DAVID SUTTON PICTURES THE KIDNEY AND URETERS ONLY FOR STUDY PURPOSE

1. 30
THE KIDNEYS AND URETER
DAVID SUTTON 94

2. DAVID SUTTON PICTURES
DR. Muhammad Bin Zulfiqar
PGR-FCPS III SIMS/SHL

3. • Fig. 30.1 Renal ultrasound demonstrating the
characteristic pattern of persistent fetal
lobulation.

4. Fig. 30.2 (A) Longitudinal renal ultrasound scan
showing a prominent column of Bertin
(arrow). (B) Transverse scan showing the same
feature (arrow).

5. • Fig. 30.3 Dromedary hump related to the
lateral border of the left kidney on IVU (A) and
ultrasound (B).

6. • Fig. 30.4 IVU showing left renal agenesis with bowel gas
within the left renal bed. The large right kidney shows a
bifid renal pelvis, the mildest form of renal duplication.

7. • Fig. 30.5 Renal dysplasia in Laurence-Moon-
Biedl syndrome showing poorly developed
papillae and small communicating calyceal
diverticula on IVU.

8. • Fig. 30.6 Malrotation of the left kidney on
IVU showing the anteriorly pointing renal
pelvis projected over the calyces.

9. • Fig. 30.7 Pelvic kidney seen on IVU (A) and
(different patient) CT (B).

10. • Fig. 30.8 Intrathoracic kidney seen on IVU (A)
and a transverse T 1 -weighted MR scan (B).

11. • Fig. 30.9 IVU (A) demonstrating a horseshoe
kidney. The isthmus of fused renal tissue
across the midline is well seen on CT (B).

13. • Fig. 30.11 (A) Main stem renal artery
supplying the upper two-thirds of the kidney
with (B) an accessory lower pole renal artery
demonstrated on angiography.

14. • Fig. 30.12 Duplex ureters on IVU: complete
bilateral (A) and partial left-sided (B).

15. • Fig. 30.13 Ultrasound of duplex kidney.

16. • Fig. 30.14 (A) Ultrasound of duplex kidney with
upper pole moiety hydronephrosis; there has
been virtually complete loss of cortex from the
upper pole moiety. Similar features seen on MRI
in a different patient with a small, chronically
hydronephrotic upper pole moiety (B).

17. Fig. 30.15 The classical drooping lily sign on IVU (A). The lower
pole moiety has been displaced inferolaterally by an upper
pole hydronephrosis. This usually occurs due to obstruction
of the upper pole moiety ureter at its orifice associated
with ectopic insertion or a ureterocele. In this case it is due
to a calculus i n the upper pole moiety ureter (B).

18. • Fig. 30.16 Triplex ureters demonstrated on
IVU.

19. • Fig. 30.17 Full length film from an IVU series showing a
non-opacified partly obstructing ureterocele surrounded by
opacified urine in the bladder (A). A later full length film
shows opacification of the distended upper moiety ureter
running down to the opacified ureterocele (B).

20. • Fig. 30.18 IVU demonstrating the
characteristic stretching of calyces by cysts in
polycystic kidneys.

21. • Fig. 30.19 Ultrasound showing relatively early
polycystic disease with multiple simple cysts
demonstrable.

22. • Fig. 30.20 CT scan showing multiple cysts in
the left kidney. The disease in this patient is
dominated by multiple hepatic cysts, the
right lobe containing a particularly large one.

23. • Fig. 30.21 Ultrasound in a patient with
tuberous sclerosis showing cysts and small
echogenic angiomyolipomas in the kidney.

24. • Fig. 30.22 Ultrasound of a patient with
tuberous sclerosis showing multiple small,
highly echogenic angiomyolipomas.

25. • Fig. 30.23 Medullary sponge kidney on IVU
showing linear (A) and saccular (B) ectasia of
the collecting ducts. This is often associated
with the formation of small calculi (C).

