Adrenals, urinary tract, testes and prostate

Functioning tumours

• 1.

  Conn's adenoma —accounts for 70% of Conn's syndrome. Usually small, homogeneous, relatively low density due to cholesterol content. 30% of Conn's syndrome is due to bilateral hyperplasia, which can occasionally be nodular and mimic an adenoma. Note that functioning and nonfunctioning adenomas are essentially indistinguishable on imaging, although functioning adenomas tend to be smaller and are more likely to be lipid-rich.

• 2.

  Phaeochromocytoma —usually large (>5 cm) with avid contrast enhancement ± central necrosis/haemorrhage (NB: it is safe to administer IV iodinated CT contrast). Often markedly T2 hyperintense on MRI. Rule of tens: 10% malignant, 10% bilateral, 10% ectopic—of these 50% are located around the kidney, particularly the renal hilum (if not seen on CT, MIBG isotope scan may be helpful). 10% show calcification. 10% are multiple and usually part of MEN 2A/B syndrome, NF1, tuberous sclerosis or vHL.

• 3.

  Cushing's adenoma —accounts for 10% of Cushing's syndrome. Usually >2 cm. 80% of Cushing's syndrome is due to excess ACTH from a pituitary adenoma (Cushing's disease) or ectopic source (small cell carcinoma, carcinoid, pancreatic NET, phaeochromocytoma, medullary thyroid carcinoma) with resultant adrenal hyperplasia. 10% of Cushing's syndrome is due to adrenal carcinoma. The differentials for an adrenal mass in Cushing's syndrome are:

  • (a)

    Functioning adenoma/carcinoma—atrophy of the contralateral adrenal is suggestive.

  • (b)

    Coincidental nonfunctioning adenoma—both adrenals may be hyperplastic (due to excess ACTH).

  • (c)

    Metastasis from small cell primary.

  • (d)

    Bilateral nodular hyperplasia—see Section 9.2 .

• 4.

  Adrenal carcinoma —rare, usually large (>5 cm). Functioning tumours (<50%) may present with Cushing's, virilization, feminization or rarely Conn's, and are more common in women.

Malignant tumours

• 1.

  Metastases —often bilateral, usually >2 cm, irregular outline with patchy contrast enhancement. Common sources include lung, breast, renal and GI tract. Metastases from melanoma and RCC are usually hypervascular and may mimic phaeochromocytoma. Recent haemorrhage into a vascular metastasis can produce patchy high attenuation on unenhanced CT. In patients without a known extraadrenal primary tumour, the vast majority of adrenal masses are benign; in the presence of a known primary malignancy 26-36% of adrenal lesions are metastatic.

• 2.

  Carcinoma —rare, aggressive. Typically a large (>5 cm), irregular, heterogeneously enhancing mass with central necrosis/haemorrhage ± foci of calcification and nodal, metastatic and/or intravenous spread. May invade the adjacent kidney, making it difficult to distinguish from an advanced RCC. Nonfunctioning tumours (>50%) are more common in men and present at a larger size than functioning tumours.

• 3.

  Lymphoma *—usually secondary in the presence of retroperitoneal nodal disease. Unilateral or bilateral adrenal masses/diffuse enlargement + mild homogeneous enhancement.

• 4.

  Neuroblastoma —very rare in adults. Usually large (>5 cm), ill-defined and heterogeneous + calcification. Commonly surrounds and displaces vessels (e.g. aorta and IVC) without causing significant narrowing. Metastases are common at presentation.

• 5.

  Sarcoma —e.g. angiosarcoma, leiomyosarcoma. Very rare. Nonspecific appearances: aggressive, irregular, heterogeneously enhancing mass.

Benign

• 1.

  Nonfunctioning adenoma —very common. Usually small (50% <2 cm), homogeneous and well-defined. If lipid-rich, will have unenhanced CT attenuation <10 HU and will drop signal on out-of-phase T1-weighted MRI.

• 2.

