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Conclusion
Diffuse renal parenchymal diseases manifest with increased parenchymal
echogenicity and maintenance or loss of corticomedullary differentiation on gray scale US.
correlation of the US pattern with patient’s clinical history and background is essential for a
correct characterization. Gray-scale US and spetral Doppler US may be used in the follow-up
of renal parenchyma diseases especially during pharmacologic medical treatment. Additional
techniques, including CEUS and US elastography, may provide additional functional
informations regarding renal parenchyma perfusion and tissue stiffness related to the amount
of fibrosis in chronic renal diseases.
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Figures
Figure 1(a, b): Normal kidney, longitudinal plane. Gray scaleUS (a) and Color Doppler
MicroDoppler US acquisition (b) are performed in real time and displayed simultaneously.
Utrasensitive Color Doppler MicroDoppler US allows visualization of renal cortical vessels up
to the capsule with distinct identification of the interlobular arteries (straight arrows).
Figure 2: Right focal acute pyelonephritis in a 25-year-old woman. There is an hyperechoic
focus (arrow) in the upper pole of the right kidney with reduced vascularity on Color Doppler
US related to acute bacterial pyelonephritis.
Figure 32 (a – h): Scheme representing the different patterns of glomerular diseases. (a)
The normal glomerulus with the endothelium surrounding the glomerular vessel lumen (red)
and the Bowman's capsule - visceral layer, namely podocytes (orange) separated by a thin
glomerular basement membrane (yellow) which derives both from endothelial and epithelial
cells, the Bowman's capsule - parietal layer (blue), and the Bowman's space (green). (b)
Focal glomerulosclerosis. Glomerular consolidation affects some, but not all, glomeruli and
initially involves only part (gray) of an affected glomerular tuft. (c) Membranous nephropathy.
There is no evident proliferation by light microscopy, with global scattered subepithelial
accumulation of immunocomplexes, between podocytes and glomerular basement
mambranemembrane, with projections which are called spikes (black spots) of basement
membrane adjacent to the deposits. (d) Membranoproliferative glomerulonephritis, with
endocapillary and mesangial hypercellularity and glomerular basement membrane double
contours due to mesangial and subendothelial deposits (gray) also with
monocyte/macrophages and mesangial cells cell vascular infiltration, (e) IgA
glomerulonephritis. Mesangioproliferative glomerulonephritis with IgA deposits,
predominantly in the mesangium (gray). (f) Crescentic rapidly progressive
glomerulonephritis. There is capillary thrombosis (violet) and necrosis and/or capillary
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hypercellularity, mesangial hypercellularity, subendothelial immune complex deposits (gray)
with cellular crescent due to proliferation of parietal epithelial cells and influx of macrophages
(gray). (g) Multiple myeloma / Amyloid nephropathy are characterized by varying degrees of
mesangial proliferation (dark red) and, in its advanced form, by nodular glomerulosclerosis.
Amyloidosis is characterized by accumulation of fibrillary deposits in the mesangium
extending along the inner surface of GBM (h) Diabetic nephropathy. There is mesangial
increase or nodular sclerosis (violet), accompanied by hyalinosis of both afferent and efferent
arterioles and thickening of the glomerular basement membrane lamina densa without
deposits.
Figure 43a, b.Images in 56-year-old man with crescentic glomerulonephritis. (a) Grayscale
US, longitudinal plane. Kidneys appear increased in dimensions and present parenchymal
thickening with compressed renal sinus and hyperechoic renal parenchyma with reduced
corticomedullary differentiation.
Figure 5a-c.Images in 45-year-old man with rapidly progressive glomerulonephritis due to
crescentic glomerulonephritis. (a) Grayscale US, longitudinal plane. Kidneys present
parenchymal thickening with compressed renal sinus and hyperechoic renal parenchyma
with reduced corticomedullary differentiation. (b) Color Doppler US. Longitudinal plane.
Renal parechyma vascularity appears reduced. (c) Increased resistive index (0.73) is
revealed on spectral Doppler US.
Figure 4a6a, b: Images in 45-year-old man with tubulointerstitial nephritis. (a) Grayscale US,
longitudinal plane. Kidneys present parenchymal thickening, hyperechoic renal parenchyma
and reduced corticomedullary differentiation. (b) Spectral Doppler US interrogation of
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interlobar arteries visualized on color Doppler US reveals increased resistive index value
(0.77).
Figure 57(a, b): Images in 45-year-old woman with IgG4-related tubulointerstitial nephritis.
(a) Grayscale US, longitudinal plane. Kidneys appear increased in dimensions withpresent
increased parenchymal thickeness, renal sinus compression and reduced corticomedullary
differentiation on grayscale ultrasound. (b) Color Doppler reveals reduced renal parenchyma
vascularity.
Figure 68: Acute transplant rejection in a 55-year-old man with treated diabetes mellitus.