26. • Fig. 30.23 Medullary sponge kidney on IVU
showing linear (A) and saccular (B) ectasia of the
collecting ducts. This is often associated with the
formation of small calculi (C).

27. • Fig. 30.24 Calyceal diverticulum initially not
seen on the 5 min IVU film (A) but fills
retrogradely with contrast on the 15 min film
(B).

28. • Fig. 30.25 Gross right
hydronephrosis with failure of
contrast excretion Thin septae
of renal tissue can just b seen
separating the dilated nor
opacified calyces. The left
kidney is also affected, albeit
to a lesser degree showing a
tight pelviureteric junction and
dilatation and clubbing of the
calyces and renal pelvis.

29. • Fig. 30.26 Bilateral pelviureteric junction obstruction (A). The left
kidney is more severely affected, with contrast still visible in the
collecting ducts as crescents. Classical right pelviureteric junction
obstruction with kinking of the upper ureter (B). The same case
after surgery (C) showing the straight medial edge of a pyeloplasty.

30. • Fig. 30.26 Bilateral pelviureteric junction obstruction (A).
The left kidney is more severely affected, with contrast still
visible in the collecting ducts as crescents. Classical right
pelviureteric junction obstruction with kinking of the upper
ureter (B). The same case after surgery (C) showing the
straight medial edge of a pyeloplasty.

31. • Fig. 30.27 Chronic right pelviureteric junction
obstruction with almost complete cortical loss
seen on CT.

32. • Fig. 30.28 Retrograde balloon dilatation of a
pelviureteric junction obstruction: the balloon
partly (A) and fully (B) dilated.

33. • Fig. 30.29 Left
megaureter on IVU
showing dilatation of
the entire length of
the ureter with
secondary
pelvicalyceal
dilatation.

34. • Fig. 30.30 Gross bilateral megaureters (A) with
calculus formation within the dilated distal
ureters (B).

35. • Fig. 30.31 Left megacalycosis with numerous
calyces showing poorly developed flattened
papillae

36. • Fig. 30.32 IVU on an infant with prune-belly
syndrome. There is gross overdistension of the
bladder, bilateral hydronephrosis and hydroureters.

37. • Fig. 30.33 Focal severe pyelonephritis
appearing as a slightly heterogeneous mass.

38. • Fig. 30.34 Emphysematous pyelitis. (A) Plain film showing
the characteristic configuration of gas in the collecting
system. (B) CT demonstrating gas within the collecting
system.

39. • Fig. 30.35 Gas bubbles shown on IVU within the
collecting system due to a fistula between the
ureter and the small bowel in Crohn's disease.

40. • Fig. 30.36 Renal abscess on postcontrast CT
showing a liquid non enhancing centre and an
irregular enhancing wall.

41. • Fig. 30.37 Perinephric abscess on CT. There is
an adjacent area of severe renal parenchymal
inflammation with a tiny associated calculus.
A small reactive pleural effusion is also
present.

42. • Fig. 30.39 Xanthogranulomatous pyelonephritis
on CT. There is a renal calculus but no
hydronephrosis. Gas is seen in the collecting
system in this case. The kidney has also begun to
shrink and there is extension of the
inflammatory process into the perinephric space
and abdominal wall.

43. • Fig. 30.38 Chronic pyonephrosis on ultrasound (A) and CT
(B). There is marked cortical loss and modest dilatation of
the collecting system. The CT also demonstrates the pelvic
calculus responsible for the development of the condition,
and a multiloculated perinephric abscess, which has
extended laterally into the abdominal wall and posteriorly
into the psoas muscle.

44. • Fig. 30.40 Urinary tract tuberculosis. The plain film (A) demonstrates calcification within
distended upper pole calyces. The IVU (B) shows strictures at the calyceal necks with hydrocalyces
and fibrous stricturing of the renal pelvis and the ureter. The tomogram from an IVU on another
patient (C) shows a stricture at the neck of the upper pole calyx. This progresses on treatment and
the full length film from the IVU performed 6 months later shows the upper pole calyx has been
completely amputated (D). Distal ureteric strictures are also present. Classical end-stage upper tract
tuberculosis is the autonephrectomy (E) in which the chronically obstructed pelvicalyceal system is
filled with calcifying caseous pus associated with complete renal parenchymal destruction. In this
case there is also similar calcifying pus in an obstructed dilated upper ureter.

