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.
2
Q
What are the most common types of kidney tumours?
A
Renal cell carcinoma ~90%
Oncocytoma ~5%
Angiomyolipoma ~2-3%
3
Q
What types of renal cell carcinomas are they and how common are they?
A
Clear cell 85%
Papillary 10%
Chromophobe 5%
4
Q
Should you perform a biopsy before deciding on active surveillance of a small renal mass?
A
No
5
Q
How often is an oncocytoma mis-diagnosed when a biopsy is performed?
A
In 35,4% of the cases
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
7
Q
At what size can you consider intervention of an angiomyolipoma?
A
> 4 cm though the evidence is weak
8
Q
Bosniak I
A
Simple cyst
9
Q
Bosniak II
A
Mildly complex benign cyst
10
Q
Bosniak IIF
A
Moderately complex cyst
Follow-up som are malignant
11
Q
Bosniak III
A
Indeterminate complex cyst
Over 50% are malignant
Surgery or active surveillance
12
Q
Bosniak IV
A
Complex cystic mass
most are malignant
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
14
Q
When resecting a kidney tumour, which tumours do you have to clamp arteries and veins both?
A
Centrally located tumours
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
16
Q
Why is Ablative therapies not recommended when compared to partial nephrectomies?
A
Higher risk of local recurrence
Worse overall survival
17
Q
What is the benefit of laprascopic radical nephrectomy vs open surgery?
A
Lower morbidity
18
Q
How does renal cell carcinoma most commonly spread?
A
Haematogenous spread
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
20
Q
When is radical nephrectomy including a thrombectomy indicated?
A
When there is a vena cava thromb and staging is N0M0
21
Q
After a radical nephrectomy, should you offer adjuvant therapy?
A
No
trials are ongoing if you could offer neadjuvant immunetherapy
22
Q
What are the most frequent sites for metastases of RCC?
A
Lung 54%
lymph nodes 22%
bone 20%
23
Q
What is the recurrence of non metastatic RCC?
A
20% inom 5år
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
25
Metastasectomy for RCC is indicated:
If complete and a favourable risk profile
26
What is the result of a complete resection of metastases in mRCC in 5-year cancer specific-survival?
74% in pulmonary
| 33% in extrapulmonary metastases
27
How do you treat brain or bone metastases of RCC?
stereotactic radiotherapy
28
Can you treat retroperitoneal recurrence of RCC?
Aggressive surgical resection offers potential cure in a substantial number of patients with retroperitoneal recurrence
29
What is a TKI?
Tyrosine kinase inhibitor
30
Give a few examples of Tyrosine kinase inhibitors (TIK:s):
Axitinib
Panzopanib
Sorafenib
Sunitinib
31
Give a few examples of mTOR inhibitors:
Temsirolimus
| Everolimus
32
Give an example of a VEGF antibody:
Bevacizumab
33
Give a few examples of a PD-1 inhibitor:
Nivolumab
| Pembrolizumab
34
Give a few examples of a PD-L1 inhibitor:
Atezolizumab
| Avelumab
35
Give an example of a drug targeting CTLA-4:
Ipilimumab
36
What types of immunotherapy are available for the treatment of RCC?
```
TKI:s
mTOR inhibitors
VEGF-antibodies
PD-1 inhibitors
PD-L1 inhibitors
drugs targeting CTLA-4
```
37
When is cytoreductive nephrectomy (CR NE) indicated in non Clear cell RCC?
Indicated if patient is not a MSKCC poor-risk patient
| MSKCC Memorial Sloan-Kettering Cancer center classification
38
Renal Mass Staging: T1a, T1b
T1a: < or = 4 cm
T1b: < or = 7 cm
39
Renal Mass Staging: T2a, T2b
T2a: < or = 10 cm
T2b: >10 cm
40
Renal Mass Staging: T3a
T3a: renal vein, pelvicalyceal, perirenal/renal sinus fat within Gerota
41
Renal Mass Staging: T3b
IVC below diaphragm
42
Renal Mass Staging: T3c
VC above diaphragm
43
Renal Mass Staging: T4
Outside of Gerota or involving adrenal
44
Stage I
T1N0M0
45
Stage II
T2N0M0
46
Stage III
T3N0-1M0
T1-2N1M0
47
Stage IV
M1
48
Postoperative Risk Stratification
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
49
Evaluation of renal mass:
- Imaging?
