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04. RCC (937) > Renal Cell Carcinoma > Flashcards

Renal Cell Carcinoma Flashcards

1
Q

What limitation does an MRI have when investigating kidney tumours?

A

It can not be used to evaluate the chest. CT is needed for that.

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2
Q

What are the most common types of kidney tumours?

A

Renal cell carcinoma ~90%
Oncocytoma ~5%
Angiomyolipoma ~2-3%

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3
Q

What types of renal cell carcinomas are they and how common are they?

A

Clear cell 85%
Papillary 10%
Chromophobe 5%

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4
Q

Should you perform a biopsy before deciding on active surveillance of a small renal mass?

A

No

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5
Q

How often is an oncocytoma mis-diagnosed when a biopsy is performed?

A

In 35,4% of the cases

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6
Q

How do you differentiate between an onocytoma and RCC?

A

Imaging characteristicts are unreliable
Biopsy only gives the right diagnosis in 64,6% of the cases
= there is no reliable way

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7
Q

At what size can you consider intervention of an angiomyolipoma?

A

> 4 cm though the evidence is weak

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8
Q

Bosniak I

A

Simple cyst

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9
Q

Bosniak II

A

Mildly complex benign cyst

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10
Q

Bosniak IIF

A

Moderately complex cyst

Follow-up som are malignant

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11
Q

Bosniak III

A

Indeterminate complex cyst

Over 50% are malignant
Surgery or active surveillance

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12
Q

Bosniak IV

A

Complex cystic mass

most are malignant

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13
Q

How many partial nefrektomies do you have to perform a year for good results (hospital volume)?

A

35-40 cases

18-20 in robot

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14
Q

When resecting a kidney tumour, which tumours do you have to clamp arteries and veins both?

A

Centrally located tumours

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15
Q

In what ways are Ablative therapies better than partial nephrectomies?

A

Less decline of renal function over 6-months

Less decline of renal function at long term follow up

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16
Q

Why is Ablative therapies not recommended when compared to partial nephrectomies?

A

Higher risk of local recurrence

Worse overall survival

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17
Q

What is the benefit of laprascopic radical nephrectomy vs open surgery?

A

Lower morbidity

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18
Q

How does renal cell carcinoma most commonly spread?

A

Haematogenous spread

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19
Q

What is the role of lymph node dissection (LND) in treating renal cancer?

A

LND is not standard

Can be considered in high risk tumours but evidence is weak

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20
Q

When is radical nephrectomy including a thrombectomy indicated?

A

When there is a vena cava thromb and staging is N0M0

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21
Q

After a radical nephrectomy, should you offer adjuvant therapy?

A

No

trials are ongoing if you could offer neadjuvant immunetherapy

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22
Q

What are the most frequent sites for metastases of RCC?

A

Lung 54%
lymph nodes 22%
bone 20%

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23
Q

What is the recurrence of non metastatic RCC?

A

20% inom 5år

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24
Q

When is cytoreductive nephrectomy (CR NE) indicated in Clear cell RCC?

A

Good performance status who do not require systemic therapy

Oligometastases when complete local treatment of the metastases can be achieved

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25
Q

Metastasectomy for RCC is indicated:

A

If complete and a favourable risk profile

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26
Q

What is the result of a complete resection of metastases in mRCC in 5-year cancer specific-survival?

A

74% in pulmonary

33% in extrapulmonary metastases

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27
Q

How do you treat brain or bone metastases of RCC?

A

stereotactic radiotherapy

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28
Q

Can you treat retroperitoneal recurrence of RCC?

A

Aggressive surgical resection offers potential cure in a substantial number of patients with retroperitoneal recurrence

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29
Q

What is a TKI?

A

Tyrosine kinase inhibitor

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30
Q

Give a few examples of Tyrosine kinase inhibitors (TIK:s):

A

Axitinib
Panzopanib
Sorafenib
Sunitinib

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31
Q

Give a few examples of mTOR inhibitors:

A

Temsirolimus

Everolimus

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32
Q

Give an example of a VEGF antibody:

A

Bevacizumab

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33
Q

Give a few examples of a PD-1 inhibitor:

A

Nivolumab

Pembrolizumab

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34
Q

Give a few examples of a PD-L1 inhibitor:

A

Atezolizumab

Avelumab

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35
Q

Give an example of a drug targeting CTLA-4:

A

Ipilimumab

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36
Q

What types of immunotherapy are available for the treatment of RCC?

A 
TKI:s
mTOR inhibitors
VEGF-antibodies
PD-1 inhibitors
PD-L1 inhibitors
drugs targeting CTLA-4
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37
Q

When is cytoreductive nephrectomy (CR NE) indicated in non Clear cell RCC?

A

Indicated if patient is not a MSKCC poor-risk patient

MSKCC Memorial Sloan-Kettering Cancer center classification

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38
Q

Renal Mass Staging: T1a, T1b

A

T1a: < or = 4 cm
T1b: < or = 7 cm

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39
Q

Renal Mass Staging: T2a, T2b

A

T2a: < or = 10 cm
T2b: >10 cm

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40
Q

Renal Mass Staging: T3a

A

T3a: renal vein, pelvicalyceal, perirenal/renal sinus fat within Gerota

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41
Q

Renal Mass Staging: T3b

A

IVC below diaphragm

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42
Q

Renal Mass Staging: T3c

A

VC above diaphragm

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43
Q

Renal Mass Staging: T4

A

Outside of Gerota or involving adrenal

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44
Q

Stage I

A

T1N0M0

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45
Q

Stage II

A

T2N0M0

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46
Q

Stage III

A

T3N0-1M0
T1-2N1M0

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47
Q

Stage IV

A

M1

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48
Q

Postoperative Risk Stratification

A

Low Risk: pT1 and Grade 1-2

Intermediate Risk: pT1 and Grade 3-4, or pT2 and any G

High Risk: pT3 and any G

Very High Risk: pT4 or pN1, sarcomatoid, rhabdoid, macroscopic R1

*Note, positive final margin should increase risk category by one level and increase clinical vigilance

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49
Q

Evaluation of renal mass:
- Imaging?
- Labs?
- CKD?

A

Get multi-phase cross sectional imaging (enhancing = greater that 20 HU)
Consider MRI if suspicion for IVC thrombus
Get CT chest for advanced tumors

If malignancy suspected –> CBC, UA, CMP, chest imaging

Solid or Bosniak 3/4 mass: Use GFR to assign CKD stage I-V
- (90+, 60+, 30+, 15+, <15 or Dialysis)

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50
Q

When to consult nephrology?

A

Consider for eGFR <45, expected postop GFR <30, proteinuria, DM with CKD

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51
Q

When to consult Med Onc?

A

Concerned for potential clinical mets
Incomplete resection

Consider adjuvant treatment for High Risk (T3 and G) or locally advanced, fully resected cancers

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52
Q

When to consult genetics?

A

Recommend for age 46 or less, multifocal/bilateral renal masses, whenever the personal/family history suggests a familial renal neoplastic syndrome

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53
Q

When to perform Renal Mass Biopsy (RMB)?

A

Consider if suspicious for hematologic/metastatic/inflammatory/infectious mass

For solid mass, multiple cores&raquo_space; FNA

PPV ~100%, NPV ~60%, Nondiagnostic ~15%

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54
Q

Partial Nephrectomy:
- When do you prioritize this?
- When do you consider it?
- Surgical considerations?

A

Prioritize PNx: cT1a (when Tx is indicated), cases with solitary kidney, bilateral tumors, familial RCC, multifocal, severe CKD

Consider PNx: young patients, multifocal masses, increased risk for future CKD (HTN, DM, urolithiasis, morbid obesity)

Surgical considerations: minimize warm ischemia time, prioritize negative margins, consider enucleation if familial RCC, multifocal or severe CKD

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55
Q

When is radical nephrectomy preferred over partial nephrectomy?

