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4. Primer / Mankad & Hoey > 4.1 Renal > Flashcards

4.1 Renal Flashcards

1
Q

Renal Embryology

A

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

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2
Q

US Medulla Cortex

A

Renal medulla hypoechoic to cortex

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3
Q

Renal Mass CT protocol

A 
Noncontrast
Corticomedullary phase (25-30 seconds)
Nephrographic phase (80 seconds)
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4
Q

Location Septum of Bertin

A

90% upper pole, 60% bilateral

Associated with bifid renal pelvis

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5
Q

Congenital megacalyces

A

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

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6
Q

Pyelocalcyceal Diverticulum Types

A

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

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7
Q

ADPKD

A 
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
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8
Q

Acquired cystic kidney disease

A

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%

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9
Q

Bosniak criteria

A
  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
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10
Q

Medullary cystic disease

A

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

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11
Q

Causes of Nephrocalcinosis

A

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

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12
Q

Medullary sponge kidney

A

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,

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13
Q

RCC Types

A

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%)

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14
Q

Oncocytoma

A

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

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15
Q

Staging RCC

A

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%))

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16
Q

Renal lymphoma

A

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)

17
Q

Renal metastases

A

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

18
Q

Angiomyolipoma

A

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

19
Q

Tuberous sclerosis

A

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%)

20
Q

Renal adenoma

A

Solid lesion < 3 cm

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

21
Q

Renal Pelvis Tumours

A

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)

22
Q

TCC of Upper Renal Tract

A

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)

23
Q

Indications for partial nephrectomy

A

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

24
Q

Von Hippel Lindau

A

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

25
Q

GU Tuberculosis

A

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

26
Q

GU Tuberculosis Imaging features

A

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

27
Q

Emphysematous pyelonephritis

A 
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
28
Q

Xanthogranulomatous pyelonephritis

A

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)

29
Q

Renal papillary necrosis and causes

A

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

30
Q

Renal Trauma Categories

A

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

31
Q

Renal Haemorrhage

A

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

32
Q

Renal infarction

A

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)

33
Q

Renal vein thrombosis

A

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

34
Q

Acute Cortical Necrosis Definition, Causes

A

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)
35
Q

Renal artery stenosis

A

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

36
Q

Renal Transplant Complications

A

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

37
Q

Causes of perirenal fluid collections post-transplant

A

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

4. Primer / Mankad & Hoey (8 decks)

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