- Labs?
- CKD?
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)
50
When to consult nephrology?
Consider for eGFR <45, expected postop GFR <30, proteinuria, DM with CKD
51
When to consult Med Onc?
Concerned for potential clinical mets
Incomplete resection
Consider adjuvant treatment for High Risk (T3 and G) or locally advanced, fully resected cancers
52
When to consult genetics?
Recommend for age 46 or less, multifocal/bilateral renal masses, whenever the personal/family history suggests a familial renal neoplastic syndrome
53
When to perform Renal Mass Biopsy (RMB)?
Consider if suspicious for hematologic/metastatic/inflammatory/infectious mass
For solid mass, multiple cores >> FNA
PPV ~100%, NPV ~60%, Nondiagnostic ~15%
54
Partial Nephrectomy:
- When do you prioritize this?
- When do you consider it?
- Surgical considerations?
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
55
When is radical nephrectomy preferred over partial nephrectomy?
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
56
When is Thermal Ablation appropriate? How to follow up?
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
57
When to consider active surveillance? Triggers for intervention?
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
58
Follow-up labs post-op?
Cr, UA, eGFR --> refer to nephrology PRN
Consider other labs as needed and if advanced disease expected (CBC, LDH, LFTs, Alk Phos, Ca++)
59
Abdominal imaging after nephrectomy and partial nephrectomy?
Chest imaging?
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
60
What to do when renal artery vasospasm during hilar dissection?
Reduced perfusion
Pale kidney
1. Reduce insufflation pressure
2. Apply topical papaverine (opium alkaloid antispasmodic vasodilator) to renal hilar vessels
61
When to consider when using argon gas laparoscopically?
Argon beam will increase abdominal pressure due to addition of argon gas
- Important to vent abdomen via a port to relieve pressure
62
Interaortocaval nodes only drain the right kidney
They drain the left kidney with advanced disease
63
Incidence of local recurrence after nephrectomy?
What does this mean for 5 year survival?
Incidence 2.9%
Poor prognosis: 5 year survival 30%
Synchronous mets at the time of recurrence are an independent predictor of poor prognosis
64
Hand-assisted lap compared to straight lap?
What does this mean for donor nephrectomies?
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.
65
Acute bleed following ligation/division of left renal hilum
Think about disruption of a lumbar vein, because this inserted into the renal vein posteriorly
66
Workflow for urine leak after partial nephrectomy
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
67
Severe, persistent back pain resistant to pain meds after renal surgery
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)
68
Proposed criteria for cytoreductive nephrectomy
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)
69
Vaccinations s/p splenectomy
Indicated due to risk of severe infection with encapsulated bacteria
SHiN - Streptococcus pneumoniae, Haemophilus influenzae type b, Neisseria meningitidis
70
New lesion with early enhancement and prompt washout at prior tumor site after partial nephrectomy
Get US with doppler to determine pseudoaneurysm vs. recurrence
71
RCC tumor thrombus levels
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
72
"Persistent central enhancement"
Tumor recurrence after cryoablation
73
Ways to optimize (lap) renal cryoablation
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
74
Small renal mass(es) are identified in conjunction with widespread LAD outside of typical LN drainage zones
Suspect renal involvement of lymphoma
Perc LN biopsy to determine Tx plan
75
Renal tumor with high signal on T1 on MRI
Fat in lesion
Think AML
Think a/w tuberous sclerosis
AML = benign tumor of perivascular epithelioid cell origin
76
MRI sequence most likely to confirm AML