  Myelolipoma —benign tumour composed of fat and haemopoietic tissue. Characteristic appearance on CT: discrete mass containing soft tissue and macroscopic fat (<−20 HU) ± calcification. On MRI the fatty component will drop signal on fatsat sequences. If large, may be hard to differentiate from retroperitoneal liposarcoma and exophytic renal AML. Nearly all are found in the adrenal, but extraadrenal tumours (presacral, perirenal, retroperitoneum, mediastinum, liver, stomach, omentum) can occur.

• 3.

  Adrenal haemorrhage —hyperattenuating mass on unenhanced CT with surrounding fat stranding. Occurs in 25% of severe trauma (usually unilateral, R>L), but can also occur in vascular masses (e.g. phaeochromocytoma, metastases), coagulopathies and severe stress (e.g. surgery, sepsis, burns, pregnancy, hypotension—often bilateral).

• 4.

  Cyst —round, well-defined, water density, nonenhancing. May contain thin septa ± mural calcification. Pseudocysts due to previous haemorrhage > true cysts. Beware of cystic tumours (e.g. some phaeochromocytomas)—look for nodular wall thickening. If multiloculated, consider lymphangioma and hydatid cyst in the differential.

• 5.

  Granulomatous disease —e.g. TB, histoplasmosis. More commonly bilateral, see Section 9.2 .

• 6.

  Haemangioma —rare. Often contains phleboliths. Typically demonstrates peripheral nodular enhancement ± partial infilling on delayed phase. Central fibrotic scar usually does not enhance. Peripheral nonfibrotic component is usually markedly T2 hyperintense. May mimic phaeochromocytoma.

• 7.

  Ganglioneuroma —rare, occurs in children or young adults. Benign counterpart of neuroblastoma, arises from sympathetic ganglia. Well-defined, often shows heterogeneous delayed enhancement. Heterogeneously T2 hyperintense on MRI ± whorled appearance. Calcification is common.

• 8.

  Other very rare lesions —adrenal lipoma, teratoma and angiomyolipoma can mimic myelolipoma due to macroscopic fat content (a fat–fluid level suggests teratoma). Schwannomas may be cystic ± calcification. Solitary fibrous tumours, leiomyomas, oncocytomas and inflammatory pseudotumours have also been rarely reported in the adrenals and present as a nonspecific solid heterogeneously enhancing mass.

• 9.

  Pseudolesions —e.g. exophytic renal/hepatic/pancreatic mass, gastric diverticulum, splenunculus, retroperitoneal varices. These can occasionally mimic an adrenal mass but IV/oral contrast and coronal reconstructions will nearly always clarify the diagnosis.

Anomalies of position

All malpositioned kidneys are malrotated. Most commonly malrotation occurs around the vertical axis with collecting structures positioned ventrally.

• 1.

  Ectopic kidney —typically sited caudal to usual site. A pelvic kidney is due to failure of renal ascent. Blood supply is from the iliac artery or aorta. Most ectopic kidneys are asymptomatic, although pelvic kidneys are more susceptible to trauma, reflux, stone formation, PUJ obstruction and infection, and may complicate natural childbirth later in life. Rarely, a kidney may herniate through a Bochdalek hernia during its ascent, giving rise to an intrathoracic kidney.

Anomalies of form

These are associated with an increased risk of reflux, infection, stone formation, PUJ obstruction and other congenital anomalies (e.g. VACTERL association; see Part 2 ).

• 1.

  Horseshoe kidney —two kidneys joined by parenchymal/fibrous isthmus, typically at the lower poles. Ascent is arrested by the inferior mesenteric artery. Most common fusion anomaly (1 in 400 births). Both kidneys are malrotated with the renal pelves and ureters situated anteriorly and renal long axis medially oriented. Associated with many congenital syndromes (e.g. Turner) and an increased risk of malignancy (Wilms, TCC, RCC).

• 2.

  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).

• 3.

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

• 4.

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

Anomalies of number

• 1.

  Unilateral renal agenesis —1 in 1000 live births. Associated with chromosomal abnormalities, VACTERL anomalies, Müllerian duct anomalies (in women) and Zinner syndrome (in men: renal agenesis + ipsilateral seminal vesicle cyst + ejaculatory duct obstruction). Hyperplastic normal solitary kidney—up to twice the normal size.