Spectral Doppler US interrogation of interlobar arteries reveals increased resistive index
values with inverted diastolic flow.
Figure 79(a, b): Images in 45-year-old woman with acute tubular necrosis. (a) Grayscale US,
longitudinal plane. Kidneys appear enlarged with increased parenchymal thickeness, and
increased parenchyma echogenicity with reduced corticomedullary differentiation on
grayscale ultrasound. (b) Spectral Doppler US interrogation of interlobar arteries reveals
increased resistive index values (0.77).
Figure 810. Images in 75-year-old man with chronic kidney disease. Gray-scale US,
longitudinal plane. Kidneys reveals diffusely irregular margins, reduced cortical thickness and
increased cortical echogenicity with increased volume of renal sinus fat.
Figure 911(a, b): 50-year-old man referred for acute renal failure due to ANCA positive
vasculitis at renal pathology. (a) At gray scale US the size of the kidneys and the cortical
thickness were normal but the corticomedullary differentiation was lost. (b) At color Doppler
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and spectral Doppler US, the cortical vascularization was reduced but the resistive index was
normal measured at 0.67.
Figure 10 12 (a, b)Patient presenting with fever and renal failure, referred for the drainage of
multiple renal abscesses. (a) Gray scale and Color Doppler US confirmed the presence of
multiple anechoic to hypoechoic round nodules (arrows) inside the renal parenchyma of both
kidneys. (b) At CEUS performed immediately before the drainage, these areas enhanced
strongly during the arterial phase, and were corresponding to multiple aneuryisms (arrows).
The histologic diagnosis of Behcet like disease was established afterwards. Aneurysms were
not indentified on color Doppler due to high flow optimization.
Figure 13(a, b) 35-year-old mam with systemic hypertension secondary to renal artery
stenosis. (a) At color Doppler US a tight stenosis is revealed at the right renal artery with
increased peak systolic velocity and spectral broadening. (b) On spectral Doppler US the
Doppler waveforms at the level of the interlobar arteries, downstream to the site of stenosis,
revealed a normal resistive index (0.62) but a tardus - parvus pattern with prolonged systolic
acceleration and small systolic amplitude with rounding of systolic peak.
Figure 1114(a, b) 36-year-old man, second transplantation due to loss of the first renal graft
after severe acute rejection. At day 13, the patient was presenting with poor recovery of renal
function and fever. (a) At gray scale US and color Doppler US, the renal transplant exhibited
a complete loss of the cortico-medullary differentiation with diffuse hyperechoic pattern of the
renal cortex, a hypoechoic area at the upper pole corresponding to a known infarct and poor
renal cortical vascularization. However, the Doppler waveforms at the level of the interlobar
arteries were normal with a resistive index measured at 0.62. (b) CEUS revealed the
presence of cortical necrosis (thin arrows) combined with medullary necrosis (thick arrows),
as this frame is acquired at 60 sec after injection. Some cortical areas remained perfused
(arrow head).
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Figure 1215: 72-year-old man presenting with chronic kidney disease due to diabetic
nephropathy. Kidneys were enlarged presenting with irregular margins, increased
echogenicity and corticomedullary difference. At spectral Doppler US, the resistive index
measured at the foot origin of the interlobar arteries are increased at 0.81.
Figure 1316(a - c) 61-year-old woman referred for acute renal failure due to antiphospholipid
syndrome. (a) At gray scale US the size and the echostructure of both kidneys were normal.
(b) Color Doppler US revealed a decrease in the intra-renal blood vessels but the resistive
index recorded at the level of the interlobar arteries was normal. (c) Contrast-enhanced US
was performed due to the discordance between the clinical status of the patient and the US
findings. It revealed the presence of patchy cortical necrosis at the lower pole (arrows) that
explained the presence of acute renal failure.
Figure 1417(a, b) 53-year-old woman presenting with renal amyloidosis and chronic kidney
disease. Note that the examination was performed after biopsy complicated with gross
hematuria. (a) At gray scale US the kidney was enlarged and the pelvi-caliceal tree was
enlarged and filled with echoic materials corresponding to clots (arrows). The renal
parenchyma was hyperechoic and the differentiation between the cortex and the medulla
was reduced. (b) Color Doppler US revealed the reduction of intra parenchymal vascularity
but the resistive index recorded at the level of the interlobar arteries was normal (0.70).
Figure 1518(a, b) 50-year-old woman presenting with HIV – associated nephropathy without
hypertension. Note that the examination was performed after biopsy complicated with gross
hematuria. (a) Gray scale US shows renal swelling, increased renal echogenicity, and loss of
corticomedullary differentiation. (b) Color Doppler US reveals reduced parenchymal
vascularity.
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Figure 196: 73-year-old woman presenting with lithium nephropathy and mild chronic kidney
disease. Gray scale US reveals reduced corticomedullary differentiation, multiple
hyperechoic cortical micro-calcifications and multiple cysts.
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