4.1 Renal

Question 1

Renal Embryology

Answer 1

Kidneys form from pro-, meso- and metanephros; first two regress and only latter persists
Ureteric bud from outgrowth of mesonephric duct
Form in sacrum and migrate caudally by 8 weeks gestation; maturation continues to 5 y/o

Question 2

US Medulla Cortex

Answer 2

Renal medulla hypoechoic to cortex

Question 3

Renal Mass CT protocol

Answer 3

Noncontrast
Corticomedullary phase (25-30 seconds)
Nephrographic phase (80 seconds)

Question 4

Location Septum of Bertin

Answer 4

90% upper pole, 60% bilateral

Associated with bifid renal pelvis

Question 5

Congenital megacalyces

Answer 5

Excess of enlarged calyces (20-25 vs normal 10-14), causing hypoplastic pyramids
No obstruction, normal renal parenchyma and function

Question 6

Pyelocalcyceal Diverticulum Types

Answer 6

Outpouching of calyx into corticomedullary region; usually asyptomatic but may cause calculi
Type 1: from minor calyx
Type 2: from infundibulum
Type 3: from renal pelvis

Question 7

ADPKD

Answer 7

Cystic dilatation of collecting tubules and nephrons; 0.1% population, 10% dialysis patients, strong penetrance
Hepatic cysts (70%), intracranial berry aneurysms (20%), pancreatic and splenic cysts  60 y/o

Question 8

Acquired cystic kidney disease

Answer 8

Multiple renal cysts developed in CRF; occur in 90% patients on dialysis
3-5 cysts in each kidney, CRF and no history of inherited cystic disease
Hemorrhagic cysts occur in 50%, can rupture
RCC develops in 7%

Question 9

Bosniak criteria

Answer 9

1. Benign simple cyst, don’t communicate with collecting system
2. Minimally complicated, benign but with concerning features
   Thin septations (20)
   2F. Multiple septa with or without perceptible but not measurable enhancement; can have thick or nodular calcification, also included if hyperattenuating and >3 cm
3. Complicated, multiloculated but with malignant features.
4. Clearly malignant with large cystic component

Question 10

Medullary cystic disease

Answer 10

Due to tubulointerstitial fibrosis
Presents with anaemia and renal failure
Small kidneys with multiple small medullary cysts, often merely causes medullary increased echogenicity, thinned cortex
Three types
Familial nephronophthisis (70%): AR, juvenile onset at 3-5 years but also adult type
Adult medullary cystic disease (15%): AD inheritance
Renal retinal dysplasia (15%): recessive, associated with retinitis pigmentosa

Question 11

Causes of Nephrocalcinosis

Answer 11

Metastatic (normal kidneys), dystrophic (injured tissue) or urine stasis
Hyperparathyroidism (primary and secondary)
Metastatic carcinoma to bone and hypercalcaemia of malignancy
Prolonged immobilisation
Sarcoidosis
Milk alkali syndrome
Hypervitaminosis D
RTA (often dense medullary calcification)
Medullary sponge kidney (urine stasis)
Hyperoxaluria
Bartter’s syndrome
Prolonged frusemide (usually premature infants)
Nephrotoxic drugs
Papillary necrosis

Question 12

Medullary sponge kidney

Answer 12

AKA Benign renal tubular ectasia, Cacchi-Ricci disease
Dysplastic cystic dilatation of papillary / medullary portions of collecting ducts, usually 20-40 y/o
75% bilateral, often asymptomatic; 10% develop progressive renal failure
IVP - striated nephrogram (brushlike), ‘bunch of flowers’ appearance
Associations: Hemihypertrophy, Beckwith-Wiedemann, Pyloric stenosis, Ehlers Danlos, RTA, any form of renal cystic disease / ectopia,

Question 13

RCC Types

Answer 13

Best evaluated in nephrographic phase, venous invasion best characterised by MRI
US: 70% hyperechoic if > 3 cm, 30% if < 3 cm