• 2.

  Bilateral renal agenesis —Potter syndrome. 1 in 10,000 live births. Invariably fatal in first few days of life due to pulmonary hypoplasia secondary to the associated oligohydramnios.

• 3.

  Supernumerary kidney —very rare. Most commonly on left side caudal to normal kidney. May be partially fused with the normal kidney mimicking a duplex kidney, but the two components will have separate arterial and venous supply.

Differential diagnosis

• 1.

  Persistent fetal lobulation —lobules overlie calyces with interlobular septa between the calyces. Normal size 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.

• 1.

  Ischaemia due to renal artery stenosis —ureteric notching (due to enlarged collateral vessels) differentiates this from the other causes in this group. See Section 9.25 .

• 2.

  Radiation nephritis —at least 23 Gy over 5 weeks. The collecting system may be normal or small. Depending on the size of the radiation field, both, one or just part of one kidney may be affected.

• 3.

  End result of renal infarction —due to previous renal artery occlusion or renal vein thrombosis. The collecting system does not usually opacify during excretion urography.

Renal = parenchymal

• 1.

  Congenital hypoplasia —<6 calyces. The pelvicalyceal system is otherwise normal.

• 2.

  Multicystic dysplastic kidney (adult) .

• 3.

  Papillary necrosis —late sequela. See Section 9.23 .

• 4.

  Postinflammatory —following acute diffuse nephritis especially in diabetes.

• 5.

  Following partial nephrectomy.

Postrenal = collecting system

Usually with a dilated collecting system.

• 1.

  Postobstructive atrophy —± thinning of the renal cortex and if there is impaired renal function this will be revealed by poor contrast medium density in the collecting system.

Prerenal = vascular

• 1.

  Arterial hypotension —distinguished by the time relationship to the contrast medium injection and its transient nature.

• 2.

  Generalized arteriosclerosis —normal calyces.

Renal = parenchymal

• 1.

  Chronic glomerulonephritis —normal calyces. Reduced nephrogram density and poor calyceal opacification.

• 2.

  Hereditary nephropathies —e.g. Alport's syndrome.

Postrenal = collecting system

• 1.

  Chronic papillary necrosis —with other signs of necrotic papillae (see Section 9.23 ).

Prerenal = vascular

• 1.

  Acute renal vein thrombosis —enlarged kidney + surrounding oedema + filling defect in the renal vein (best seen on CT). On US the kidney may be hyper- or hypoechoic ± absent Doppler venous flow ± visible thrombus. Echogenic streaks may be seen radiating from the renal hilum (representing thrombosed veins). Most common causes are nephrotic syndrome (in adults) and dehydration/sepsis (in children). Many other causes including intrinsic renal diseases (pyelonephritis, glomerulonephritis, amyloid), hypercoagulable states (pregnancy, OCP, malignancy, thrombophilia), extrinsic compression (by tumour, nodes or RPF), vasculitis, sickle cell disease, trauma, transplant rejection. Beware of tumour thrombus due to renal vein invasion from RCC—this shows enhancement, whereas bland thrombus is nonenhancing.

• 2.

  Acute arterial infarction —well-defined wedge-shaped areas of reduced Doppler flow on US and reduced enhancement on CT. Usually embolic, may be bilateral.

Renal = parenchymal

• 1.

  Duplex kidney —50% are bigger than the contralateral kidney; 40% are the same size; 10% are smaller.

• 2.

  Compensatory hypertrophy —for an atrophic/absent contralateral kidney.

• 3.

  Crossed fused ectopia —see Section 9.4 .

• 4.

  Acute pyelonephritis —impaired excretion of contrast medium ± dense nephrogram. Attenuated calyces but may have nonobstructive pelvicalyceal or ureteric dilatation. Completely reversible within a few weeks of clinical recovery.

• 5.

  Diffuse infiltrative tumour —e.g. lymphoma/leukaemia (usually bilateral).