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
77
Drug that can be used to shrink AMLs
Everolimus (Afinitor)
Tumor growth typically resumes when treatment is discontinued
Can watch AMLs when small, can cause problems if >4 cm
78
Benign tumor in 20yo with elevated peripheral renin
Juxtaglomerular tumor
Tumor secretes renin
patients typically <20yo
Cured with surgery
79
Rare, extremely aggressive tumor associated with sickle cell trait
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
80
Treatment for metastatic renal medullary carcinoma
Carboplatin + paclitaxel is first line (not upfront surgical resection)
Gemcitabine + adriamycin is 2nd line
81
Collecting duct RCC
More aggressive --> younger age of presentation
Resistant to standard chemos for RCC, but sometimes responsive to gemcitabine and cisplatin chemos (behave more like UCC)
82
Renal pseudotumor
Column of Bertin
Focal cortical hyperplasia
Best established with DMSA scan
83
How to follow patients with oncocytoma or indeterminate histology on renal mass biopsy
Follow with same imaging protocols used for untreated low risk renal cancers due to risk of substantial growth and risk of inaccurate biopsy results
84
How to distinguish between oncocytoma and RCC?
Technetium-sestamibi nuclear scanning
- oncocytoma will have high radiotracer uptake
- RCC will have low radiotracer uptake
85
Preferred regimens for relapse or stage IV metastatic CCRCC (favorable and poor/intermediate risk)
Pembrolizumab + axitinib - Keynote-426
Nivolumab + cabozantinib - CheckMate-9ER
Pembrolizumab + lenvatinib - CLEAR
Cabozantinib monotherapy (CABOSUN) is a preferred option for poor/intermediate risk
86
Metastatic RCC sites with worst to best prognosis
Brain, liver, bone, LNs, lung, adrenal
87
What labs do you need to monitor Sunitinib with/for?
Associated with hypothyroidism - get thyroid labs
88
Renovascular fistulae treatment
- If asymptomatic due to biopsy?
- If asymptomatic due to RCC?
- What symptoms do they cause when symptomatic?
- Cirsoid AV fistula?
- 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.
89
Von Hippel Lindau
- Inheritance pattern?
- Manifestations?
- Gene associated?
- Gene location?
- Leading cause of death in VHL?
- 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
90
Medication that is FDA approved for treatment of VHL-associated RCC? Mechanism?
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)
91
Hereditary syndrome with type 1 papillary RCC?
- Gene?
- Location of gene?
Hereditary papillary renal cell carcinoma
RAre
cMet codes for RTK protein --> papillary RCCs only, no extra-renal findings
92
Hereditary syndrome with type 2 papillary RCC?
Gene?
Location of gene?
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
93
Birt-Hogg-Dube
- Gene?
- Gene location?
- Tumor type?
- Manifestations?
Gene - BHD1
On 17p11
Mutated gene codes for folliculin --> painless fibrofolliculomas (benign)
Bilateral RCCs (chromophobe RCC or oncocytomas)
Lung cysts, risk of pneumothorax
94
Tuberous Sclerosis
- Inheritance pattern?
- Manifestations?
- 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
95
Lynch syndrome
- Where are mutations?
- What organs most likely to get cancer?
= Hereditary Non-polyposis Colorectal Cancer
- Genes MLH1, MSH2/6, PMS2
- Colorectal, endometrial, digestive, ovarian, upper tract cancers
96
Cowden Syndrome
PTEN hamartoma syndrome
PTEN = phosphatase and tensin homolog mutations
--> hamartomas
Endometrial and kidney cancers
97
Li-Fraumeni Syndrome
Tumor suppressor p53 mutation
Breast cancer, osteosarcoma, soft tissue sarcoma, leukemia, lymphoma
98
Neurofibromatosis
Caused by oncogene mutation in MF1 (csome 17) or NF2 (csome 22)
Classically manifests with cafe au lait spots
99
MEN 2A
Gain of function in RET proto-oncogene
Medullary thyroid cancer, parathyroid hyperplasia, pheochromocytoma
100
MEN 2B
Gain of function in RET proto-oncogene
Medullary thyroid cancer, pheochromocytoma, marfanoid body habitus, mucosal neuroma
101
RCC Screening?