Clear cell (65%) - proximal tubule
Papillary (15%) - chromophil, proximal tubule
Chromophobe (10%) - intercalated cell of cortical collecting duct
Oncocytoma (5%)
Unclassified (5%)

Question 14

Oncocytoma

Answer 14

From epithelial cells of proximal tubule, usually well-differentiated and benign but need resection
Central stellate scar (25-33% on CT) and spoke wheel (angiography), usually homogeneous enhancement, can’t differentiate from RCC on imaging, but FNA can discriminate

Question 15

Staging RCC

Answer 15

I: kidney only
II: extrarenal ± adrenal involvement, but confined within Gerota’s fascia
III: A - renal vein, B - lymph node metastases, C - both
IV: A - direct extension to other organs through Gerota’s fascia; B - metastases (lung (55%) > liver > bone > adrenal > contralateral kidney (10%))

Question 16

Renal lymphoma

Answer 16

Occurs in 8% lymphoma patients, 75% bilateral, NHL > HL.
Characteristically, renal vessels remain patent despite encasement
MR: hypointense to cortex on T1W, heterogeneously hypo to isointense on T2W
Patterns (five):
Mulitple renal masses (59%)
Solitary mass (3%)
Renal invasion (contiguous RP spread)
Perirenal (10%)
Diffuse renal infiltration (rare)

Question 17

Renal metastases

Answer 17

Fifth most common metastatic site, mainly haematogenous spread
Lung, breast and contralateral kidney
Colonic metastases often solitary and exophytic
Melanoma metastases often have perinephric extension

Question 18

Angiomyolipoma

Answer 18

Benign hamartomas - blood vessels, smooth muscle, fat; DO NOT contain calcification
Can cause pain, haematuria, anaemia
Usually multiple in tuberous sclerosis (80% of TS have AML)
Sporadic form commonest (80-90%): F/M = 4/1, usually middle aged; thus 4 cm often resected / ablated.
Intratumoural fat almost diagnostic (CT or chemical shift), 5% do not contain fat
May extend into renal vein and IVC

Question 19

Tuberous sclerosis

Answer 19

AD, variable penetrance; >50% sporadic
Epilepsy, mental retardation and adenoma sebaceum
Also subependymal nodules, giant cell astrocytoma, peripheral tubers, retinal hamartomas, cardiac rhabdomyomas, lymphangioleiomyomatosis, shagreen patches, subungual fibromas, bone cysts
50% have renal lesions
Bilateral renal cysts
Multiple AMLs are sine qua non of TS (15% patients)
RCC (1-2%)

Question 20

Renal adenoma

Answer 20

Solid lesion < 3 cm

Now considered renal carcinoma (adenocarcinoma) in evolution and treated with partial nephrectomy

Question 21

Renal Pelvis Tumours

Answer 21

Tend to maintain reniform outline of kidney
Inverted Papilloma (No malignant potential, 20% risk of associated urothelial malignancy)
TCC
SCC (5% renal pelvis tumours, <1% all renal tumours)
Collecting Duct Carcinoma (rare, aggressive, possible from distal collecting ducts of Bellini, often infiltrative rather than expansile)

Question 22

TCC of Upper Renal Tract

Answer 22

Often multifocal; 40-80% have bladder TCC but only 3% bladder TCC later develop upper renal tract TCC
10% of upper renal tract neoplasms, 2-4% bilateral, 2-7% calcification
Hyperechoic on US and hyperattenuating on CT
Causes faceless kidney - obliteration of sinus fat and infiltration of parenchyma
Stippling sign on IVP - tracking of contrast interstitially in papillary lesion
Stricturing - thus can mimic renal TB
60% ipsilateral recurrence and 50% have lung metastases
Stage I and II: limited to lamina propria / muscular layer, III: renal parenchyma / adjacent fat, IV: metastatic (usually liver, lung, bones)