A

Radical only preferred over partial if:
1. High tumor complexity and pNx would be difficult even in experienced hands
2. No preexisting CKD or proteinuria
3. Normal contralateral kidney and new baseline GFR likely to be >45

Consider radical when oncologic potential is suggested by tumor size, RMB, and/or imaging characteristics

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56
Q

When is Thermal Ablation appropriate? How to follow up?

A

Consider for cT1a <3cm AFTER renal mass biopsy
Radio and cryo are options
Counsel slightly worse outcomes (i.e. local recurrence rates)
Can repeat ablation as needed

Obtain pre and post contrast abdominal imaging within 6 months of ablation, then follow IR postop protocol

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57
Q

When to consider active surveillance? Triggers for intervention?

A

Consider especially for <2cm, repeat imaging in 3-6 months
Consider RMB for mass with solid component
Individualize surveillance based on growth rate and shared decision making (SDM)

Potential triggers for intervention in healthier patients?
- Growth to >3cm
- >5mm/year of growth

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58
Q

Follow-up labs post-op?

A

Cr, UA, eGFR –> refer to nephrology PRN

Consider other labs as needed and if advanced disease expected (CBC, LDH, LFTs, Alk Phos, Ca++)

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59
Q

Abdominal imaging after nephrectomy and partial nephrectomy?

Chest imaging?

A

CT w/ and w/o contrast or MRI for 5 years
Consider switching LR and IR patients to alternating cross sectional imaging and abdominal US

SDM for further imaging after 5 years

LR: yearly for 5 years
IR + TA: 6, 12, 24, 36, 48, 60 (q6m for a year)
HR: 6, 12, 18, 24, 30, 36, 48, 60 (q6m for 3 years)
VHR: 3, 6, 9, 12, 18, 24, 30, 36, 48, 60 (every 3 months for a year, then every 6 months to 3 years, then yearly)

Chest imaging: CXR for LR+IR, CT for HR and VHR
SDM after 5 years

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60
Q

What to do when renal artery vasospasm during hilar dissection?

A

Reduced perfusion
Pale kidney

  1. Reduce insufflation pressure
  2. Apply topical papaverine (opium alkaloid antispasmodic vasodilator) to renal hilar vessels
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61
Q

When to consider when using argon gas laparoscopically?

A

Argon beam will increase abdominal pressure due to addition of argon gas
- Important to vent abdomen via a port to relieve pressure

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62
Q

Interaortocaval nodes only drain the right kidney

A

They drain the left kidney with advanced disease

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63
Q

Incidence of local recurrence after nephrectomy?
What does this mean for 5 year survival?

A

Incidence 2.9%
Poor prognosis: 5 year survival 30%

Synchronous mets at the time of recurrence are an independent predictor of poor prognosis

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64
Q

Hand-assisted lap compared to straight lap?

What does this mean for donor nephrectomies?

A

Hand-assisted lap has higher rates of wound complications (infections and hernias)

In setting of donor nephrectomy, warm ischemia time of donor kidney is reduced because specimen can be quickly removed via hand-port. Other outcomes are similar to straight lap.

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65
Q

Acute bleed following ligation/division of left renal hilum

A

Think about disruption of a lumbar vein, because this inserted into the renal vein posteriorly

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66
Q

Workflow for urine leak after partial nephrectomy

A

Start with perc drain placement if drain not already present
If leak persists, make sure drain isn’t directly on leak site, and take off of suction
Place urethral catheter and do RPG + ureteral stent
If unable to place stent, place PCN

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67
Q

Severe, persistent back pain resistant to pain meds after renal surgery

A

Consider rhabdomyolysis (if pain contralateral to side of surgery, check CK)
Pancreatic injury (if pain is on left following left-sided renal surgery, check amylase and lipase)

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68
Q

Proposed criteria for cytoreductive nephrectomy

A

Ability to resect >75% of the tumor
No brain mets (need to be treated with radiation or surgery prior to cNx)
Adequate pulmonary and cardiac reserve
ECOG performance status of 0-1

(0=Fully active, able to carry on all pre-disease performance without restriction
1=Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature, e.g., light house work, office work)

Predominantly clear-cell histology
Disease has not progressed through systemic therapy (sunitinib)

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69
Q

Vaccinations s/p splenectomy

A

Indicated due to risk of severe infection with encapsulated bacteria

SHiN - Streptococcus pneumoniae, Haemophilus influenzae type b, Neisseria meningitidis

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70
Q

New lesion with early enhancement and prompt washout at prior tumor site after partial nephrectomy

A

Get US with doppler to determine pseudoaneurysm vs. recurrence

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71
Q

RCC tumor thrombus levels

A

0 = renal vein
1 = <2cm into IVC
2 = >2cm into IVC but still below hepatic veins
3 = above hepatic veins but below diaphragm
4 = above diaphragm

3 and 4 may need bypass during sugrery

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72
Q

“Persistent central enhancement”

A

Tumor recurrence after cryoablation

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73
Q

Ways to optimize (lap) renal cryoablation

A

Real-time intraop US to monitor progression of cryo lesion
Cryoprobe tip at deepest margin of tumor
Target temperature below -40C
Extend the cryo lesion ~1cm beyond the margin of the tumor
Active double freeze-thaw cycle

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74
Q

Small renal mass(es) are identified in conjunction with widespread LAD outside of typical LN drainage zones

A

Suspect renal involvement of lymphoma

Perc LN biopsy to determine Tx plan

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75
Q

Renal tumor with high signal on T1 on MRI

A

Fat in lesion
Think AML
Think a/w tuberous sclerosis

AML = benign tumor of perivascular epithelioid cell origin

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76
Q

MRI sequence most likely to confirm AML

A

T2 with fat suppression

On CT, suspect AML if negative HU (fat) are mentioned

Angioembolization often effective, particularly in setting of acute bleed
If massive, will need nephrectomy

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77
Q

Drug that can be used to shrink AMLs

A

Everolimus (Afinitor)
Tumor growth typically resumes when treatment is discontinued

Can watch AMLs when small, can cause problems if >4 cm

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78
Q

Benign tumor in 20yo with elevated peripheral renin

A

Juxtaglomerular tumor
Tumor secretes renin
patients typically <20yo
Cured with surgery

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79
Q

Rare, extremely aggressive tumor associated with sickle cell trait

A

Renal medullary carcinoma

  • Arises from collecting duct
    <100 cases ever
    Mean survival <6 months
    75% on right side
    Central/infiltrative, not amenable to partial
    Does not typically respond to chemo/immunotherapies
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80
Q

Treatment for metastatic renal medullary carcinoma

A

Carboplatin + paclitaxel is first line (not upfront surgical resection)

Gemcitabine + adriamycin is 2nd line

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81
Q

Collecting duct RCC

A

More aggressive –> younger age of presentation

Resistant to standard chemos for RCC, but sometimes responsive to gemcitabine and cisplatin chemos (behave more like UCC)

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82
Q

Renal pseudotumor

A

Column of Bertin
Focal cortical hyperplasia

Best established with DMSA scan

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83
Q

How to follow patients with oncocytoma or indeterminate histology on renal mass biopsy

A

Follow with same imaging protocols used for untreated low risk renal cancers due to risk of substantial growth and risk of inaccurate biopsy results

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84
Q

How to distinguish between oncocytoma and RCC?