Renal US for ESRD patients after 3 years of dialysis
HLRCC patients at age 8
VHL patients at age 16
102
Favorable molecular markers for survival in RCC
Absent vimentin, absent p53, High CAIX
103
Bosniak 1 Classification
Simple cyst, imperceptible wall, no work-up indicated
0% chance of malignancy
104
Bosniak 2
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
Bosniak 2F
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
Bosniak 3
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
Bosniak 4
Clearly malignant
Solid mass with large cystic or necrotic component
Treatment: partial or radical nephrectomy
~100% risk of cancer
108
Lit: localized RCC in VHL
Belzutifan for localized RCC in VHL
HIF-2a inhibition can shrink small RCCs in VHL
109
Lit: Radical Nx with or without LND
EORTC
Completely LND NOT needed during radical nephrectomy for N0M0 RCC
- OS, PFS, time to progression and complications rates didn't differ
110
Lit: EORTC partial vs radical nephrectomy and renal function
Partial nephrectomy is better than radical nephrectomy for preserving renal function... duh
Similar for OS, median follow-up 9.3 years
111
Lit: Cytoreductive nephrectomy and interferon
SWOG 8949 2001
cytoreductive nephrectomy and interferon improved median OS by 3 months (11 vs. 8) over interferon alone
112
Lit: EORTC cytoreductive nephrectomy trial 2001
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
Lit: CARMENA 2018 (cNx)
cNx + sunitinib has WORSE median OS than sunitinib alone (!)
114
Lit: SURTIME 2018 (cNx)
Sunitinib + delayed cNx (when indicated) has better OS than upfront cNx
115
Lit: (not) ASSURE(d) 2016
Adjuvant systemic therapy after rNx
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
Lit: S-TRAC 2016
Adjuvant systemic therapy after rNx
Adjuvant sunitinib improves median DFS by one year over placebo (no OS benefit)
RCT
Locoregional high risk RCC patients
117
Lit: KEYNOTE-564 2021
Adjuvant systemic therapy after rNx
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
Lit: Global ARCC - Temsirolimus, Interferon-a or both?
2007
Advanced RCC
Temsirolimus identified as best choice for poor-prognosis RCC
RCT
Temsirolimus - mTOR inhibitor
IFN - activates inflammatory and immune responses
119
Lit: Sunitinib vs. IFN-a for mRCC?
2007
Advanced RCC
Sunitinib > IFN-a for mRCC
PFS and objective response rate better
RCT
Sunitinib - TKI --> VEGF and PDGFR
IFN - activates inflammatory and immune responses
120
Lit: TARGET 2007
Advanced RCC
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
Lit: RECORD-1 2008
Advanced RCC
mccRCC patients who fail sunitinib should get Everolimus
RCT
everolimus --> mTOR inhibitor
PFS was improved in the everolimus group compared to placebo
122
Lit: COMPARZ 2013
Advanced RCC
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
Lit: METEOR 2015
Advanced RCC
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
Lit: CheckMate 025 2015
Advanced RCC
Nivolumab has better OS than everolimus for advanced RCC s/p 1-2 anti-angiogenic Txs (sunitinib)
RCT
125
Lit: CABOSUN 2017
Advanced RCC
Cabozantinib extends PFS vs. sunitinib in poor/intermediate risk met ccRCC
RCT
Previously untreated patients
126
Lit: CheckMate 214 2018
Advanced RCC
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
Lit: IMmotion151 2019
Advanced RCC
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
Lit: KEYNOTE 426 2019
Advanced RCC
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