45. • Fig. 30.40 Urinary tract tuberculosis. The plain film (A) demonstrates calcification
within distended upper pole calyces. The IVU (B) shows strictures at the calyceal
necks with hydrocalyces and fibrous stricturing of the renal pelvis and the ureter.
The tomogram from an IVU on another patient (C) shows a stricture at the neck of
the upper pole calyx. This progresses on treatment and the full length film from
the IVU performed 6 months later shows the upper pole calyx has been
completely amputated (D). Distal ureteric strictures are also present. Classical end-
stage upper tract tuberculosis is the autonephrectomy (E) in which the chronically
obstructed pelvicalyceal system is filled with calcifying caseous pus associated with
complete renal parenchymal destruction. In this case there is also similar calcifying
pus in an obstructed dilated upper ureter.

46. • Fig. 30.40 Urinary tract tuberculosis.
The plain film (A) demonstrates
calcification within distended upper
pole calyces. The IVU (B) shows
strictures at the calyceal necks with
hydrocalyces and fibrous stricturing
of the renal pelvis and the ureter.
The tomogram from an IVU on
another patient (C) shows a stricture
at the neck of the upper pole calyx.
This progresses on treatment and
the full length film from the IVU
performed 6 months later shows the
upper pole calyx has been
completely amputated (D). Distal
ureteric strictures are also present.
Classical end-stage upper tract
tuberculosis is the autonephrectomy
(E) in which the chronically
obstructed pelvicalyceal system is
filled with calcifying caseous pus
associated with complete renal
parenchymal destruction. In this
case there is also similar calcifying
pus in an obstructed dilated upper
ureter.

47. • Fig. 30.41 Full length film
from an IVU showing
changes of schistosomiasis
including bladder wall
calcification with
secondary ureteric and
pelvicalyceal dilatation.
(Courtesy of Dr Shadley
Fataar, Royal Hospital,
Muscat, Oman.)

48. • Fig. 30.42 IVU films showing the features of reflux nephropathy. (A) Severe right-
sided disease with a small kidney, widespread cortical loss (maximal at the upper
pole) and clubbing of the calyces. (B) Right-sided duplex system with diseased
lower pole moiety showing clubbing of the calyces and cortical loss. The lower
moiety ureter also shows persistent dilatation due to previous severe reflux.

49. • Fig. 30.43 Reflux nephropathy developing following fashioning of an ileal conduit.
(A) Normal kidneys preoperatively (right upper pole compound calyx noted
incidentally). (B,C) Six months and 3 years later showing non-obstructive dilatation
of the pelvicalyceal systems and ureters due to reflux from the conduit (proven
with loopography) and progressive cortical loss, especially on the left.

50. • Fig. 30.43 Reflux
nephropathy developing
following fashioning of an
ileal conduit. (A) Normal
kidneys preoperatively (right
upper pole compound calyx
noted incidentally). (B,C) Six
months and 3 years later
showing non-obstructive
dilatation of the pelvicalyceal
systems and ureters due to
reflux from the conduit
(proven with loopography)
and progressive cortical loss,
especially on the left.

51. • Fig. 30.44 Pyeloureteritis cystica. (A) Plain films showing a renal
pelvic calculus (and incidental pancreatic calcification). (B) IVU
demonstrating mild hydronephrosis due to the calculus, and
multiple filling defects from the pelviureteric junction downwards
due to the cyst of pyeloureteritis cystica

52. • Fig. 30.45 Renal sinus lipomatosis. CT
demonstrates bilateral renal atrophy with
increase in the volume of sinus fat.