A

Technetium-sestamibi nuclear scanning
- oncocytoma will have high radiotracer uptake
- RCC will have low radiotracer uptake

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85
Q

Preferred regimens for relapse or stage IV metastatic CCRCC (favorable and poor/intermediate risk)

A

Pembrolizumab + axitinib - Keynote-426
Nivolumab + cabozantinib - CheckMate-9ER
Pembrolizumab + lenvatinib - CLEAR

Cabozantinib monotherapy (CABOSUN) is a preferred option for poor/intermediate risk

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86
Q

Metastatic RCC sites with worst to best prognosis

A

Brain, liver, bone, LNs, lung, adrenal

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87
Q

What labs do you need to monitor Sunitinib with/for?

A

Associated with hypothyroidism - get thyroid labs

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88
Q

Renovascular fistulae treatment
- If asymptomatic due to biopsy?
- If asymptomatic due to RCC?
- What symptoms do they cause when symptomatic?
- Cirsoid AV fistula?

A
  • If asymptomatic due to biopsy? 70% will close spontaneously, observe
  • If asymptomatic due to RCC? Nephrectomy
  • What symptoms do they cause when symptomatic? HTN, hematuria, high output heart failure. Treat with embo, ligation, partial or complete nephrectomy
  • Cirsoid AV fistula? Cirsoid means to resemble a varix. These are too complex for angioembolization. Treatment of choice is nephrectomy.
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89
Q

Von Hippel Lindau
- Inheritance pattern?
- Manifestations?
- Gene associated?
- Gene location?
- Leading cause of death in VHL?

A
  • Inheritance pattern? AD
  • Manifestations? Hemangioblastomas of retina, cerebellum, medulla (~70%, get brain/spine MRI when diagnosed), cavernous hemangiomas in skin, mucosa and organs, pancreatic masses. About half will develop multiple bilateral RCCs and other tumors associated with deletion of the tumor suppressor gene VHL on 3p
  • Gene associated? (VHL (tumor suppressor gene))
  • Gene location? Short arm of 3p25
  • Leading cause of death in VHL? Kidney cancer

Ipsilateral cysts should be removed at time of partial nephrectomy (when a solid mass is >3 cm) because they can harbor carcinoma

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90
Q

Medication that is FDA approved for treatment of VHL-associated RCC? Mechanism?

A

Belzutifan (HIF-2a inhibitor)

Common side effects include anemia (from reduced epo), and fatugue

When VHL (a TSG) is deleted, causes constitutive expression of HIF (a transcription factor), which activated angiogenic growth factors (like VEGF, EPO)

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91
Q

Hereditary syndrome with type 1 papillary RCC?
- Gene?
- Location of gene?

A

Hereditary papillary renal cell carcinoma

RAre
cMet codes for RTK protein –> papillary RCCs only, no extra-renal findings

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92
Q

Hereditary syndrome with type 2 papillary RCC?
Gene?
Location of gene?

A

Hereditary leiomyomatosis RCC (HLRCC)
FH gene codes for fumarate hydratase (TSG) –> painful leiomyomas (cutaneous, uterine) + papillary RCC –> bad disease, patients may die young –> start annual screening with contrasted MRI at age 8

Surveillance of tumors not recommended, take them out

1q42

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93
Q

Birt-Hogg-Dube
- Gene?
- Gene location?
- Tumor type?
- Manifestations?

A

Gene - BHD1
On 17p11

Mutated gene codes for folliculin –> painless fibrofolliculomas (benign)
Bilateral RCCs (chromophobe RCC or oncocytomas)

Lung cysts, risk of pneumothorax

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94
Q

Tuberous Sclerosis
- Inheritance pattern?
- Manifestations?

A
  • AD
    Facial lesions (adenoma sebaceum)
    Hypopigmented “ash leaf spots” on skin
    Cortical and retinal hamartomas
    Seizures/epilepsy
    Mental retardation
    Renal cysts
    Renal AMLs
    Cardiac rhabdomyomas
    Increased incidence of astrocytomas
    Incomplete penetrance, variable presentation
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95
Q

Lynch syndrome
- Where are mutations?
- What organs most likely to get cancer?

A

= Hereditary Non-polyposis Colorectal Cancer
- Genes MLH1, MSH2/6, PMS2

  • Colorectal, endometrial, digestive, ovarian, upper tract cancers
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96
Q

Cowden Syndrome

A

PTEN hamartoma syndrome

PTEN = phosphatase and tensin homolog mutations

–> hamartomas
Endometrial and kidney cancers

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97
Q

Li-Fraumeni Syndrome

A

Tumor suppressor p53 mutation

Breast cancer, osteosarcoma, soft tissue sarcoma, leukemia, lymphoma

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98
Q

Neurofibromatosis

A

Caused by oncogene mutation in MF1 (csome 17) or NF2 (csome 22)
Classically manifests with cafe au lait spots

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99
Q

MEN 2A

A

Gain of function in RET proto-oncogene

Medullary thyroid cancer, parathyroid hyperplasia, pheochromocytoma

100
Q

MEN 2B

A

Gain of function in RET proto-oncogene

Medullary thyroid cancer, pheochromocytoma, marfanoid body habitus, mucosal neuroma

101
Q

RCC Screening?

A

Renal US for ESRD patients after 3 years of dialysis
HLRCC patients at age 8
VHL patients at age 16

102
Q

Favorable molecular markers for survival in RCC

A

Absent vimentin, absent p53, High CAIX

103
Q

Bosniak 1 Classification

A

Simple cyst, imperceptible wall, no work-up indicated

0% chance of malignancy

104
Q

Bosniak 2

A

Minimally complex
A few thin, <1 mm septations or thin calcifications
Non-enhancing high-attenuation (due to proteinaceous or hemorrhagic contents)

Risk of malignancy ~0%

105
Q

Bosniak 2F

A

Minimally complex
Increased number of septa
Minimally thickened with nodular or thick calcifications
May be perceived but not measurable enhancement of a hairline smooth thin septa

Hyperdense cyst >3cm in diameter, mostly intrarenal
No enhancement
Requiring follow-up - US or CT around 6 months

Cancer risk 5-10%

106
Q

Bosniak 3

A

Indeterminate, thick, nodular, multiple septa or wall with measurable enhancement, hyperdense on CT

Tx: partial nephrectomy or ablation in poor surgical candidates

~50% risk of cancer

107
Q

Bosniak 4

A

Clearly malignant
Solid mass with large cystic or necrotic component

Treatment: partial or radical nephrectomy

~100% risk of cancer

108
Q

Lit: localized RCC in VHL

A

Belzutifan for localized RCC in VHL
HIF-2a inhibition can shrink small RCCs in VHL

109
Q

Lit: Radical Nx with or without LND

A

EORTC
Completely LND NOT needed during radical nephrectomy for N0M0 RCC
- OS, PFS, time to progression and complications rates didn’t differ

110
Q

Lit: EORTC partial vs radical nephrectomy and renal function

A

Partial nephrectomy is better than radical nephrectomy for preserving renal function… duh

Similar for OS, median follow-up 9.3 years

111
Q

Lit: Cytoreductive nephrectomy and interferon

SWOG 8949 2001

A

cytoreductive nephrectomy and interferon improved median OS by 3 months (11 vs. 8) over interferon alone

112
Q

Lit: EORTC cytoreductive nephrectomy trial 2001

A

Cytoreductive nephrectomy + interferon improves median OS by 10 months (17 vs. 7) over interferon alone

A combined analysis for SWOG and WORTC studies similarly revealed a survival benefit with cNx (13.6 vs. 7.8 months)

113
Q

Lit: CARMENA 2018 (cNx)

A

cNx + sunitinib has WORSE median OS than sunitinib alone (!)