Lit: TIVO-3 2020
Advanced RCC
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
Lit: CheckMate 9ER 2021
Advanced RCC
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
Lit: CLEAR 2021
Advanced RCC
(Lenvatinib + pembrolizumab) > (lenvatinib + temsirolimus) > sunitinib for PFS in previously untreated, advanced RCC
Pembrolizumab = IgG4k mAb to PD-1
Lenvatinib = TKI--> VEGF, FGFR, PDGFR
132
Sunitinib mechanism
TKI --> VEGF + PDGFR
Decreases tumor angiogenesis and growth
133
Sunitinib side effects
Myelosuppression, nephrotoxicity, hepatotoxicity, diarrhea, fatigue, nausea, stomatitis, vomiting, HTN, HTN, Hand-Foot Sx, rash
134
Sorafenib mechanism
TKI --> VEGF + PDGFR + RAF kinase
Decreases tumor angiogenesis and growth
135
Sorafenib side effects
Cardiac ischemia or infarction (3%), lymphopenia, hepatotoxicity, diarrhea, fatigue, nausea, anorexia, vomiting, HTN, rash
136
Tivozanib mechanism
TKI --> VEGF
Decreases tumor angiogenesis and growth
137
Tivozanib side effects
HTN, fatigue, diarrhea, rash, hoarse voice
138
Cabozantinib mechanism
TKI --> VEGF + MET + TAM
Decreases tumor angiogenesis and growth
139
Cabozantinib side effects
GI perforation and fistula
HTN
Fatigue
Diarrhea
Rash
Seizures
Jaw osteonecrosis
Anorexia
HA
Dizziness
140
Nivolumab mechanism
IgG4 mAb to PD-1
Decreases T-cell suppression
Increases T-cells killing cancer cells
141
Nivolumab side effects
Immune-mediated inflammation, hypothyroidism or hyperthyroidism, pancreatitis with Type I DM, colitis, rash, peripheral edema, neuropathy
142
Ipilimumab mechanism
IgG1-mAb to CTLA-4
Decreases T-cell suppression
Increases T-cells killing cancer cells
143
Ipilimumab side effects
Colitis
Diarrhea
Fever
Stomach pain
Bloating
Difficulty breathing
144
Atezolizumab mechanism
IgG4-mAb to PD-L1
Decreases T-cell suppression
Increases T-cells killing cancer cells
145
Atezolizumab side effects
Fatigue
Anorexia
Nausea
UTI
146
Bevacizumab mechanism
IgG1-mAb to VEGF
Decreased tumor angiogenesis
Increased apoptosis
147
Bevacizumab side effects
HTN
Rash
Nose bleeds
Infection
148
Lenvatinib mechanism
TKI --> VEGF + FGFR + PDGFR
Decreased tumor angiogenesis
Increased apoptosis
149
Lenvatinib side effects
HTN
Diarrhea
Fatigue
Anorexia
Hypotension
Thrombocytopenia
150
Pembrolizumab mechanism
IgG4-mAb to PD-1
Decreased T-cell suppression
Increased T-cells killing cancer cells
(Same mechanism as nivolumab?)
151
Pembrolizumab side effects
Immune-mediated inflammation
Hypo- or hyperthyroidism
Pancreatitis with Type 1 DM
Colitis
Rash
Fatigue
Diarrhea
Nausea
152
Axitinib mechanism
TKI --> VEGF, PDGFR, c-kit
Decreases tumor angiogenesis and growth
153
Axitinib side effects
Diarrhea
HTN
Fatigue
Anorexia
Nausea
Dysphonia
Hand-foot sxs
Weight loss
Vomiting
Constipation
154
Pazopanib mechanism
TKI --> VEGF, PDGFR, FGFR, c-kit
Decreased tumor angiogenesis and growth
155
Pazopanib side effects
Nausea
Vomiting
Diarrhea
HTN
Anorexia
Rash
Hair Loss
Fatigue
156
Temsirolimus mechanism
mTOR inhibitor
Decreased protein synthesis
Decreased tumor survival and growth
157
Temsirolimus side effects
Fatigue
Rash
Mucositis
Myelosuppression
Hyperglycemia
158
Everolimus mechanism
mTOR inhibitor
Decreased protein synthesis
Decreased tumor survival and growth
159
Everolimus side effects
Fatigue
Rash
Diarrhea
Stomatitis
Infections
Myelosuppression
Hyperglycemia
160
What percentage of surgically resected tumors \< 4 cm are benign?