53. • Fig. 30.46 Right renal cyst on IVU appearing as
a welldefined avascular mass displacing the
adjacent calyces.

54. • Fig. 30.47 Renal cyst on ultrasound (A) appearing as a well-
defined echo-free mass without significant wall thickness
and distal acoustic enhancement. On CT the cyst is of water
density (B) and shows no enhancement with intravenous
contrast (C). On MRI the cyst has the same signal intensity
as water, being low signal on the T,-weighted sequence ( D)
and high signal on the T2 –weighted sequence (E).

55. • Fig. 30.47 Renal cyst on ultrasound (A) appearing
as a well-defined echo-free mass without
significant wall thickness and distal acoustic
enhancement. On CT the cyst is of water density
(B) and shows no enhancement with intravenous
contrast (C). On MRI the cyst has the same signal
intensity as water, being low signal on the T,-
weighted sequence ( D) and high signal on the T2
–weighted sequence (E).

56. • Fig. 30.47 Renal cyst on ultrasound (A) appearing as a
well-defined echo-free mass without significant wall
thickness and distal acoustic enhancement. On CT the
cyst is of water density (B) and shows no enhancement
with intravenous contrast (C). On MRI the cyst has the
same signal intensity as water, being low signal on the
T,-weighted sequence ( D) and high signal on the T2 –
weighted sequence (E).

57. • Fig. 30.48 High-density cyst on
unenhanced (A) and postcontrast
(B) CT shows no enhancement,
indicating its probably benign
nature. Ultrasound (C)
demonstrates no internal echoes,
offering further reassurance.

58. • Fig. 30.49 Multiloculated cyst on CT with
substantial calcific area (A). Different patient
on ultrasound (B) also demonstrating
considerable wall calcification.

59. • Fig. 30.50 Well-defined cystic lesion with
substantial irregular enhancing areas
signifying probable malignancy.

60. • Fig. 30.51 Ultrasound appearances of
angiomyolipomas. (A) Large lower pole
predominantly echogenic mass (solitary
angiomyolipoma). (B) Multiple well-defined
purely echogenic masses (multiple
angiomyolipomas in tuberous sclerosis).

61. • Fig. 30.52 CT showing pre dominantly fat-density
solitary angiomyolipoma (A) and multiple purely
fat-density bilateral angiomyolipomas (B) in
tuberous sclerosis. The latter case has presented
with a left-sided perinephric haemorrhage seen
as a soft-tissue rim around the kidney but
delineated externally by the perinephric fascia.

62. • Fig. 30.53 Large left-sided angiomyolipoma
with small fat-density areas but
predominantly appearing as an enhancing
soft-tissue mass.

63. • Fig. 30.54 Left-sided angiomyolipoma with
brisk haemorrhage, some of which is
sufficiently acute to appear as ill-defined high-
density areas on CT.

64. • Fig. 30.55 Renal cell carcinoma on IVU. The
tumour appears as a large left lower pole
mass distorting the adjacent pelvicalyceal
system.

65. • Fig. 30.56 Renal cell carcinoma on
ultrasound. Two examples, one appearing as
a solid mass of intermediate echogenicity
replacing the normal renal architecture (A)
and the other similar apart from substantial
central necrosis (B).

66. • Fig. 30.57 Renal cell carcinoma on CT
appearing as a heterogeneously enhancing
mass associated with destruction of the
normal renal architecture.

67. • Fig. 30,58 Stage I renal cell carcinoma on
postcontrast CT. The tumour is small and
confined to the kidney.

68. • Fig. 30.59 Stage II renal cell carcinoma on
postcontrast CT. The tumour extends to the
margin of the kidney and shows some local
nodular extension through the renal capsule.

69. • Fig. 30.60 Renal cell carcinoma with vascular
involvement. (A) Ultrasound shows tumour as a soft-
tissue nodule of intermediate echogenicity within the
inferior vena cava. Postcontrast CT (B, different case)
shows a right renal cell carcinoma extending along the
renal vein into the inferior vena cava and (C) into the
contralateral renal vein.