• 6.

  Malakoplakia —renal involvement may be diffuse causing enlargement.

Postrenal = collecting system

• 1.

  Obstructed kidney —dilated calyces and renal pelvis.

• 2.

  Xanthogranulomatous pyelonephritis —staghorn calculus is typically present with dilated calyces and a contracted renal pelvis (bear's paw appearance) ± distortion of the renal outline and perinephric stranding.

• 3.

  Pyonephrosis —obstructed kidney + echogenic pus in collecting system + urothelial thickening.

Developmental

• 1.

  Bilateral duplex kidneys .

• 2.

  Autosomal recessive polycystic kidney disease * —infantile form. On US, smooth enlarged hyperechoic kidneys with numerous tiny cysts and echobright foci.

Inflammation/oedema

• 1.

  Acute glomerulonephritis —many different causes including Wegener's granulomatosis, microscopic polyangiitis, Goodpasture's syndrome, SLE, HSP, infections, drugs. Renal cortex may be diffusely hyperechoic on US.

• 2.

  Acute tubular necrosis —usually due to hypoperfusion or toxins (e.g. drugs, iodinated contrast, haemolysis, rhabdomyolysis). Hyperechoic (or normal) renal cortex on US. Persistent nephrogram on delayed postcontrast CT.

• 3.

  Acute cortical necrosis —>50% of cases are related to pregnancy (placental abruption, infected abortion, preeclampsia). Other causes include shock, sepsis, trauma, hyperacute transplant rejection, HUS, sickle cell disease, NSAIDs. Enhancing medulla and renal capsule with nonenhancing cortex on CT. Hypoechoic renal cortex on US. Cortical calcification is a late finding.

• 4.

  Acute interstitial nephritis —most commonly an allergic drug reaction. Other causes include autoimmune disease, acute transplant rejection and various infections. Renal cortex may be hyperechoic on US.

• 5.

  Polyarteritis nodosa —microaneurysms of renal artery branches + small renal infarcts.

Deposition of abnormal proteins

• 1.

  Amyloid —secondary > primary amyloid. Kidneys may be enlarged in acute disease ± focal mass lesions. Chronic deposition results in small kidneys ± amorphous calcifications.

• 2.

  Multiple myeloma * —kidneys may be enlarged ± focal masses. Usually in the setting of disseminated skeletal disease.

Neoplastic infiltration

Leukaemia and lymphoma *—usually bilateral.

Miscellaneous

• 1.

  Bilateral hydronephrosis .

• 2.

  Acute renal papillary necrosis (see Section 9.23 ).

• 3.

  Acute uric acid nephropathy/tumour lysis syndrome —massive tumour lysis following chemotherapy results in acute kidney injury due to precipitation of uric acid and calcium phosphate crystals in the renal tubules. Usually occurs in the setting of advanced lymphoma or leukaemia. CT may show enlarged kidneys with acute stone formation and/or milk of calcium in the collecting systems ± obstruction.

• 4.

  Early diabetic nephropathy —renal echotexture is usually normal.

• 5.

  Sickle cell anaemia* —in early disease. The renal pyramids are often echobright on US ± papillary necrosis. The kidneys atrophy in chronic disease.

• 6.

  HIV-associated nephropathy —bilateral enlarged hyperechoic kidneys + urothelial thickening ± effacement of renal sinus fat.

• 7.

  Acromegaly* and gigantism —as part of the generalized visceromegaly. Tall stature, obesity and steroid use can also result in large kidneys with normal echotexture.

Dystrophic calcification due to localized disease

Usually in one kidney or focally in one kidney.

• 1.

  Infections

  • (a)

    Chronic pyelonephritis —focal unilateral/asymmetrical cortical calcification with associated parenchymal scarring. Pyogenic abscesses can rarely calcify.

  • (b)

    Tuberculosis *—variable appearance of nodular, curvilinear or amorphous calcification, usually within dilated calyces or tuberculous abscess → end-stage putty kidney. Typically multifocal with calcification elsewhere in the urinary tract. In the early stage there may be triangular ring-like medullary calcification due to papillary necrosis. The urogenital tract is the second commonest site of involvement after the lungs.