114
Q

Lit: SURTIME 2018 (cNx)

A

Sunitinib + delayed cNx (when indicated) has better OS than upfront cNx

115
Q

Lit: (not) ASSURE(d) 2016

Adjuvant systemic therapy after rNx

A

Adjuvant targeted therapy (sunitinib or sorafenib) does not improve disease free survival (DFS) over placebo

Stopped early due to side effects with no evidence of improved DFS with either therapy

Non-metastatic patients

116
Q

Lit: S-TRAC 2016

Adjuvant systemic therapy after rNx

A

Adjuvant sunitinib improves median DFS by one year over placebo (no OS benefit)

RCT
Locoregional high risk RCC patients

117
Q

Lit: KEYNOTE-564 2021

Adjuvant systemic therapy after rNx

A

Adjuvant pembro improves DFS s/p rNx for high-risk RCC

RCT
OS data immature, but seems to favor pembro group at 24 months

118
Q

Lit: Global ARCC - Temsirolimus, Interferon-a or both?
2007

Advanced RCC

A

Temsirolimus identified as best choice for poor-prognosis RCC

RCT
Temsirolimus - mTOR inhibitor
IFN - activates inflammatory and immune responses

119
Q

Lit: Sunitinib vs. IFN-a for mRCC?
2007

Advanced RCC

A

Sunitinib > IFN-a for mRCC
PFS and objective response rate better

RCT
Sunitinib - TKI –> VEGF and PDGFR
IFN - activates inflammatory and immune responses

120
Q

Lit: TARGET 2007

Advanced RCC

A

Sorafenib > placebo for mRCC s/p 1 prior systemic therapy

RCT
Sorafenib - TKI –> VEGF, PDGFR and RAF kinase
- Significant SE profile includes rare cardiac ischemia

121
Q

Lit: RECORD-1 2008

Advanced RCC

A

mccRCC patients who fail sunitinib should get Everolimus

RCT
everolimus –> mTOR inhibitor

PFS was improved in the everolimus group compared to placebo

122
Q

Lit: COMPARZ 2013

Advanced RCC

A

Pazopanib is non-inferior to sunitinib for m-ccRCC and has superior safety profile

Pazopanib –> TKI - VEGF, PDGFR, fibroblast growth factor receptor (FGFR), and c-kit

RCT
Median PFS and OS were similar and non-inferior to sunitinib

123
Q

Lit: METEOR 2015

Advanced RCC

A

Cabozantinib has better PFS than everolimus for RCC with progression through a VEGFR-targeted treatment

Median PFS and rate or progression or death favored cabozantinib

124
Q

Lit: CheckMate 025 2015

Advanced RCC

A

Nivolumab has better OS than everolimus for advanced RCC s/p 1-2 anti-angiogenic Txs (sunitinib)

RCT

125
Q

Lit: CABOSUN 2017

Advanced RCC

A

Cabozantinib extends PFS vs. sunitinib in poor/intermediate risk met ccRCC

RCT
Previously untreated patients

126
Q

Lit: CheckMate 214 2018

Advanced RCC

A

Nivolumab + ipilimumab has better 18 month OS than sunitinib for poor and intermediate risk patients with untreated advanced RCC (with clear cell component)

RCT
Previously untreated

Ipilimumab = monoclonal Ab to CTLA-4 –> inhibits T-cell suppression

127
Q

Lit: IMmotion151 2019

Advanced RCC

A

Atezolizumab + bevacizumab > sunitinib for PD-L1+ mRCC patients

RCT
Patients with mRCC (cc or sarcomatoid)

Atezolizumab = igG4l mAb to PD-L1
Bevacizumab = mAb that inhibits VEGF-A to block angiogenesis

128
Q

Lit: KEYNOTE 426 2019

Advanced RCC

A

Pembro + axitinib has increased 1-yr OS over sunitinib REGARDLESS of PD-L1 status

Pembrolizumab = IgG4k mAb to PD-1
Axitinib = TKI –> VEGFR, c-kit, PDGFR

129
Q

Lit: TIVO-3 2020

Advanced RCC

A

Tivozanib has better PFS than sorafenib in mRCC s/p multiple prior systemic Tx

RCT

Tivozanib = potent and selective TKI –> VEGF
Sorafenib = TKI –> VEGF, RAF kinase, PDGFR

130
Q

Lit: CheckMate 9ER 2021

Advanced RCC

A

Cabozantinib + nivolumab has better OS than sunitinib for previously untreated advanced or mRCC

RCT
Cabozantinib = TKI –> VEGF, MET, TAm
Nivolumab = IgG4 mAb to PD-1 –> inhibits T cell suppression

Cabo/nivo patients have increase QoL

131
Q

Lit: CLEAR 2021

Advanced RCC

A

(Lenvatinib + pembrolizumab) > (lenvatinib + temsirolimus) > sunitinib for PFS in previously untreated, advanced RCC

Pembrolizumab = IgG4k mAb to PD-1
Lenvatinib = TKI–> VEGF, FGFR, PDGFR

132
Q

Sunitinib mechanism

A

TKI –> VEGF + PDGFR
Decreases tumor angiogenesis and growth

133
Q

Sunitinib side effects

A

Myelosuppression, nephrotoxicity, hepatotoxicity, diarrhea, fatigue, nausea, stomatitis, vomiting, HTN, HTN, Hand-Foot Sx, rash

134
Q

Sorafenib mechanism

A

TKI –> VEGF + PDGFR + RAF kinase
Decreases tumor angiogenesis and growth

135
Q

Sorafenib side effects

A

Cardiac ischemia or infarction (3%), lymphopenia, hepatotoxicity, diarrhea, fatigue, nausea, anorexia, vomiting, HTN, rash

136
Q

Tivozanib mechanism

A

TKI –> VEGF
Decreases tumor angiogenesis and growth

137
Q

Tivozanib side effects

A

HTN, fatigue, diarrhea, rash, hoarse voice

138
Q

Cabozantinib mechanism

A

TKI –> VEGF + MET + TAM
Decreases tumor angiogenesis and growth

139
Q

Cabozantinib side effects

A

GI perforation and fistula
HTN
Fatigue
Diarrhea
Rash
Seizures
Jaw osteonecrosis
Anorexia
HA
Dizziness

140
Q

Nivolumab mechanism

A

IgG4 mAb to PD-1
Decreases T-cell suppression
Increases T-cells killing cancer cells

141
Q

Nivolumab side effects

A

Immune-mediated inflammation, hypothyroidism or hyperthyroidism, pancreatitis with Type I DM, colitis, rash, peripheral edema, neuropathy

142
Q

Ipilimumab mechanism

A

IgG1-mAb to CTLA-4
Decreases T-cell suppression
Increases T-cells killing cancer cells

143
Q

Ipilimumab side effects

A

Colitis
Diarrhea
Fever
Stomach pain
Bloating
Difficulty breathing

144
Q

Atezolizumab mechanism

A

IgG4-mAb to PD-L1
Decreases T-cell suppression
Increases T-cells killing cancer cells

145
Q

Atezolizumab side effects

A

Fatigue
Anorexia
Nausea
UTI

146
Q

Bevacizumab mechanism

A

IgG1-mAb to VEGF
Decreased tumor angiogenesis
Increased apoptosis

147
Q

Bevacizumab side effects

A

HTN
Rash
Nose bleeds
Infection

148
Q

Lenvatinib mechanism

A

TKI –> VEGF + FGFR + PDGFR
Decreased tumor angiogenesis
Increased apoptosis

149
Q

Lenvatinib side effects

A

HTN
Diarrhea
Fatigue
Anorexia
Hypotension
Thrombocytopenia

150
Q

Pembrolizumab mechanism

A

IgG4-mAb to PD-1
Decreased T-cell suppression
Increased T-cells killing cancer cells

(Same mechanism as nivolumab?)

