Adrenals, urinary tract and testes

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Adrenals, urinary tract and testes


Adrenal calcification

1. Cystic disease – similar to that seen in the child. Blunt abdominal trauma is a much more common cause in adults. Bilateral in 15% of cases.

2. Carcinoma – irregular punctate calcifications seen in 30%. Average size of tumour is 14 cm and there is frequently displacement of the ipsilateral kidney.

3. Addison’s disease – now most commonly due to autoimmune disease or metastasis. Historically, when TB was a frequent cause, calcification was a common finding.

4. Ganglioneuroma – 40% occur over the age of 20 years. Slightly flocculent calcifications in a mass, which is usually asymptomatic. Large tumours may cause displacement of the adjacent kidney and/or ureter.

5. Inflammatory – primary tuberculosis and histoplasmosis.

6. Phaeochromocytoma – calcification is rare but when present is usually an ‘egg-shell’ pattern.


Incidental adrenal mass (unilateral)

Adrenal ‘incidentalomas’ are seen in 1% of all CT examinations. The normal length of adrenal limbs is variable: can be up to 4 cm. The width of a limb is normally < 1 cm. A mass < 3 cm in diameter is likely to be benign (87% cases) and a mass > 5 cm in diameter is probably malignant. On unenhanced scans a mass < 10 HU is likely to be a benign lipid-rich adenoma. For indeterminate lesions, i.e. those > 10 HU, a contrast-enhanced scan with delayed imaging is required to assess degree of enhancement and washout values. Chemical shift MRI has also proved useful in characterization by assessing for the presence of microscopic fat. 18FDG-PET and 18FDG-PET/CT have also been used to differentiate benign from malignant tumours. For patients in whom the incidentaloma comprises a metastasis, 18FDG-PET/CT may be useful to detect other metastases and to find the primary tumour when this has not previously been diagnosed. Also in adrenocortical cancer, 18FDG-PET/CT can be used for staging of the disease. Ultimately, biopsy may be required.

Functioning tumours

1. Conn’s adenoma – accounts for 70% of Conn’s syndrome. Usually small, 0.5–1.5 cm. Homogeneous, relatively low density due to build-up of cholesterol. 30% of Conn’s syndrome due to hyperplasia, which can occasionally be nodular and mimic an adenoma.

2. Phaeochromocytoma – usually large, > 5 cm, with marked contrast enhancement (beware hypertensive crisis with i.v. contrast medium). 10% malignant, 10% bilateral, 10% ectopic (of these 50% are located around the kidney, particularly the renal hilum. If CT does not detect, MIBG isotope scan may be helpful). 10% are multiple and usually part of MEN II syndrome, neurofibromatosis or von Hippel–Lindau.

3. Cushing’s adenoma – accounts for 10% of Cushing’s syndrome. Usually > 2 cm in diameter. 40% show slight reduction in density. 80% of Cushing’s syndrome due to excess ACTH from pituitary tumour or ectopic source (small cell carcinoma, pancreatic islet cell, carcinoid, medullary carcinoma of thyroid, thymoma) which causes adrenal hyperplasia not visible on CT scan. 10% of Cushing’s syndrome due to adrenal carcinoma. The possibilities for adrenal mass in Cushing’s syndrome are:

4. Adrenal carcinoma – 50% present as functioning tumours (Cushing’s 35%, Cushing’s with virilization 20%, virilization 20%, feminization 5%).

Malignant tumours

1. Metastases – may be bilateral, usually > 2–3 cm, irregular outline with patchy contrast enhancement. Recent haemorrhage into a vascular metastasis (e.g. melanoma) can give a patchy high density on precontrast scan. In patients without a known extra-adrenal primary tumour the vast majority of adrenal masses are benign; even in the presence of a known primary malignant tumour many adrenal masses will still be benign (40% are metastases).

2. Carcinoma – typical features are:

3. Lymphoma – 25% also involve kidneys at autopsy. Lymphadenopathy will be seen elsewhere.

4. Neuroblastoma – > 5 cm. Calcification in 90%. Extends across midline. Nodes commonly surround and displace the aorta and inferior vena cava.


1. Non-functioning adenoma – occurs in 5% at autopsy. Usually relatively small (50% < 2 cm), homogeneous and well-defined.

2. Myelolipoma – 0.2% at autopsy. Rare benign tumour composed of adipose and haemopoietic tissue. 85% are found in the adrenal but extra-adrenal tumours (liver, retroperitoneum, pelvis) have been reported. Low attenuation on CT and may enhance. Mean diameter of 10 cm.