  • (c)

    Xanthogranulomatous pyelonephritis —large obstructive calculus in 80% of cases.

  • (d)

    Hydatid —the cyst is usually polar and calcification is curvilinear or heterogeneous. 50% of echinococcal cysts calcify.

• 2.

  Tumours —e.g. RCC, Wilms tumour, TCC, metastasis.

• 3.

  Cysts —rim/septal calcification, usually related to previous infection or haemorrhage. Common in ADPKD.

• 4.

  Vascular —e.g. in a chronic perinephric haematoma, or curvilinear calcification in atherosclerotic/aneurysmal renal arteries.

Calcium-containing

75% are calcium oxalate/phosphate. Usually very dense (up to 1700 HU on CT). Causes include:

• 1.

  With normocalcaemia —obstruction, UTI, prolonged bed rest, dehydration, congenital renal anomalies (e.g. horseshoe kidney), calyceal/bladder diverticula, Cushing's syndrome, type 1 renal tubular acidosis, medullary sponge kidney, idiopathic hypercalciuria.

• 2.

  With hypercalcaemia —hyperparathyroidism, milk-alkali syndrome, excess vitamin D, sarcoidosis, idiopathic infantile hypercalcaemia.

Pure calcium oxalate

Due to hyperoxaluria. Can lead to oxalosis (deposition of oxalate in extrarenal organs) if untreated.

• 1.

  Secondary hyperoxaluria —mainly in patients with Crohn's disease, small bowel resection, high vitamin C intake or chronic renal failure/dialysis.

• 2.

  Primary hyperoxaluria —rare, autosomal recessive, typically presents in childhood. Radiologically: cortical and medullary nephrocalcinosis (generally diffuse and homogeneous), recurrent renal stones, dense vascular calcification, osteopenia or renal osteodystrophy and abnormal metaphyses (dense/lucent bands).

Struvite

Account for 15% of calculi overall, and 70% of staghorn calculi. Caused by urease-producing bacterial UTI (e.g. Proteus , Klebsiella , Pseudomonas , Enterobacter —not E. coli ); more common in women.

Cystine

Due to inherited cystinuria, presents in younger patients. Stones are usually <550 HU on CT, often large in size (may be staghorn) and homogeneous in density.

Uric acid

Usually <500 HU on CT, typically form in acidic urine. Causes include:

• 1.

  With hyperuricaemia —gout, myeloproliferative disorders and tumour lysis syndrome.

• 2.

  With normouricaemia —idiopathic or associated with acidic, concentrated urine, e.g. in hot climates and in chronic diarrhoea (including ileostomy patients).

Xanthine

Rare, due to xanthinuria, which may be primary (hereditary xanthinuria) or secondary (due to allopurinol). Stones are radiolucent on plain film but radiopaque on CT.

Stones radiolucent on CT (soft-tissue attenuation)

Rare. Suspect in patients with ureteric obstruction without a visible cause on unenhanced CT. CT urography will show the stone as a filling defect.

• 1.

  Protease inhibitors, e.g. Indinavir —used in HIV treatment. Most common medication-induced calculus—other causes include sulphonamides, ciprofloxacin, ephedrine, guaifenesin.

• 2.

  Matrix —mainly composed of mucoproteins. Tend to occur in patients with a history of UTIs, renal stones or proteinuria on dialysis.

Nonstone genitourinary

• 1.

  Pyelonephritis —asymmetric perinephric stranding or mild renal enlargement. Mild disease may have no signs on unenhanced CT. Post IV contrast, pyelonephritis may be seen as a focal region of low attenuation or a more widespread striated enhancement of the kidney. Renal or perinephric abscesses are rare sequelae.

• 2.

  Congenital PUJ obstruction —hydronephrosis with a sudden transition to normal at the PUJ without a visible cause on CT.

• 3.

  Ureteric obstruction by any other cause .

• 4.

  Cystitis .

• 5.

  Renal neoplasm —e.g. RCC, TCC.