Question 23

Indications for partial nephrectomy

Answer 23

Solitary RCC <7 cm confined to kidney
RCC in solitary kidney
Significant risk of later CRF

Question 24

Von Hippel Lindau

Answer 24

AD, almost 100% penetrance
Usually renal cysts
25-40% develop clear cell RCC (often 30-40 y/o), often synchronous / metachronous; often screen from 20’s.
Also have pancreatic cysts (30%), islet cell tumours, phaeochromocytomas (10%, often multiple and ectopic, 50-80% bilateral), retinal angiomas, ANS haemangioblastomas
More rarely endolymphatic sac tumours, cystadenomas of epididymis, broad ligament cysts

Question 25

GU Tuberculosis

Answer 25

Second most common site of TB, usually haematogenous spread, may be asymptomatic Active / healed pulmonary TB in 50% 50% calcification (amorphous granular if active, dense punctate if healed tuberculomas - putty kidney) Usually bilateral asymmetrical involvement, 25% unilateral Tubercles become cavities, communicating with calyces, which then stricture, can cause autonephrectomy Can cause epididymitis, hydrocoele, testicular mass, prostatitis, female infertility

Question 26

GU Tuberculosis Imaging features

Answer 26

Kidneys - Smudged papillae, moth-eaten calyx, 'hiked-up' pelvis - cephalad retraction of infero-medial margin of pelvis at PUJ Ureters - Usually unilateral, beaded corkscrew appearance (alternating scarring & dilatation), aperistaltic and shortened (pipestem) Bladder - Chronic interstitial cystitis causing fibrosis; Small, trabeculated, VU reflux, wall rarely calcified Prostate - Dense calcification

