30THE KIDNEYS AND URETER

DAVID SUTTON 94

DAVID SUTTON PICTURES

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

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

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

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

• 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.

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

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

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

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

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

• 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.

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

• Fig. 30.13 Ultrasound of duplex kidney.

• 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).

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).

• Fig. 30.16 Triplex ureters demonstrated on IVU.

• 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).

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

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

• 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.

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

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

• 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).

• 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).

• 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).

• 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.

• 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.

• 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.

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

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

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

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

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

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

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

• 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.

• 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.

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

• 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.

• 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.

• 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.

• 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.

• 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.

• 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.

• 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.)

• 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.

• 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.

• 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.

• 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

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

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

• 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).

• 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).

• 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).

• 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.

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

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

• 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).

• 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.

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

• 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.

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

• 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).

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

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

• 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.

• 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.

• 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.

• 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.

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

• 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).

• 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).

• 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.

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

• 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.

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

• 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.

• 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.

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

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

• 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).

• 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).

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

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

• 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.

• 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.

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

• 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.

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

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

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

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

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

• 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).

• 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).

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.

• 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.

• 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).

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).

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

• Fig. 30.89 Ultrasound showing a relatively marked hydronephrosis.

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

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

• 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.

• 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.

• 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.

• 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).

• 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).

• Fig. 30.94 Ultrasound of chronic• demonstrating cortical loss• H ??????????????????????????????????????

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• Fig. 30.95 Persistent dilatation of the upper two-thirds of the right ureter due to previous pregnancy.

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

• 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.

• 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).

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

• 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.

• 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).

• 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.

• 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.

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

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

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

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

• 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.

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

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

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

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

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

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

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

• 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).

• 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).

• Fig. 30.122 Mechanical causes of renal failure.

• 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).

• 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).

• 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.

• 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.