3. Angiomyolipoma – adrenal lesions are very rare in practice. Usually contain vascular tissue and fat density.

4. Cyst – well-defined, water density.

5. Post-traumatic haemorrhage – homogeneous, hyperdense. Occurs in 25% of severe trauma, 20% bilateral, 85% on right. Adrenal haemorrhage can also occur in vascular metastases, anticoagulant treatment and severe stress (e.g. surgery, sepsis, burns, hypotension).

6. Granulomatous disease (TB, histoplasmosis) – present as diffuse enlargement or as discrete mass. Can have a central cystic component, with/without calcification.


Bilateral adrenal masses

1. Metastases – bilateral in 15%. Common at autopsy. Most common primary sites are lung or breast; also melanoma, renal cell carcinoma, gastrointestinal tract, thyroid, contralateral adrenal gland. Usually does not affect adrenal function; may cause adrenal insufficiency if extensive (replacing > 80% of adrenal gland).

2. Phaeochromocytoma – bilateral in 10%.

3. Hyperplasia – adrenogenital syndromes result in symmetrically enlarged and thickened adrenal glands. Adrenocortical hyperplasia can cause bilateral adrenal enlargement but usually these are not visible on CT.

4. Spontaneous adrenal haemorrhage.

5. Lymphoma – primary adrenal lymphoma is rare. Usually presents with bilateral adrenal masses, often with adrenal hypofunction. Usually diffuse large B-cell lymphomas. Adrenal involvement occurs at autopsy in up to 25% with disseminated lymphoma, usually with no associated adrenal insufficiency.

6. Granulomatous disease – histoplasmosis/TB. Can be acute or chronic. Patients with adrenal masses and adrenal failure caused by chronic disseminated histoplasmosis may have symptoms and CT findings that are indistinguishable from those of malignancy.


Adrenal pseudotumours

Soft-tissue density in the location of the adrenal glands on plain films of the abdomen or on CT. This almost always occurs on the left side. Right-sided lesions are usually liver, gallbladder or renal masses.

The right adrenal lies behind the IVC and above the right kidney, i.e. not on the same slice as the kidney. The left adrenal lies in front of the upper pole of the left kidney, i.e. on the same slice as the kidney – do not mistake upper pole of left kidney for an adrenal mass.


Congenital renal anomalies

These may be anomalies of position, of form or of number.

Anomalies of form

1. Horseshoe kidney – two kidneys joined by parenchymal/fibrous isthmus. Most common fusion anomaly with incidence of 1 in 400 births. Fusion of right and left kidneys at lower pole in 90%. Abnormal axis of each kidney (bilateral malrotation). Renal pelves and ureters situated anteriorly and renal long axis medially oriented. Associated with other anomalies in 50% (e.g. vesicoureteral reflux, ureteral duplication, genital anomalies, Turner’s syndrome).

2. Pancake/discoid kidney – bilateral fused pelvic kidneys, usually near the aortic bifurcation.

3. Crossed renal ectopia – kidney is located on opposite side of midline from its ureteral orifice. Usually L > R. The lower kidney is usually ectopic. In 90% there is fusion of both kidneys (= crossed fused ectopia). May be associated with anorectal anomalies and renal dysplasia. Slightly increased incidence of calculi.

4. Renal hypoplasia – incomplete development results in a smaller (< 50% of normal size) kidney with fewer calyces and papillae. Normal function.


Localized bulge of the renal outline


1. Cyst – well-defined nephrographic defect with a thin wall on the outer margin. Beak sign. Displacement and distortion of smooth-walled calyces without obliteration.

2. Tumour – mostly renal cell carcinoma in adults and Wilms’ tumour in children. See 8.21.

3. Fetal lobation – the lobule directly overlies a normal calyx. Normal interpapillary line. See 8.8.

4. Dromedary hump – on the midportion of the lateral border of the left kidney. Occurs secondary to prolonged pressure by spleen during fetal development. The arc of the interpapillary line parallels the renal contour.

5. Splenic impression – on the left side only. This produces an apparent bulge inferiorly.

6. Enlarged septum of Bertin – overgrowth of renal cortex from two adjacent renal lobules. Usually between upper and interpolar portion. Excretory urography shows a pseudomass with calyceal splaying and associated short calyx ± attempted duplication. Tc-DMSA accumulates normally or in excess. On US echogenicity is usually similar to normal renal cortex but may be of increased echogenicity. CT – enhances similar to cortex.

7. Localized compensatory hypertrophy – e.g. adjacent to an area of pyelonephritic scarring.

8. Acute focal nephritis (lobar nephronia) – usually an ill-defined hypoechoic mass on US, but may be hyperechoic. CT shows an ill-defined, low-attenuation, wedge-shaped mass with reduced contrast enhancement.