Question 27

Emphysematous pyelonephritis

Answer 27

``` Usually diabetic & E Coli (gas forming gram negatives) infection, occasionally non-DM with obstruction Best diagnosed on CT, often requires nephrectomy if severe Type 1 (pyelonephritis): Destruction > one third renal parenchyma, 70% mortality, gas in parenchyma Type 2 (pyelitis): Destruction < one third parenchyma, 20% mortality, renal/perirenal collection with gas in collecting system ```

Question 28

Xanthogranulomatous pyelonephritis

Answer 28

Replacement of renal parenchyma by lipid laden macrophages, begins in pelvis and extends to cortex and medulla Multiple low attenuation (-10 to 30 HU) xanthomatous masses (may show fine calcifications, thin rim of peripheral enhancement) ± thickened Gerota's fascia ± psoas abscess Chronic indolent bacterial infection, usually E Coli or Proteus; 10% diabetic, typically middle aged females 90% diffuse, 10% focal Absent / decreased contrast excretion on affected side 75% due to staghorn calculus; 25% due to PUJ obstruction or tumour May lead to replacement lipomatosis (severe parenchymal atrophy)

Question 29

Renal papillary necrosis and causes

Answer 29

Ischaemic coagulative necrosis of pyramids / medullary papillae; chronic tubulointerstitial nephropathy; predominantly affects medulla Gradual development of cleft in papilla ± sloughing ± rimlike calcification 'Lobster claw' initially, then 'ring sign' around sequestered sloughed papilla, ultimately calyceal blunting after necrosis and absorption Causes (due to ischaemic and/or infective necrosis) DM Analgesia Sickle cell Pyelonephritis Renal vein thrombosis Tuberculosis Obstructive uropathy

Question 30

Renal Trauma Categories

Answer 30

80% blunt trauma, 20% penetrating Absence of haematuria does not preclude serious renal injury I (75-85%): Contusions, small lacerations with no communication with collecting system (includes isolated subcapsular and perinephric haematomas, conservative management II (10%): Laceration through cortex ± urine extravasation; may be managed conservatively III (5%): Multiple deep lacerations with renal pedicle injury IV (rare): PUJ avulsion / laceration of renal pelvis

Question 31

Renal Haemorrhage

Answer 31

Suburothelial - thickened wall of pelvis / proximal ureter due to blood Subcapsular - recent blood is higher attenuation than parenchyma, kidney flattened with elevated capsule, eventually may calcify; if large and chronic may cause hypertension (Page kidney) Perinephric - usually extends below renal margin

Question 32

Renal infarction

Answer 32

Due to RA thrombosis or embolism, vasculitis, trauma, sickle cell, aortic dissection Renal Artery Occulsion may present with Severe flank pain, haematuria, albuminuria, leukocytosis, fever, tender renal mass; or may be asymptomatic Types Global: Non-enhancing kidney, high density capsular rim (collateral perfusion) Large branch occlusion: Wedge shaped defect, base on capsule, apex towards hilum, ± cortical rim enhancement Small vessel occlusion (emboli, vasculitis, sickle cell): Multiple, often bilateral infarcts, 'slit-like' in sickle cell, may show cortical rim enhancement (unlike pyelonephritis)

Question 33

Renal vein thrombosis

Answer 33

Causes smooth, swollen kidney with variable contrast excretion (can be dense nephrogram) ± occluded collecting system Can cause cortical rim sign; varices may indent pelvis / ureter CT: prolonged corticomedullary differentiation, characteristic fine linear densities extending from kidney to perirenal space, enhance post contrast US: Initially hypoechoic, then hyperechoic at 10 days due to cellular infiltrates / fibrosis; in late phase (several weeks) small hyperechoic kidney with loss of corticomedullary differentiation If complete acute occlusion, can cause infarction Causes: Malignant (extrinsic compression or direct extension) Primary renal disease (membranous GN commonest, SLE, amyloid) Secondary from IVC thrombosis Infants: sickle cell, haemoconcentration (diarrhoea, sepsis), hypoxia in congenital heart disease, maternal diabetes

Question 34

Acute Cortical Necrosis Definition, Causes

Answer 34

Pathological progression of ATN; Ischaemic cortical necrosis with medullary sparing; usually bilateral Acute: unenhanced cortex between enhancing medulla and enhancing cortical rim Chronic: small smooth kidneys, may show cortical calcification ``` Causes (60% ischaemia, 40% nephrotoxins): Haemorrhage (classically 3rd trimester) Septic abortion Trauma with shock Severe dehydration Haemolytic uraemic syndrome Acute aortic dissection Transfusion reaction Toxins (including snake venom) ```

Question 35

Renal artery stenosis

Answer 35

Causes: atherosclerosis (90%; narrows ostium or proximal 2 cm of RA), FMD (mid-distal RA, 'string of beads') Causes 1-5% HTN in young adults CECT: Prolonged CMD implies significant stenosis CEMRA: Highly sensitive in proximal RAS Angiography: Gold standard, but can't assess haemodynamic significance of lesion US: Peak systolic velocity > 150 cm/s, acceleration time > 0.07 s (parvus et tardus waveform), post-stenotic spectral broadening / flow reversal

Question 36

Renal Transplant Complications

Answer 36

ATN (normal flow, reduced excretion) - rarely occurs > 1 month post transplant Rejection (Resistive index >0.7 ([systolic-diastolic]/systolic, nonspecific), 90% show increased size (but normally decreased if chronic); thickened cortex; large renal pyramids with indistinct CM junction, focal hypechoic areas in cortex / medulla (20%), increased cortical echogenicity (15%)); hyperacute rejection shows decreased flow but delayed excretion Cyclosporine toxicity - similar pattern to ATN but later post-transplant, rare within first month Arterial occlusion (87% success of angioplasty for anastomotic stenosis) Venous occlusion (RVT normally occurs in first 3 days post transplant) Urinary leak Urinary obstruction

Question 37

Causes of perirenal fluid collections post-transplant

Answer 37

Lymphocoele (10-20% at 1-4 months post transplant; usually inferomedial to kidney and linear septations present in 80%) Abscess (usually develops within weeks) Urinoma (develops in first month, generally near VUJ, may be cold on nuclear medicine if not active) Haematoma