15-20%
161
What percentage of RCC cases are familial? What are syndromes?
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
Major subtypes of RCC?
clear cell
papillary 1 or 2
chromophobe
collecting duct
unclassified
uncommon: acquired cystic, clear cell tubulo papillary, renal medullary (sickle cell)
163
Advanced PE findings?
Paraneoplastic syndromes (htn, polycythemia, hypercalcemia)
adenopathy
varicocele
164
Name benign renal tumors?
Papillary adenoma
Oncocytoma
AML
Metanephric adenoma
Adult cystic nephroma
Mixed epithelial stromal tumors
Juxtaglomerular cell tumor
165
What is T1 renal tumor? subtypes?
T1 → _\<_ 7 cm in greatest dimension, _limited to kidney_
T1a _\<_ 4 cm
T1b \< 4 cm, but not _\>_ 7 cm
166
Describe renal tumor T2:
T2 → \>7 cm in greatest dimension, _limited to kidney_
T2a → \> 7 cm but _\<_ 10 cm
T2b → \> 10 cm
167
Describe renal mass T3:
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
Describe renal mass T4:
T4 → invades beyond Gerota's (including contiguous adrenal extension)
169
Define renal cancer N and M stages:
Nx → LN not assessed
N0 → no region LN mets
N1 → mets to regional LN
M0 → no distant mets
M1 → distant mets
170
Describe renal mass stages:
171
Describe the treatment options for clinically localized renal cancer:
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
In a patient with renal mass, clinicians SHOULD obtain which imaging? How is mass characterized?
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
Nephrometry Score
RENAL
Radius, Exophytic/Endophyic, Nearness to CS, A/P, Location re: polar lines
174
In patients with suspected renal cancer, clinician SHOULD obtain which labs? Metastatic eval?
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
What makes a renal mass higher risk?
presence of thrombi, presumed adenopathy, larger tumor size, infiltrative appearance, extensive tumor necrosis, severe relevant sxs or PE findings
176
In patient with solid or Bosniak 3 or 4 mass, in addition to labs and metastatic workup, what other classifications SHOULD be done?
GUIDELINE STATEMENT 3
Assign CKD stage base on GFR and degree proteinuria
177
In regards to counseling for suspicious renal mass, who SHOULD be considered as players of the multidisciplinary team?