151
Q

Pembrolizumab side effects

A

Immune-mediated inflammation
Hypo- or hyperthyroidism
Pancreatitis with Type 1 DM
Colitis
Rash
Fatigue
Diarrhea
Nausea

152
Q

Axitinib mechanism

A

TKI –> VEGF, PDGFR, c-kit
Decreases tumor angiogenesis and growth

153
Q

Axitinib side effects

A

Diarrhea
HTN
Fatigue
Anorexia
Nausea
Dysphonia
Hand-foot sxs
Weight loss
Vomiting
Constipation

154
Q

Pazopanib mechanism

A

TKI –> VEGF, PDGFR, FGFR, c-kit
Decreased tumor angiogenesis and growth

155
Q

Pazopanib side effects

A

Nausea
Vomiting
Diarrhea
HTN
Anorexia
Rash
Hair Loss
Fatigue

156
Q

Temsirolimus mechanism

A

mTOR inhibitor
Decreased protein synthesis
Decreased tumor survival and growth

157
Q

Temsirolimus side effects

A

Fatigue
Rash
Mucositis
Myelosuppression
Hyperglycemia

158
Q

Everolimus mechanism

A

mTOR inhibitor
Decreased protein synthesis
Decreased tumor survival and growth

159
Q

Everolimus side effects

A

Fatigue
Rash
Diarrhea
Stomatitis
Infections
Myelosuppression
Hyperglycemia

160
Q

What percentage of surgically resected tumors < 4 cm are benign?

A

15-20%

161
Q

What percentage of RCC cases are familial? What are syndromes?

A

4-6%

Von Hippel-Lindau (VHL)

Birt Hogg-Dube (BHD)

Hereditary leiomyomatosis RCC (HLRCC)

Succinate dehydrogenase deficiency

Tuberous sclerosis

BAP-1

PTEN hamartoma (Cowden Syndrome)

162
Q

Major subtypes of RCC?

A

clear cell

papillary 1 or 2

chromophobe

collecting duct

unclassified

uncommon: acquired cystic, clear cell tubulo papillary, renal medullary (sickle cell)

163
Q

Advanced PE findings?

A

Paraneoplastic syndromes (htn, polycythemia, hypercalcemia)

adenopathy

varicocele

164
Q

Name benign renal tumors?

A

Papillary adenoma

Oncocytoma

AML

Metanephric adenoma

Adult cystic nephroma

Mixed epithelial stromal tumors

Juxtaglomerular cell tumor

165
Q

What is T1 renal tumor? subtypes?

A

T1 → < 7 cm in greatest dimension, limited to kidney

T1a < 4 cm

T1b < 4 cm, but not > 7 cm

166
Q

Describe renal tumor T2:

A

T2 → >7 cm in greatest dimension, limited to kidney

T2a → > 7 cm but < 10 cm

T2b → > 10 cm

167
Q

Describe renal mass T3:

A

T3 → tumor extends into major veins or perinephric tissues, but not to adrenal or beyond Gerota’s

T3a → into renal vein or its segmental branches, or invades pelvicalyceal system, or invades perirenal and/or renal sinus fat but not beyond Gerota’s

T3b → Grossly extends into vena cava below diaphragm

T3c → extends into vena cava above diaphragm or invades wall of vena cava

168
Q

Describe renal mass T4:

A

T4 → invades beyond Gerota’s (including contiguous adrenal extension)

169
Q

Define renal cancer N and M stages:

A

Nx → LN not assessed

N0 → no region LN mets

N1 → mets to regional LN

M0 → no distant mets

M1 → distant mets

170
Q

Describe renal mass stages:

A
171
Q

Describe the treatment options for clinically localized renal cancer:

A

Active surveillance → cT1a < 4 cm → risk of mets <2%

Radical Nx → historically entire kidney, Gerota’s/ Zuckerkandel’s fascia, regional LN, and adrenal

Partial Nx → NSS

Thermal ablation → RFA and cryoablation

172
Q

In a patient with renal mass, clinicians SHOULD obtain which imaging? How is mass characterized?

A

GUIDELINE STATEMENT 1

High-quality, multiphase, cross-sectional abdominal imaging (CT/MRI)

eGFR < 45 → hydration or MRI (especially characterizing small lesions < 2 cm)

NSF (CKD 4/5 → < 0.07%)

Characterize stage (size cranio-caudal, transverse, and A/P, morphology, involvement of vasculature, adenopathy)

Nephrometry score, PADUA score, C-index

Complexity (Bosniak 3 → irregular walls/septa + enhancement ~50% malignant; Bosniak 4 → complex cystic lesions, enhancing ~75-90% malginant)

Degree of contrast enhancement (> 15-20 HU on CT or 20% on MRI)

Presence or absence of fat

173
Q

Nephrometry Score

A

RENAL

Radius, Exophytic/Endophyic, Nearness to CS, A/P, Location re: polar lines

174
Q

In patients with suspected renal cancer, clinician SHOULD obtain which labs? Metastatic eval?

A

GUIDELINE STATEMENT 2

CMP, CBC, UA (proteinuria important prognostic factor)

UA 1+ protein → Protein: Cr or Alb:Cr

Elevated ALP → consider bone mets

Chest imaging → CXR or CT(evaluate for thoracic mets based on risk of dz)

175
Q

What makes a renal mass higher risk?

A

presence of thrombi, presumed adenopathy, larger tumor size, infiltrative appearance, extensive tumor necrosis, severe relevant sxs or PE findings

176
Q

In patient with solid or Bosniak 3 or 4 mass, in addition to labs and metastatic workup, what other classifications SHOULD be done?

A

GUIDELINE STATEMENT 3

Assign CKD stage base on GFR and degree proteinuria

177
Q

In regards to counseling for suspicious renal mass, who SHOULD be considered as players of the multidisciplinary team?

A

GUIDELINE STATEMENT 4

Urologist → lead counseling process

IR → RMB or ablation

Nephrologist → CKD, proteinuria, DMII, ongoing renal protection

Pathologist → GU dedicated, also evaluation of normal parenchyma

Medical Oncologist → poss neoadjuvant or adjuvant trials, recurrence

Genetic Counseling → 4-6% familial, multifocal or b/l

178
Q

Clinicians SHOULD provide counseling that includes current perspectives about tumor biology and what patient-specific risk assessment:

A

GUIDELINE STATEMENT 5

Sex, tumor size/complexicty, histology, imaging characteristics

cT1a (low oncologic risk → indolent, <2% risk mets)

179
Q

When counseling treatment options for renal mass, clinicians SHOULD review the most common urologic and non-urologic morbidities of each treatment pathway including:

A

GUIDELINE STATEMENT 6

the importance of age, comorbidities/frailty, and life expectancy

RN → greatest risk dec. GFR or de novo CKD, favorable peri-op outcomes and low risk of complication compared to PN

PN → excellent preservation of GFR, higher risk txf, urine leak or other complications needing additional tx (stent, drains, embolization of pseudo-aneurysm)

TA → inferior RFS, most favorable peri-operative outcome profile (best for small peripheral tumors)

AS → favorable oncologic and OS outcomes in well-selected patients; possible anxiety or poor outcomes

180
Q

What SHOULD clinicians review in regards to renal function recovery related to renal mass management:

A

GUIDELINE STATEMENT 7

Progressive CKD

ST and LT need for RRT

LT OS considerations

181
Q

Clinicians SHOULD refer to nephrology renal mass patients with:

A

GUIDELINE STATEMENT 8

High risk of CKD progression (eGFR < 45), confirmed proteinuria, DMII pre-existing CKD, or expected GFR < 30 after sx

182
Q

In regards to renal cancer, when is genetic counseling RECOMMENDED:

A

GUIDELINE STATEMENT 9

< 46 yo

Multifocal or b/l masses

personal hx suggests familial renal neoplastic syndrome

1st or 2nd degree relative with hx of renal cancer or known clinical/genetic dx of familial neoplastic syndrome (even if kidney cancer not observed)

path demonstrates histologic features suggestive of syndrome

183
Q

Syndrome: Von Hippel-Lindau (VHL)

A

Gene: VHL

Clear cell RCC, renal cysts, hemangioblastomas of CNS, retinal angiomas, pheochromocytoma

184
Q

Syndrome: Hereditary Papillary Renal Carcinoma (HRPC)

A

Gene: MET

Type 1 papillary RCC

185
Q

Syndrome: Birt Hogg-Dube (BHD)

A

Gene: FLCN

chromophobe RCC, oncocytoma, hybrid oncocytic/chromophobe tumors (HOCTs), cc RCC (less common), renal cysts, cutaneous fibrofolliculomas, lung cysts, spontaneous PTX

186
Q

Syndrome: Hereditary Leiomyomatosis and RCC (FH)

A

Gene: FH

type 2 papillary or CD RCC, cutaneous leioyomyomas, uterine leiyomyomas

187
Q

Syndrome: Succinate Dehydrogenase Kidney Cancer (SDH-RCC)

A

Gene: SDHB/C/D

ccRCC, choromophobe RCC, type 2 papillary RCC, oncocytoma, pheochromocytoma/paraganglioma

188
Q

Syndrome: BAP-1 Tumor Predisposition Syndrome

A

Gene: BAP-1

ccRCC, uveal melanoma

189
Q

Syndrome: Tuberous Sclerosis Complex

A

Gene: TSC 1 or 2

AML, ccRCC, oncocytoma, lymphangioleiyomyomastosis (LAM), seizures, developmental delay

190
Q

Syndrome: Cowden/PTEN Syndrome associated RCC (CS-RCC)

A

Gene: PTEN

Thyroid, breast, and endometrial cancer, mucocutaneous lesions, RCC with papillary mc, other forms of RCC including cc

191
Q

When considering RMB what SHOULD be counseled?

A

GUIDELINE STATEMENT 10

generally safe & complications low risk: hematoma, pain, hematuria, PTX, hemorrhage (txf)

Sensitivity 9.67%, Specificity 94.4%, PPV 98.8% (core), NPV 60-80%

non-diagnostic rate 14%, concern for missed histologic heterogeneity

Discussion:

RMB is safe and low risk (no reported tumor seeding)

Dx of RCC is highly reliable

LImits:

Benign bx must be distinguished from non-dx

Benign is not always correct

Grade concordance from bx to sx is not perfect

Oncocytic neoplasm are diagnostic dilemma

Bx or aspiration of cystic mass not advised (spillage)

192
Q

When concerned about hematologic, metastatic, inflammatory, or infectious mass, clinicians SHOULD consider? What type of cancers are common?

A

GUIDELINE STATMENT 11

RMB

Lymphoma, lung, melanoma, colon, thyroid

193
Q

RMB SHOULD be obtained on utility-based approach when it may influence mgmt. It is NOT required when:

A

GUIDELINE STATMENT 12

Young or healthy patients who are unwilling to accept uncertainties

older or frail patients who will be managed conservatively no matter results

194
Q

How SHOULD RMB be done?

A

GUIDELINE STATEMENT 13

Multiple core biopsies and preferred over FNA

195
Q

Why is NSS (PNx) important? When is it appropriate to consider?

A

GUIDELINE STATEMENT 14

for mgmt of cT1a mass

**reduces risk of CKD or CKD progression and is associated with favorable outcomes

GUIDELINE STATEMENT 15

solid or Bosniak 3 or 4 complex cystic masses in anatomically or functional solitary kidney, bilateral tumors, known familial RCC, pre-existing CKD, or proteinuria

GUIDELINE STATEMENT 16

solid or Bosniak 3 or 4 complex cystic masses who are young, multifocal masses, or comorbidities likely to impact GFR in future (htn, DM, stones, obesity)

196
Q

Intraoperatively, how SHOULD clinicians prioritize nephron sparing and balance with what other goals?

A

GUIDELINE STATEMENT 17

optimize nephron mass preservation

avoid prolonged warm ischemia (<25-30 mins)

GUIDELINE STATEMENT 18

Prioritize negative sx margins

Enucleation should be considered in pts with familial RCC, multifocal dz, severe CKD

*depends on tumor characteristics, growth pattern, interface with normal tissue

197
Q

When SHOULD a clinician consider RNx?

A

GUIDELINE STATEMENT 19

Solid or Bosniak 3 or 4 complex cystic renal mass with:

increased oncologic potential (size, RMB, imaging features)

ALL of following:

high tumor complexity (PN challenging in experienced hands)

no pre-existing CKD or proteinuria

normal contralateral kidney (new baseline GFR would be >45)

198
Q

Patients undergoing renal sx, SHOULD have LND when?

A

GUIDELINE STATEMENT 20

clnically concerning regional LAN, perform LND including all clinically positive nodes for staging (no real survival benefit)

(concerning features: > 10 cm mass, clinical stage T¾, high grade tumors (3 or 4), sarcomatoid features, histologic tumor necrosis)

199
Q

For patients with renal mass, when SHOULD adrenalectomy be performed?

A

GUIDELINE STATEMENT 21

imaging and/or intraoperative findings suggest mets or direct invasion of adrenal gland

pT4 (contiguous)

M+ if hematogenous

200
Q

How SHOULD renal mass surgery be performed?

A

GUIDELINE STATEMENT 22

Minimally invasive (when it would not compromise outcomes)

*benefits in ST complications, fewer longer term

201
Q

After PNx of RNx, adjacent renal parenchyma SHOULD be evaluated:

A

GUIDELINE STATEMENT 23

evaluate for intrinsic renal dz and particularly for CKD or risk factors for CKD

202
Q

When SHOULD clinicians refer to medical oncology for renal masses?

A

GUIDELINE STATEMENT 24

whenever there is concern for potential clinical mets or incompletely resected dz (macroscopic positive margin or gross residual dz)

patients with high-risk or locally advanced, fully resected renal cancers should be counseled of risk, benefits of adjuvant tx and encourage to participate in trials

203
Q

What types of TA can be considered for renal mass? Who SHOULD be considered?

A

GUIDELINE STATEMENT 26

radiofrequency ablation (RFA) and cryoablation

GUIDELINE STATEMENT 25

consider as alternative mgmt of cT1a solid masses < 3 cm (percutaneous preferred over sx approach)

204
Q

Describe RFA and cyroablation:

A

RFA → high frequency alternative current (460-500 kHz) to induce frictional agitation and heating in adjacent tissues

Cryo → temp -20 to -40 C, resulting in coagulative necrosis

205
Q

When treating with TA, what SHOULD be performed prior to or at time of tx? What should counseling include?

A

GUIDELINE STATEMENT 27

RMB to provide pathologic dx and guide surveillance

GUIDELINE STATEMENT 28

info regarding increased likelihood of persistence or local recurrence vs. sx which may be addressed with repeat ablation or further intervention

206
Q

Patient related factors for AS vs. Expectant Mgmt vs. Intervention

A
207
Q

When SHOULD AS be utilized?