• 6.

  Perinephric/subcapsular haemorrhage —if no history of trauma or coagulopathy, consider the possibility of an underlying tumour.

• 7.

  Renal infarction or renal vein thrombosis —difficult to appreciate on unenhanced CT. Perinephric stranding may be the only visible sign. Acute thrombus within the renal vein may appear hyperattenuating compared to flowing blood in the IVC.

Gynaecological

• 1.

  Adnexal masses —most commonly ovarian cysts (usually haemorrhagic), tuboovarian abscesses, dermoid cysts, endometriomas and ovarian neoplasms.

• 2.

  Cervical cancer —which may involve the distal ureters.

• 3.

  Degenerating or torted fibroids .

• 4.

  Ectopic pregnancy .

Gastrointestinal

• 1.

  Appendicitis —if pain is right-sided.

• 2.

  Diverticulitis —usually left-sided. Meckel's diverticulitis may occur on either side.

• 3.

  Abdominal hernias —particularly inguinal.

• 4.

  Fat necrosis —e.g. epiploic appendagitis (usually left-sided) or omental infarction (usually right-sided).

• 5.

  Other bowel pathology — e.g. obstruction, intussusception, ischaemia, IBD or tumour.

Pancreatic and hepatobiliary disorders

• 1.

  Gallstones .

• 2.

  Pancreatitis and pancreatic tumours .

Vascular

• 1.

  Renal artery aneurysm .

• 2.

  Ruptured abdominal aortic aneurysm —a crescent-shaped area of high attenuation (> intraluminal blood) in the wall of an AAA on unenhanced CT is a sign of impending rupture. Periaortic stranding or haemorrhage (>60 HU) indicates active bleeding.

• 3.

  Aortic dissection —high attenuation in the aortic wall on unenhanced CT indicates intramural haematoma. Displacement of intimal calcification into the aortic lumen and/or renal infarction may be seen.

• 4.

  SMA thrombosis, embolism or dissection —pain may radiate to one side. Difficult to appreciate on unenhanced CT, may see vessel enlargement, perivascular stranding, high-attenuation blood clot within the vessel or displacement of intimal calcification (in the case of dissection) + signs of bowel ischaemia.

• 5.

  Intraperitoneal and retroperitoneal haemorrhage —e.g. due to trauma, anticoagulants, coagulopathy, vasculitis (PAN), splenic rupture and certain neoplasms.

• 6.

  Rectus sheath haematoma —hyperattenuating compared with normal muscle on unenhanced CT. Usually due to anticoagulants/coagulopathy.

Musculoskeletal

• 1.

  Mechanical low back pain .

• 2.

  Osteoporotic fracture —usually in the elderly.

• 3.

  Bone metastases and myeloma .

• 4.

  Psoas haematoma .

• 5.

  Discitis —difficult to appreciate on unenhanced CT. May see endplate irregularity and fat stranding adjacent to a disc.

Medullary (pyramidal)

The first three causes account for 70% of cases.

• 1.

  Medullary sponge kidney —developmental anomaly causing cystic dilatation of the small collecting ducts in the medullary pyramids; may involve a variable portion of one or both kidneys. The dilated tubules fill with contrast during an IVU, giving a characteristic ‘paintbrush’ appearance to the pyramids. The tubules may contain small calculi, giving rise to medullary nephrocalcinosis—this usually manifests as focal or asymmetrical clusters of punctate calcification. Kidneys may be enlarged or normal in size. Echobright medullary pyramids on US (even without calcification). MRI may show cystic nature of pyramids on T2 sequences. Associated with Caroli disease of the liver.

• 2.

  Hyperparathyroidism * —usually bilateral and symmetrical, diffuse rather than punctate.

• 3.

  Renal tubular acidosis (type 1) —most common cause in children, may be associated with osteomalacia or rickets. Calcification tends to be more severe and confluent than in other causes; typically bilateral and symmetrical. Kidneys are usually of normal size.

• 4.

  Renal papillary necrosis —calcification of necrotic papillae. Usually asymmetrical. See Section 9.23 .