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
Clinicians SHOULD provide counseling that includes current perspectives about tumor biology and what patient-specific risk assessment:
GUIDELINE STATEMENT 5
Sex, tumor size/complexicty, histology, imaging characteristics
cT1a (low oncologic risk → indolent, \<2% risk mets)
179
When counseling treatment options for renal mass, clinicians SHOULD review the most common urologic and non-urologic morbidities of each treatment pathway including:
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
What SHOULD clinicians review in regards to renal function recovery related to renal mass management:
GUIDELINE STATEMENT 7
Progressive CKD
ST and LT need for RRT
LT OS considerations
181
Clinicians SHOULD refer to nephrology renal mass patients with:
GUIDELINE STATEMENT 8
High risk of CKD progression (eGFR \< 45), confirmed proteinuria, DMII pre-existing CKD, or expected GFR \< 30 after sx
182
In regards to renal cancer, when is genetic counseling RECOMMENDED:
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
Syndrome: Von Hippel-Lindau (VHL)
Gene: VHL
Clear cell RCC, renal cysts, hemangioblastomas of CNS, retinal angiomas, pheochromocytoma
184
Syndrome: Hereditary Papillary Renal Carcinoma (HRPC)
Gene: MET
Type 1 papillary RCC
185
Syndrome: Birt Hogg-Dube (BHD)
Gene: FLCN
chromophobe RCC, oncocytoma, hybrid oncocytic/chromophobe tumors (HOCTs), cc RCC (less common), renal cysts, cutaneous fibrofolliculomas, lung cysts, spontaneous PTX
186
Syndrome: Hereditary Leiomyomatosis and RCC (FH)
Gene: FH
type 2 papillary or CD RCC, cutaneous leioyomyomas, uterine leiyomyomas
187
Syndrome: Succinate Dehydrogenase Kidney Cancer (SDH-RCC)
Gene: SDHB/C/D
ccRCC, choromophobe RCC, type 2 papillary RCC, oncocytoma, pheochromocytoma/paraganglioma
188
Syndrome: BAP-1 Tumor Predisposition Syndrome
Gene: BAP-1
ccRCC, uveal melanoma
189
Syndrome: Tuberous Sclerosis Complex
Gene: TSC 1 or 2
AML, ccRCC, oncocytoma, lymphangioleiyomyomastosis (LAM), seizures, developmental delay
190
Syndrome: Cowden/PTEN Syndrome associated RCC (CS-RCC)
Gene: PTEN
Thyroid, breast, and endometrial cancer, mucocutaneous lesions, RCC with papillary mc, other forms of RCC including cc
191
When considering RMB what SHOULD be counseled?
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
When concerned about hematologic, metastatic, inflammatory, or infectious mass, clinicians SHOULD consider? What type of cancers are common?
GUIDELINE STATMENT 11
RMB
Lymphoma, lung, melanoma, colon, thyroid
193
RMB SHOULD be obtained on utility-based approach when it may influence mgmt. It is NOT required when:
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
How SHOULD RMB be done?
GUIDELINE STATEMENT 13
Multiple core biopsies and preferred over FNA
195
Why is NSS (PNx) important? When is it appropriate to consider?
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
Intraoperatively, how SHOULD clinicians prioritize nephron sparing and balance with what other goals?
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
When SHOULD a clinician consider RNx?
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
Patients undergoing renal sx, SHOULD have LND when?
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
For patients with renal mass, when SHOULD adrenalectomy be performed?
GUIDELINE STATEMENT 21
imaging and/or intraoperative findings suggest mets or direct invasion of adrenal gland
pT4 (contiguous)
M+ if hematogenous
200
How SHOULD renal mass surgery be performed?
GUIDELINE STATEMENT 22
Minimally invasive (when it would not compromise outcomes)
\*benefits in ST complications, fewer longer term
201
After PNx of RNx, adjacent renal parenchyma SHOULD be evaluated:
GUIDELINE STATEMENT 23
evaluate for intrinsic renal dz and particularly for CKD or risk factors for CKD
202
When SHOULD clinicians refer to medical oncology for renal masses?
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
What types of TA can be considered for renal mass? Who SHOULD be considered?
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
Describe RFA and cyroablation:
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
When treating with TA, what SHOULD be performed prior to or at time of tx? What should counseling include?
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
Patient related factors for AS vs. Expectant Mgmt vs. Intervention
207
When SHOULD AS be utilized?
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
When is intervention RECOMMENDED over AS? When is AS possible in this case?
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
Follow up after intervention of renal mass: benign vs. malignant?
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
What follow up labs for malignant renal mass s/p tx?
GUIDELINE STATEMENT 35
Cr, eGFR, UA
CBC, LDH, LFT, ALP, Ca → discretion of MD or if advanced dz
211
When following patient s/p tx for renal mass, when do you refer to nephrology?
GUIDELINE STATEMENT 36
with progressive renal insufficiency or proteinuria
212
When do you perform bone scan for renal mass f/up post tx? When head or spine CT/MRI?