9. Abscess – loss of renal outline and psoas margin on the control film. Scoliosis concave to the involved side. Initially there is no nephrographic defect, but following central necrosis there will be a central defect surrounded by a thick irregular wall. Adjacent calyces are displaced or effaced.

10. Non-functioning moiety of a duplex – usually a hydronephrotic upper moiety. Delayed films may show contrast medium in the upper moiety calyces. Lower moiety calyces display the ‘drooping lily’ appearance.


Unilateral scarred kidney



Unilateral small smooth kidney

In all these conditions chronic unilateral disease is associated with compensatory hypertrophy of the contralateral kidney.

Prerenal = vascular

Usually with a small volume collecting system. This is a sign of diminished urinary volume and, together with global cortical thinning, delayed opacification of the calyces, increased density of the opacified collecting system and delayed washout following oral fluids or diuretics, indicates ischaemia.


Bilateral small smooth kidneys

Postrenal = collecting system

Chronic papillary necrosis (see 8.26) – with other signs of necrotic papillae.


Unilateral large smooth kidney

Renal = parenchymal


Bilateral large smooth kidneys

It is often difficult to distinguish, radiologically, the members of this group from one another. The appearance of the nephrogram may be helpful – see 8.25. Associated clinical and radiological abnormalities elsewhere are often more useful, e.g. in sickle-cell anaemia, Goodpasture’s disease and acromegaly.


Renal calcification

Dystrophic calcification due to localized disease

Usually one kidney or part of one kidney.

1. Infections

2. Tumours

3. Cysts – usually related to previous infection or haemorrhage.

4. Vascular


Renal calculi

Nephrolithiasis is the most common cause of calcification within the kidney. 12% of the population develop a renal stone by the age of 70.


Mimics of renal colic on unenhanced CT urography

9–29% of patients presenting with flank pain may have alternative diagnoses rather than renal colic at unenhanced CT. A renal or ureteric stone will be detected on CT in 33–55% of patients with acute flank pain. If unenhanced CT demonstrates unilateral perinephric stranding or nephromegaly but no stones, the use of intravenous contrast should be considered.

Non-stone genitourinary

Sometimes occult malignancies may result in spontaneous haemorrhage and flank pain. If an isolated subcapsular or perinephric haemorrhage is seen, an underlying neoplasm should be suspected.

Extraurinary tract disease.


1. Appendicitis – the normal appendix is usually less than 6 mm wide, thin walled, and may contain an appendicolith. Gas in the lumen may be both a normal and abnormal finding. Look for dilatation of the appendix to more than 6 mm, inflammatory stranding of the periappendiceal or pericaecal fat, and surrounding phlegmon or abscess. A faecalith within a fluid collection in the right lower quadrant is very helpful for making the diagnosis of a perforated appendicitis.

2. Diverticulitis – characteristic findings include inflammation of pericolic fat related to diverticula, focal colonic wall thickening, thickening of adjacent fascia, thickening of the root of the mesentery and intra-abdominal abscess. Most inflamed diverticula are usually within the sigmoid or descending colon.

3. Small bowel diverticulitis and Meckel diverticulitis may mimic renal colic.

4. Abdominal hernias.

5. Small bowel obstruction.

6. Intussusception.

7. Colon carcinomas.

8. Inflammatory bowel disease.

9. Pancreatic and hepatobiliary disorders


1. Renal infarction – unilateral perinephric stranding is suggestive of a dissection flap into the renal artery.

2. Renal vein thrombosis.

3. Renal artery aneurysm.

4. Ruptured abdominal aortic aneurysm – crescent-shaped area of high attenuation, higher than intraluminal blood, in the wall of an abdominal aortic aneurysm. Periaortic stranding or haemorrhage, > 60 HU is indicative of active bleeding.

5. Aortic dissection – high attenuation on unenhanced CT in the wall of the aorta indicates intraluminal haematoma, displacement of intimal calcification into the aortic lumen; renal infarction.

6. Isolated SMA dissection – rare; signs include perivascular fat stranding, vessel enlargement, irregular contour and displacement of intimal calcification. Secondary signs of bowel compromise are bowel wall thickening, pneumatosis and bowel distension.

7. SMA thrombosis or embolism – may present with pain radiating to one side; the signs are an enlarged vessel, perivascular stranding and high-attenuation material within the vessel caused by clotted blood.

8. Intraperitoneal and retroperitoneal haemorrhage – trauma-related, spontaneous haemorrhage is usually related to use of anticoagulants, also in bleeding diatheses, vasculitis (polyarteritis nodosa), splenic rupture and certain neoplasms.

9. Musculoskeletal pain