• 5.

  Causes of hypercalcaemia or hypercalciuria —e.g. malignancy (bone metastases, myeloma, paraneoplastic syndromes), sarcoidosis, hypervitaminosis D, milk-alkali syndrome and idiopathic hypercalciuria.

• 6.

  Preterm neonates —in up to two-thirds. Risk factors include extreme prematurity, severe respiratory disease, gentamicin use, and high urinary oxalate and urate excretion. Echobright medullary pyramids on US, typically bilateral and symmetrical. The majority resolve spontaneously by midchildhood. Main differential in this patient group is papillary necrosis, which also produces echobright medullary pyramids but is usually asymmetrical and results in sloughing of papillae within weeks.

• 7.

  Hyperoxaluria —typically causes diffuse cortical and medullary nephrocalcinosis as well as nephrolithiasis. Primary form presents in childhood.

Cortical

• 1.

  Acute cortical necrosis —classically ‘tramline’ calcification, occurs in the chronic phase.

• 2.

  Chronic glomerulonephritis —bilateral curvilinear or punctate cortical calcification.

• 3.

  Chronic infection —multifocal nodular cortical calcification can occur with HIV-related renal infections, e.g. Pneumocystis jirovecii , Mycobacterium avium complex (MAC) and CMV.

• 4.

  Chronic renal transplant rejection —due to cortical necrosis.

• 5.

  Hyperoxaluria —typically causes diffuse cortical and medullary nephrocalcinosis.

• 6.

  Alport syndrome —rare inherited disorder (most commonly X-linked), presents in adolescence or early adulthood with progressive renal failure and deafness. Renal calcification can look identical to hyperoxaluria.

Renal dysplasia

• 1.

  Multicystic dysplastic kidney —due to ureteric atresia during early fetal life; usually diagnosed antenatally. Multiple cysts replace the kidney with intervening echobright dysplastic tissue (no functioning renal tissue). Typically involutes over time. Associated with contralateral PUJ obstruction (PUJO) and reflux. Typically involves the whole kidney but can rarely be segmental (in the case of a duplex kidney with antenatal atresia of only one ureter), thereby mimicking a multiloculated cystic mass.

• 2.

  Localized cystic renal disease —a nonencapsulated cluster of variable-sized cysts replacing part of one kidney. May occasionally involve the entire kidney but is always unilateral.

Polycystic kidney disease*

• 1.

  Autosomal recessive polycystic kidney disease *—presents antenatally or in infancy/childhood. Bilateral enlarged echogenic kidneys with multiple microcysts, most of which are too small to resolve individually (often seen as tiny echobright foci). See Part 2 for other features and associations.

• 2.

  Autosomal dominant polycystic kidney disease *—usually presents in adulthood (or earlier if undergoing screening). Enlarged kidneys with numerous cysts of varying sizes. See Part 2 for other features and associations.

Cystic tumours

• 1.

  Multilocular cystic nephroma —nonhereditary, benign. Usually presents in young children (not neonates) or middle-aged women. Multilocular cystic mass with a fibrous capsule. Linear septal and capsular enhancement is often seen on CT/MRI, but nodular enhancement should not be present. Cannot be reliably differentiated from cystic RCC.

• 2.

  Multilocular cystic RCC —5% of RCCs are cystic (variant of clear cell RCC). Nodular components on imaging suggest RCC.

• 3.

  Mixed epithelial and stromal tumour —rare, typically seen in perimenopausal women particularly those taking OCP/hormone replacement therapy. Complex multiloculated cystic mass on imaging, often with enhancing nodular components ± calcification. Indistinguishable from cystic RCC on imaging.

• 4.

  Angiomyolipoma with epithelial cysts —rare cystic variant of AML. Indistinguishable from cystic RCC on imaging.

• 5.

  Primary renal sarcoma —e.g. leiomyosarcoma, angiosarcoma. Rare and aggressive, usually solid but can occasionally be predominantly cystic with enhancing nodular components.

• 6.

  Cystic Wilms tumour —extremely rare in adults.