A

GUIDELINE STATEMENT 29

For solid renal mass < 2 cm, or complex but cystic

*Repeat imaging in 3-6 mo to assess growth/change, then periodic imaging based on growth rate

GUIDELINE STATEMENT 30

For solid or Bosniak 3 or 4 cystic complex mass, WHEN anticipated risk of intervention or competing risk of death outweigh oncologic benefits (asx pts periodic imaging)

GUIDELINE STATEMENT 31

For patients with solid or Bosniak 3 or 4 WHEN risk/benefit is equivocal and who prefer AS, consider RMB

208
Q

When is intervention RECOMMENDED over AS? When is AS possible in this case?

A

GUIDELINE STATEMENT 32

solid or Bosniak 3 or 4 mass with oncologic benefits of intervention > risks of tx and risk of death

**Median growth rates > 5 mm/year are indicative of oncologically active tumors

AS with potential for delayed intervention → only if patient understands and willing to accept associated oncologic risk

Encourage RMB for additional stratification

continues to prefer AS → close clinical and cross sectional imaging continued

209
Q

Follow up after intervention of renal mass: benign vs. malignant?

A

GUIDELINE STATEMENT 33

Discuss implications of stage, grade, and histology including risk of recurrence and sequelae of tx

Benign → occasional clinical eval and labs (no imaging)

GUIDELINE STATEMENT 34

Periodic H&P, labs, imaging for mets and local recurrence based on stage

210
Q

What follow up labs for malignant renal mass s/p tx?

A

GUIDELINE STATEMENT 35

Cr, eGFR, UA

CBC, LDH, LFT, ALP, Ca → discretion of MD or if advanced dz

211
Q

When following patient s/p tx for renal mass, when do you refer to nephrology?

A

GUIDELINE STATEMENT 36

with progressive renal insufficiency or proteinuria

212
Q

When do you perform bone scan for renal mass f/up post tx? When head or spine CT/MRI?

A

GUIDELINE STATEMENT 37

clinical sxs bone pain, elevated ALP, or imaging suggestive of bony mets

GUIDELINE STATEMENT 38

Acute neuro sxs

GUIDELINE STATEMENT 39

site specific imaging warranted by sxs

PET should not be routinely used (selectively)

213
Q

Patients renal mass with suggestive sxs/signs of mets next steps?

A

GUIDELINE STATEMENT 40

evaluate to define extent of dz

refer to med onc

sx or ablation considered with isolated or oligo-mets

214
Q

In pts with new renal primary or local recurrence, what is next steps?

A

GUIDELINE STATEMENT 41

met evaluation including chest and abdomen

if isolated to ipsilateral kidney and/or retroperitoneum, sx resection or ablation can be considered

215
Q

Describe risk categories of patients s/p PNx or RNx:

A

GUIDELINE STATEMENT 42

See table, sx margins positive → increase risk category by one level

216
Q

Recurrence rates by risk level for renal mass post sx:

A

pT1 → 9.2% (Grade 1: 6.4%, Grade 2: 15.4%)

pT2 → 32% (organ confined RCC, Grade 3 or 4: 20-30%)

pT4 (most present mets) → 64.7% (N1 → CSS 2.8 y, 64.3% mortality after recurrence)

217
Q

Follow up after TA:

A

GUIDELINE STATEMENT 45

bx confirmed malignancy or non-dx

CTU/MRU w/in 6 mo (then follow same as intermediate risk category)

218
Q

f/up schedule after surgery for renal cancer:

A

GUIDELINE STATEMENT 43 and 44

Low risk → pT1, G1 or 2 → CT/MRI and CXR/CT q 12 mo

*after 2 years abd US alternating with CT/MRI can be considered

*after 5 y joint decision making

Intermediate risk → pT1 grade 3 or 4, pT2 any grade → CT/MRI and CXR/CT at 6 mo, then q 12 mo for 5 years (can consider abd US after 2 years alternating)

High risk → pT3 any grade → CT/MRI and CXR/CT q 6 mo for 3 y, then q 12 mo for 5 years

Very high risk → pT4 or N1 or sarcomatoid, rhabdoid, macro pos margin → CT/MRI q 3 mo x 1year, then q 6 mo years 2-3, then annually

219
Q

f/up algorithm table for renal mass

A
220
Q

Describe an extraperitoneal flank approach for Nx:

A
  1. Anesthesia, Foley, SCDs, abx
  2. Position lateral decubitus (side down opposite tumor), flexion to increase space btw ribs, pressure points padded, secured to table, right arm supported in anatomic position to protect brachial plexus
  3. Incise btw 11-12 ribs, dissect through flank layers, care to avoid perforating nerves
  4. Enter retroperitoneum, divide lumbodorsal fascia, avoid entry to pleura posteriorly and peritoneum anteriorly
  5. Mobilize kidney w/in Gerota’s posteriorly, laterally, superiorly, and anteriorly
  6. ID ureter
  7. Place kidney on anterior and medial traction to isolate hilum
  8. Dissect artery posteriorly
  9. Defat kidney near renal mass, maintain fat pedicle to possibly use for reconstruction
  10. Use US if needed to define boundaries and depth
  11. Mannitol??? /IVF (out of favor…)
  12. Clamp RA, surround kidney in slush
  13. Incise capsule 1 cm from tumor edge, excise tumor with neg margin
  14. Sample areas from bed if concern of incomplete excision
  15. Assess and repair CS
  16. Achieve hemostasis with focal suture ligatures, electrocautery, and hemostatic agents
  17. Reconstruct and reinforce defect (bolsters)
  18. Remove clamp ASAP
  19. Assess for arterial pulse/perfusion kidney
  20. Assess for hemostasis
  21. Re-approximate perinephric fat pedicle
  22. Place drain in proximity of kidney
  23. Inspect retroperitoneum, peritoneal boundary and pleura
  24. Inspect vasculature
  25. Remove flexion, reapproximate ribs
  26. Close muscle and facial layers
  27. Close skin
221
Q

How do you manage an acute post operative urine leak?

A
  1. vast majority close with conservative mgmt
  2. small leaks → adjust drain to make sure not contributing, suction on renorrhaphy vs. obs
  3. larger or persistent leaks → urinary diversion, stent, IR drain/PCN; with stent need Foley to prevent VUR
  4. Secondary closure, fistula repair, nx (challenging cases or nephrocutaneous fistula)
  5. Algorithm:

leak from drain → take off suction → adjust away from anastomosis

Insert stent → placed PCN → IR drain urinoma → antegrade stent

222
Q

Most important prognostic determinant of RCC?

A

local tumor extent/size/stage

histologic subtype

surgical margins

regional nodal status

evidence of distant met status

performance status

223
Q

What about margins?

A

<1 cm margins not associated with higher rates of local recurrence

positive margin slightly higher risk of local recurrence (but with adequate surveillance, no statistically higher mortality)

224
Q

What are risk factors and pathogenesis of ccRCC? what about VHL association?