70. • Fig. 30.60 Renal cell carcinoma with vascular
involvement. (A) Ultrasound shows tumour as a soft-
tissue nodule of intermediate echogenicity within the
inferior vena cava. Postcontrast CT (B, different case)
shows a right renal cell carcinoma extending along the
renal vein into the inferior vena cava and (C) into the
contralateral renal vein.

71. • Fig. 30.61 Heterogeneous mass of renal
carcinoma in the right kidney on MRI (T 2 -
weighted sequence) extending along the right
renal vein into the inferior vena cava.

72. • Fig. 30.62 Large right renal cell carcinoma
with lymph node metastases including a large
node that is displacing the inferior vena cava
anteriorly.

73. • Fig. 30.63 Stage IV tumours. Left renal cell
carcinoma with areas of calcification seen on
the unenhanced CT (A). The tumour has
invaded into the tail of the pancreas (B). Right
renal cell carcinoma invading the psoas
muscle, anterior abdominal wall and adjacent
bowel (C).

74. • Fig. 30.63 Stage IV tumours. Left renal cell carcinoma
with areas of calcification seen on the unenhanced CT
(A). The tumour has invaded into the tail of the
pancreas (B). Right renal cell carcinoma invading the
psoas muscle, anterior abdominal wall and adjacent
bowel (C).

75. • Fig. 30.64 Right renal angiogram (A)
demonstrating the malignant circulation of a
renal cell carcinoma. Embolisation with an
intra-arterial coil (B) has been performed.

76. • Fig. 30.65 Renal lymphoma on postcontrast
CT. There are bilateral relatively well-defined
intermediate to low-density deposits of
lymphoma.

77. • Fig. 30.66 Renal metastasis on STIR sequence
(A) and T-weighted MRI (B). Features of the
mass are essentially identical to a primary
renal cell carcinoma.

78. • Fig. 30.67 Renal oncocytoma on CT appearing
as a well-defined intensely enhancing mass
with central non-enhancing scar.

79. • Fig. 30.68 (A) Large transitional cell carcinoma seen as a
substantial filling defect in the left renal pelvis. (B) More subtle
transitional cell carcinoma al most completely obliterating the left
upper pole major calyx and showing marked irregularity of the
remaining urothelium in that area.

80. • Fig. 30.69 Well-defined
serpiginous filling
defect in the right renal
pelvis extending a little
way into the upper
ureter. This represents
thrombus in a patient
overcoagulated with
warfarin and presenting
with haematuria. The
filling defect and
haematuria resolved
completely once
normal coagulation was
restored.

81. • Fig. 30.70 Relatively echo-poor deposits of
transitional cell carcinoma obliterating the
normal renal architecture in the upper pole.

82. • Fig. 30.71 Substantial transitional cell
carcinoma showing a mixed echopoor and
echogenic pattern and a mild associated
hydronephrosis.

83. • Fig. 30.72 Infiltrating left upper pole
transitional cell carcinoma with similar
density to normal renal tissue obliterating
the sinus fat (A) and enhancing slightly less
than normal renal tissue (B).

84. • Fig. 30.73 Squamous cell carcinoma
developing within a chronic hydronephrosis
(A). The tumour has extended out of the
collecting system and is invading the psoas
muscle (B).

85. • Fig. 30.74 Ultrasound of a Wilms‘ tumour
showing the characteristic irregular
multicystic appearance.

86. • Fig. 30.75 CT scan of bilateral Wilms' tumours
showing an irregular multicystic appearance.

87. • Fig. 30.76 Multilocular cystic nephroma on
ultrasound (A) and CT before (B) and after (C)
contrast. Note the lesion typically bulging into
the renal pelvis.

88. • Fig. 30.76 Multilocular cystic nephroma on
ultrasound (A) and CT before (B) and after (C)
contrast. Note the lesion typically bulging into
the renal pelvis.