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
Patients renal mass with suggestive sxs/signs of mets next steps?
GUIDELINE STATEMENT 40
evaluate to define extent of dz
refer to med onc
sx or ablation considered with isolated or oligo-mets
214
In pts with new renal primary or local recurrence, what is next steps?
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
Describe risk categories of patients s/p PNx or RNx:
GUIDELINE STATEMENT 42
See table, sx margins positive → increase risk category by one level
216
Recurrence rates by risk level for renal mass post sx:
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
Follow up after TA:
GUIDELINE STATEMENT 45
bx confirmed malignancy or non-dx
CTU/MRU w/in 6 mo (then follow same as intermediate risk category)
218
f/up schedule after surgery for renal cancer:
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
f/up algorithm table for renal mass
220
Describe an extraperitoneal flank approach for Nx:
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
How do you manage an acute post operative urine leak?
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
Most important prognostic determinant of RCC?
local tumor extent/size/stage
histologic subtype
surgical margins
regional nodal status
evidence of distant met status
performance status
223
What about margins?
\<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
What are risk factors and pathogenesis of ccRCC? what about VHL association?
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
Describe trans peritoneal lap Nx:
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
Common locations of positioning injuries for renal sx:
Brachial plexus
Lateral popliteal nerve
Femoral nerve
Sciatic Nerve
\*usually resolve 4-6 weeks, can last up to 2y
227
What are insufflation/access related complications and treatment:
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
Name vascular complications and tx of lap surgery:
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
Complications of PNx:
Intraoperative hemorrhage
Delayed bleeding
Persistent leak from CS
Perirenal abscess
Urinoma
Reno-cutaneous fistula
Acute tubular necrosis
Conversion to RN
230
what control is needed with IVC thrombectomy?
* **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
IVC thrombus classification:
* 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](https://university.auanet.org/core/oncology-adult/renal-neoplasms/index.cfm?&ct=732f2f653c1b8c46b85ee264ee17f16de174c7f79db565af72a4abdf1b3b918781d11542c0555f10607f8cc4042a0197acb826bb3f2978aa6b6572e6d708a06d#ref_9036)
* **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
Where does RCC metastasize?
Lung → 50%
Liver → 33%
Bone 32 → 32
Brain → 25%
233
5 year survival for RN by stage?
Stage 1 → 95%
Stage II → 85%
Stage III → 60%
Stage IV → 20%
234
What are s/s important to ask at renal mass f/up after Nx or PNx? PE components?
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
Labs to consider for f/up of post sx renal mass??
CBC, LDH, LFTs, UA, BUN/Cr (eGFR), ALP (sxs)
236
What is ddx of post sx bone pain (ribs) and elevated ALP on f/up?
Hyperthyroidism
Pregnancy
Hepatitis
Biliary Obstruction
Non malignant bone conditions (Pagets)
Bone mets
237
What is ddx of solid enhancing renal mass?
RCC
vascular malformation
infarct
urothelial carcinoma
oncocytoma
AML
metanephric adenoma
Met dz
renal abscess
XGP
238
What are risk factors for AKI with IV contrast?
htn
pre-existing CKD
hemodynamic instability
volume depletion
Age \> 75 yo
CHF
High volume contrast media
239
What tactics can be utilized to prevents kidneys with IV contrast load?
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
What do you look at for post-ablation CT?
additional, new renal nodules
satellite or port site soft tissue nodules
size change of mass (increase or decrease)
enhancement
241
what are tx options for post ablation failure?
salvage RNx
salvage PNx
repeat bx
repeat ablation
242
MC IVC injuries during PNx or Nx
avulsion of right adrenal vein from IVC or right gonadal from IVC
243
Define Bosniak classification of renal cystic tumors:
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
Early Post-Op complication of PNx?
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
Late Post-op complications of PNx?
1. UJPO: scarring around hilum and UPJ
2. HTN, with renal trauma also 5% (page kidney)
3. AVM