A

family hx, smoking, hereditary, obesity, HD

arises from PCT, associated with defects in VHL (60% sporadic)

VHL → works as tumor suppressor to inhibit ubiquitination of HIF → when mutated HIF builds up overproducing VEGF, GLUT-1 TGF-a, PDGF → angiogenesis, proliferation

225
Q

Describe trans peritoneal lap Nx:

A
  1. anesthesia, foley, NGT
  2. lateral decubitus (tumor side up), 45 degree angle, pad pressure points (peroneal nerve, brachial plexus stretch injury)
  3. trochar placement to triangulate kidney
  4. Veress → incision at umbilical camera site → Kelly clamp to spread fat, ID fascia → grasp fascia using Kocher, upward traction, pass veress (2 pops) → 10 cc syringe, inject 5 cc saline without force to confirm intraperitoneal → advance needle 1 cm, no resistance → confirm low starting pressure → remove Veress, place trochar, attach gas, pass camera to inspect
  5. Hasson → consider with prev. abd sx → ID fascia, incised, peritoneum incised → 2 heavy sutures placed on either size of incision (incorporate fascia/peritoneum) → Hasson trochar in place and insufflation started
  6. Place working trochars under direct vision
  7. take down colon (white line of Toldt), care not to enter Gerota’s (left splenic flexure mobilized → drop from field, care to avoid tail of pancreas
  8. ID ureter on psoas
  9. gonadal ID and traced to hilum
  10. RV skeletonized (care not to avulse adrenal vein or lumbar (entering posterior RV)
  11. ID RA posterior and superior (make sure 1)
  12. Secure RA with Weck Clips (2-3, 1 on kidney side) or Stapler, Take vein with stapler
  13. Take gonadal and ureter, dissect free posterior, lateral, and superior aspect of kidney, place in bag
  14. Extract in lap bag to facilitate removal and reduce incision site implants
  15. Port sites > 10 mm closed
226
Q

Common locations of positioning injuries for renal sx:

A

Brachial plexus

Lateral popliteal nerve

Femoral nerve

Sciatic Nerve

*usually resolve 4-6 weeks, can last up to 2y

227
Q

What are insufflation/access related complications and treatment:

A

gas embolus → Millwheel murmur, CV collapse, head/neck cyanosis, dysrhythmia, hypoxia, decreased end tidal CO2 → terminate insufflation, release pneumo, left lateral decubitus, cardiopulmonary resuscitation, aspiration of gas via central line, 100% O2

Veress needle/trochar placement → major vascular injury → leave needle in place, use second Veress and try to repair injury → if trochar injury, open conversion, explore and repair → do not remove until conversion made and ID location and severity

Extraperitonal insufflation → high intra-abd pressure after small volume insufflated, subq emphysema, pneumoscrotum, PTX, pneumomediastinum → reposition insufflation needle

228
Q

Name vascular complications and tx of lap surgery:

A

mgmt. based on severity of injury: clip vessel, increase pressure, apply pressure (gauze or instrument), biosealants (slow ooze), oversew, convert to open/hand assist (leave instrument on bleed), lower pressure to 5 mHg at end to ensure no active bleeding (watch trochar removal)

post operative bleeding → prolonged pain, distention, tachy, fall in hct → CT AP, obs. vs. exploration

Hollow viscus → electrocautery, access (needle/trochar), blind passage of instruments

Recognize in OR → repair, abx irrigation, broad spectrum

Post op → trochar site pain, fever, leukopenia with left shift, low threshold for CT w/oral contrast and delayed views to visualize colon

Solid Viscus → veress, trochar, retraction (do gently)

Minor injury → biosealants, argon beam, cellulose gauze, open if fail

Kidney trochar injury → if Gerota’s intact, stable RP hematoma, patient stable _> conservative obs

Explore if expanding hematoma, vascular instability, or unknown extent of injury

229
Q

Complications of PNx:

A

Intraoperative hemorrhage

Delayed bleeding

Persistent leak from CS

Perirenal abscess

Urinoma

Reno-cutaneous fistula

Acute tubular necrosis

Conversion to RN

230
Q

what control is needed with IVC thrombectomy?

A
  • Prior to IVC thrombectomy vascular occlusion should include:
    • Renal artery supplying the affect kidney with tumor thrombus
    • Infrarenal IVC below thrombus
    • Lumbar veins feeding in to the IVC
    • Contralateral renal vein
    • Hepatic blood supply for thrombus that extends about the hepatic veins. A Pringle maneuver is performed to decreased hepatic blood flow by placing a clamp across the hepatic artery and portal vein within the hepatoduodenal ligament. This is mainly done for level 3 or higher tumor thrombus.
    • Suprarenal IVC above the thrombus
231
Q

IVC thrombus classification:

A
  • In the eighth edition AJCC staging manual, venous invasion is classified by the T stage according to the extent of invasion as described below:
    • T3a tumor grossly extends into the renal vein or its segmental (muscle containing) branches
    • T3b tumor grossly extends into the vena cava below the diaphragm
    • T3c tumor grossly extends into the vena cava above the diaphragm
  • However, the Neves Zincke classification is more useful from a technical surgical approach:113
    • Level 0: Tumor thrombus limited to renal vein
    • Level 1: Extending ≤2 cm above the renal vein
    • Level 2: Extending >2 cm above the renal vein but below the hepatic veins
    • Level 3: At or above the hepatic veins but below the diaphragm
    • Level 4: Extending above the diaphragm
232
Q

Where does RCC metastasize?

A

Lung → 50%

Liver → 33%

Bone 32 → 32

Brain → 25%

233
Q

5 year survival for RN by stage?

A

Stage 1 → 95%

Stage II → 85%

Stage III → 60%

Stage IV → 20%

234
Q

What are s/s important to ask at renal mass f/up after Nx or PNx? PE components?

A

History:

abdominal/flank/bladder pain or tenderness

fatigue

gross hematuria

weight loss

lower extremity edema

neuro complaints

MSK pain

SOB

PE:

LN, lower extremities, neuro exam, VS (weight and BP), abdominal exam

235
Q

Labs to consider for f/up of post sx renal mass??

A

CBC, LDH, LFTs, UA, BUN/Cr (eGFR), ALP (sxs)

236
Q

What is ddx of post sx bone pain (ribs) and elevated ALP on f/up?

A

Hyperthyroidism

Pregnancy

Hepatitis

Biliary Obstruction

Non malignant bone conditions (Pagets)

Bone mets

237
Q

What is ddx of solid enhancing renal mass?

A

RCC

vascular malformation

infarct

urothelial carcinoma

oncocytoma

AML

metanephric adenoma

Met dz

renal abscess

XGP

238
Q

What are risk factors for AKI with IV contrast?

A

htn

pre-existing CKD

hemodynamic instability

volume depletion

Age > 75 yo

CHF

High volume contrast media

239
Q

What tactics can be utilized to prevents kidneys with IV contrast load?

A

adequate oral hydration

IV NaCl or NaCO3 solution

discontinue nephrotoxic meds

stop metformin and restart in 48 h

use lowest dose

iso- or low osmolar IV contrast agent

NAC

240
Q

What do you look at for post-ablation CT?

A

additional, new renal nodules

satellite or port site soft tissue nodules

size change of mass (increase or decrease)

enhancement

241
Q

what are tx options for post ablation failure?

A

salvage RNx

salvage PNx

repeat bx

repeat ablation

242
Q

MC IVC injuries during PNx or Nx

A

avulsion of right adrenal vein from IVC or right gonadal from IVC

243
Q

Define Bosniak classification of renal cystic tumors:

A

Bosniak 1: simple cyst, 0% malignancy

Bosniak 2: minimally complex cyst, 0% malignancy

Bosniak 2F: more minimally complex cyst, 5% malignancy

Bosniak 3: indeterminate, 55% malignancy

Bosniak 4: clearly malignant, 100% malignancy

244
Q

Early Post-Op complication of PNx?

A
  1. Delayed bleeding
    1. work up pseudo-aneurysm with CT w/IV contrast → call IR for embolization
  2. Urinoma
    1. Place ureteral stent anf oley
    2. If persists, IR drain
  3. Perinephric abscess
    1. evaluate for urinoma source
    2. IR rain
    3. if persists, consider open drainage
245
Q

Late Post-op complications of PNx?

A
  1. UJPO: scarring around hilum and UPJ
  2. HTN, with renal trauma also 5% (page kidney)
  3. AVM

04. RCC (937) (10 decks)

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