89. • Fig 30. 77 CT of renal sarcoma showing
generally expanded kidney with areas of
tumour enhancing less well than normal renal
tissue.

90. • Fig. 30.78 Contrast CT scan of a renal infarct in
a patient with arteritis. The left kidney is
almost entirely non perfused apart from a
partial peripheral rim.

91. • Fig. 30.79 CT angiogram (coronal
reconstruction). A tight stenosis of the origin
of the right renal artery is demonstrated.

92. • Fig. 30.80 Angiogram demonstrating multiple
short smooth stenoses of the right renal
artery in fibromuscular dysplasia.

93. • Fig. 30.81 (A) Small right renal calculus visible
on plain film and larger calculus (B) in the left
lower pole major calyx.

94. • Fig. 30.82 Multiple punctate calculi in
hyperoxaluria secondary to small bowel
resection.

95. • Fig. 30.83 Plain film showing large right
staghorn calculus.

96. • Fig. 30.84 Radiolucent urate calculus, not visible
on plain film, appearing as a welldefined filling
defect in the collecting system of the left kidney
(A). A larger mass is also visible distorting the left
pelvicalyceal system. CT confirms that the small
filling defect is a urate calculus (B) and the larger
one a parapelvic cyst (C).

97. • Fig. 30.84 Radiolucent urate calculus, not visible on
plain film, appearing as a welldefined filling defect in
the collecting system of the left kidney (A). A larger
mass is also visible distorting the left pelvicalyceal
system. CT confirms that the small filling defect is a
urate calculus (B) and the larger one a parapelvic cyst
(C).

98. Fig. 30.85 Dense nephrogram with delay in appearance
of contrast in the left collecting system characteristic
of high-grade obstruction (A). Eventually contrast
outlines a mildly distended ureter down to a calculus at
the left vesicoureteric junction (B) with the calculus
just visible on the plain film (Q.

99. • Fig. 30.85 Dense
nephrogram with
delay in appearance
of contrast in the left
collecting system
characteristic of high-
grade obstruction (A).
Eventually contrast
outlines a mildly
distended ureter down
to a calculus at the left
vesicoureteric junction
(B) with the calculus
just visible on the plain
film (Q.

100. • Fig. 30.86 Pyelosinus extravasation (A) in high-grade obstruction
with leakage of contrast around the upper pole calyces, which have
become ill defined. Contrast is entering the lymphatic vessels
(arrow), pyelolymphatic extravasation. More profuse extravasation
is occasionally seen with forniceal rupture (B).

101. Fig. 30.87 Full length film from an IVU series (A)
showing stasis and mild fullness in the left ureter
and considerable oedema around the
vesicoureteric junction due to a small calculus
visible on the plain film (B).

102. • Fig. 30.88 Small ureteric calculus (small
arrow) associated with haematuria and
thrombus (large arrow).

103. • Fig. 30.89 Ultrasound showing a relatively
marked hydronephrosis.

104. • Fig. 30.90 Small solitary renal calculus on
ultrasound seen as an echogenic focus with
marked distal acoustic shadowing.

105. • Fig. 30.91 Small calculus in the distal dilated
ureter seen as an echogenic focus on
ultrasound.

106. • Fig. 30.92 CT demonstrating subtle dilatation of the right
ureter (A) down to a small ureteric calculus (small arrow, B).
Perinephric stranding is just visible off the lower pole of the
kidney (B) indicating significant obstruction is present.
Calculus demonstrated at the left vesicoureteric junction on
a different patient (C). Phleboliths (D) may lie close to the
expected course of the ureter but do not have the soft-
tissue rim of the ureteric wall related to them. Other
potentially confusing calcific opacities include arterial
calcification and osteophytes (E), fortunately on the
opposite side to the symptoms in this patient, a dilated
ureter being visible as well as considerable perinephric
oedema around the lower pole of the left kidney.

107. • Fig. 30.92 CT demonstrating subtle dilatation of the right
ureter (A) down to a small ureteric calculus (small arrow, B).
Perinephric stranding is just visible off the lower pole of the
kidney (B) indicating significant obstruction is present.
Calculus demonstrated at the left vesicoureteric junction on
a different patient (C). Phleboliths (D) may lie close to the
expected course of the ureter but do not have the soft-
tissue rim of the ureteric wall related to them. Other
potentially confusing calcific opacities include arterial
calcification and osteophytes (E), fortunately on the
opposite side to the symptoms in this patient, a dilated
ureter being visible as well as considerable perinephric
oedema around the lower pole of the left kidney.

108. • Fig. 30.92 CT demonstrating subtle dilatation of the right ureter (A)
down to a small ureteric calculus (small arrow, B). Perinephric
stranding is just visible off the lower pole of the kidney (B)
indicating significant obstruction is present. Calculus demonstrated
at the left vesicoureteric junction on a different patient (C).
Phleboliths (D) may lie close to the expected course of the ureter
but do not have the soft-tissue rim of the ureteric wall related to
them. Other potentially confusing calcific opacities include arterial
calcification and osteophytes (E), fortunately on the opposite side
to the symptoms in this patient, a dilated ureter being visible as
well as considerable perinephric oedema around the lower pole of
the left kidney.

109. • Fig. 30.93 CT showing modest perinephric stranding characteristic
of significant obstruction from a ureteric calculus (A). In addition
to these changes this second case shows a small fluid collection
adjacent to the anterior lip of the renal hilum indicating a forniceal
rupture (B). The acute hydronephrosis is generally mild, as
demonstrated in this third example (C), but the asymmetry
between the sides is useful (although this patient demonstrates a
slightly full extrarenal pelvis on the asymptomatic side). There is
mild perinephric stranding on the symptomatic (left) side but
considerable ill-definition around the renal pelvis, suggesting some
extravasation into the renal sinus. This can be seen to track down
along the dilated ureter, giving it a shaggy appearance (D).

110. • Fig. 30.93 CT showing modest perinephric stranding characteristic of significant
obstruction from a ureteric calculus (A). In addition to these changes this second
case shows a small fluid collection adjacent to the anterior lip of the renal hilum
indicating a forniceal rupture (B). The acute hydronephrosis is generally mild, as
demonstrated in this third example (C), but the asymmetry between the sides is
useful (although this patient demonstrates a slightly full extrarenal pelvis on the
asymptomatic side). There is mild perinephric stranding on the symptomatic (left)
side but considerable ill-definition around the renal pelvis, suggesting some
extravasation into the renal sinus. This can be seen to track down along the dilated
ureter, giving it a shaggy appearance (D).

111. • Fig. 30.94 Ultrasound of chronic
• demonstrating cortical loss
• H
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112. • Fig. 30.95 Persistent dilatation of the upper
two-thirds of the right ureter due to previous
pregnancy.

114. • Fig. 30.97 Contrast CT showing large
predominantly posterior perinephric
haemorrhage.

115. • Fig. 30.98 Contrast CT showing a laceration of
the kidney in the vicinity of the anterior lip of
the renal sinus with a large associated
haemorrhage.

116. • Fig. 30.99 Contrast CT showing a fracture
through the centre of the kidney with
considerable circumferential perinephric
haemorrhage (A). Two months after
conservative management there has been
impressive healing of the kidney and
resorption of most of the haemorrhage (B).

117. • Fig. 30.100 Contrast CT showing a shattered
kidney (multiple fractures).

118. • Fig. 30.101 Contrast CT of traumatic renal
arterial avulsion. The left kidney is completely
non-enhancing (non perfused). There is a small
amount of blood along the line of the renal
vessels and a modest haemorrhage related to the
spleen.

119. • Fig. 30.102 Stab wound resulting in laceration
of the lower pole of the right kidney with
considerable associated haematoma shown
on contrast CT (A). This was successfully
treated with selective coil embolisation (B).

120. • Fig. 30.103 Bilateral extravasation from the
distal ureters following radical pelvic surgery. The
ureters also show smooth tapered stricturing in
the pelvis with bilateral hydronephrosis and
dilatation of the proximal ureters, worse on the
right.

122. • Fig. 30.105 Ultrasound of a patient with
medullary sponge kidney showing multiple small
echogenic areas in the papillae due to tiny calculi
in the collecting duct (A). There is also
hydronephrosis and proximal hydroureter due to
a ureteric calculus. Plain film nephrocalcinosis (B)
in a different patient.

123. • Fig. 30.106 Plain film showing extremely
dense nephrocalcinosis due to
hyperparathyroidism.

124. • Fig. 30.107 Plain film showing moderately
dense nephrocalcinosis due to secondary
hyperoxaluria.

125. • Fig. 30.108 Early papillary necrosis with
erosions around the margins of some of the
papillae.

126. • Fig. 30.109 Papillary necrosis with more
widespread erosions into and around the
papillae and a classic ball-in-cup configuration
visible.

128. • Fig. 30.111 Retrograde ureterogram showing
a sloughed fragment of a large renal cell
carcinoma seen lying within the ureter and
causing obstruction above it.

129. • Fig. 30.112 IVU showing an irregular filling
defect in the distal right ureter (A). This is
better seen on the retrograde study (B).

130. • Fig. 30.113 Full length film from an IVU
showing an abrupt smooth stricture in the
distal ureter due to endometriosis.

131. • Fig. 30.114 Short tight stricture in the distal
left ureter due to involvement in a previous
diverticular abscess.

132. • Fig. 30.115 Bilateral medial deviation of the
lower ureters due to physiological psoas
muscle hypertrophy.

133. • Fig. 30.116 Retroperitoneal fibrosis on IVU.
There is marked abrupt deviation of both
upper ureters with a right-sided
hydronephrosis.

134. • Fig. 30.117 CT demonstration of
retroperitoneal fibrosis with classical
appearance of the aorta as if taped down by a
sheet of tissue.

135. • Fig. 30.118 CT of malignant para-aortic and
paracaval lymphadenopathy causing ureteric
obstruction. Note the anterior displacement
of the aorta off the spine.

136. • Fig. 30.119 IVU showing
the characteristic lateral
displacement of the
ureter following surgery
for retroperitoneal fibrosis
(only the right side has
been operated on, as the
left kidney was already
severely damaged).

137. • Fig. 30.120 (A) Surface-shaded 3D reconstruction
of a spiral CT of the left kidney demonstrating
renal morphology and vascular anatomy. The
cortical defect seen caudally represented a renal
cyst on axial images. Note the mild renal artery
stenosis, which was confirmed angiographically
(B).

139. • Fig. 30.122
Mechanical causes of
renal failure.

140. • Fig. 30.123 Duplex demonstrates an increased
and turbulent flow at the origin of the renal
artery (A) with associated damped flow at
segmental level (B) indicating renal artery
stenosis. This occurred early post transplant and
was secondary to anastomotic stricture
confirmed at angiography (C).

141. • Fig. 30.123 Duplex demonstrates an increased and
turbulent flow at the origin of the renal artery (A) with
associated damped flow at segmental level (B)
indicating renal artery stenosis. This occurred early
post transplant and was secondary to anastomotic
stricture confirmed at angiography (C).

142. • Fig. 30.124 (A) Selective angiography of the renal transplant
demonstrates early iliac vein filling due to an arteriovenous fistula
in the lower pole. (B) Supraselective embolisation with coils has
occluded the arteriovenous fistula with very little infarction of renal
cortex.

143. • Fig. 30.125 (A) Duplex
demonstrates complete reversal of
flow in this patient with renal vein
thrombosis. Similar appearances can
be seen with severe graft rejection.
(B) Renal scintigraphy in the same
patient fails to demonstrate any
uptake of tracer in the graft site in
the right iliac fossa.