Download renal cell carcinoma

Nephrology Case Presentation
Staci Smith DO
November 20, 2009
Case Presentation
 55 yo CM with CKD 3 ( baseline Cr 1.5-1.8) presents to
GVH ER with nausea , vomiting, and inability to keep
liquids or any medicines down since surgery last Friday. Pt
noticed that his abdomen has become progressively larger
. He has not been passing flatus or had any recent BM.
 Pt has been hypotensive with sbp’s in the 90’s
 NG tube was placed in the ER with 1800 cc of green liquid
output returned immediately.
Pertinent Review of Systems
 Positive for fatigue, decreased appetite and po intake,
increased abdominal girth as well as ab pain (now 10/10)
 Decreased BM’s and flatus
 Renal / Urinary specific
 Chronic foamy urine
 Positive bilateral renal carcinoma
 Decreased urinary output for past two days
 No recent OTC NAIDS
 No gross hematuria, known UTI’s, recent contrast or
colonic prep, incontinence, bph, history of stones, need
for any dialysis
Outpatient Medications
 1.Lisinopril / HCTZ 20 /12.5 one daily.
2. Glyburide 5 mg twice a day.
3. Neurontin 300 mg three times a day.
4. Aspirin 81 mg daily.
5. Multivitamin one p.o. daily.
6. Lantus 50 units subcutaneous p.m plus sliding scale
insulin
7. Norvasc 10 mg daily.
8. Coreg 25 mg twice a day.
9. Plavix 75 mg daily.
10.Crestor 20 mg p.o. every p.m.
11.TriCor 145 mg daily
Past Medical History
 1. CKD 3 - baseline Cr 1.5-1.8
2. Bilateral renal masses, worrisome for renal cell
carcinoma
3. Hypertension
4. Coronary artery disease
5. Hypercholesterolemia
6. MI
7. Peripheral vascular disease
8. Diabetes mellitus, type 2, insulin requiring
9. Tobacco abuse
Patient History
 Past Surgical History
 1. Right partial nephrectomy at OSU a week ago
2. He has had heart catheterization with PTCA.
3. Lipoma removal on the scalp.
4. Left lower extremity angioplasty in 2006
 Allergies
 none
 SHx
 Only positive for tobacco abuse x 30yrs, but quit one week ago
 FHx
 No family members on HD or immediate family with cancers
 Positive family history of DM and HTN
Important History
 Notably, the pt has a history of bilateral renal masses
since April 2009
 Partial right nephrectomy at OSU last Monday
 Previous poor outpatient follow up since April 2009
 Seen at Cassano Nephro only once in initial consult
 Multiple phone calls to stress importance of timely follow up
ER Physical Exam
 VS: BP 106/92- 92 HR, 96.7 F,15 RR, 95% on 2L oxygen
 Gen: Appears uncomfortable; no acute distress
 HEENT: Atraumatic, normocephalic. EOMI. Sclerae
anicteric. Mucous membranes are dry
 CV: HRR without murmur, rub, click, or gallop. S1, S2
 Pulm: CTAB without wheezing,rhonchi, or crackles
 Ab: Distended. Positive bowel sounds. He does have lap
trocar insertion site with mild erythema, and his belly has
voluntary guarding.
 Ext: No clubbing, cyanosis, or edema. No calf tenderness
bilaterally. Distal peripheral pulses are 2/4. No Lindsay’s
nails
 Neuro: There is no asterixis. CN 2-12 GI
ER Initial Labs
 134
3.5
88
34
49
6.1

No Ca, Mg, Phos, UA

20.5

Cr back in Oct 2009 = 1.5
15.0
46.3
474
172
ER Initial Labs
 CT scan – without contrast
 high-grade small bowel obstruction at the level
of the ventral hernia
 large amount of subcutaneous emphysema,
small amount of retroperitoneal and
smaller amount of intraperitoneal gas regional
to the right kidney where there
has been recent surgical intervention
Cause of the Patient’s Acute Kidney Injury ?
 Multifactorial
 hypovolemia
 Secondary to GI loss with nausea and vomiting
 Poor po intake with outpatient diuretics (HCTZ)
 hypotension in the prescence of OP ACE-I
 Bp 90/46 in ER
 rule out urinary obstruction
 nurses unable to place Foley
 can bladder scan
What is Acute Kidney Injury?
 An abrupt reduction in kidney function within
48 hours
 absolute increase in serum creatinine of > 0.3 mg/dl
 a percentage increase of 50%
 a reduction in urine output
 documented oliguria of < 0.5 ml/kg/hr for > 6 hours
 realize that acute kidney injury may be a precursor to
CKD, and CKD can also lead to AKI
Stages of AKI
Stage
Cr Criteria
Urine Output
Criteria
1
↑ Serum Cr of >0.3
mg/dl or increase to
≥150% - 200% from
baseline
<0.5ml/kg/hr for > 6hr
2
Increase serum
creatinine to > 200%-
<0.5ml/kg/hr for >12
hrs
300% from baseline
3
Increase serum creatinine
to >300% from baseline
(or serum creatinine
≥4.0mg/dl with an acute
rise of at least 0.5 mg/dl)
<0.3ml/kg/hr x 24 hrs or
anuria x 12 hr
AKI – RIFLE Criteria
Initial Renal US Report May 2009
 Right kidney measures 11.04 x 7.25 x 7.25 cm
 no hydronephrosis seen
 5.92 x 4.99 x 4.3 cm hypoechoic solid-appearing mass
within the cortex of the superior pole
 lesion demonstrates mildly increased flow
 also a 2.26 x 1.95 x 2.70 cm either complex cyst with
septation or two small adjacent cysts within the inferior
pole of the right kidney
 Left kidney measures 11.42 x 5.06 x 5.82 cm
 exophytic 1.9 x 1.5 x 1.7 cm hypoechoic solidappearing mass at the superior pole of the left kidney
with vascular flow
 no hydronephrosis
Initial CT Scan Report May 2009
 5.8 x 4.2 cm partially exophytic mixed attenuation lesion
arising from the superior pole of the right kidney
 most consistent with renal cell carcinoma until proven
otherwise.
 Small exophytic lesion in upper pole of the left kidney
 19 mm in diameter
 given its vascularity on the recent ultrasound a solid
lesion is suspected
Renal cell carcinoma
Renal cell carcinoma
 originate within the renal cortex
 80 to 85 % of all primary renal neoplasms
 transitional cell carcinomas
 renal pelvis are the next most common – 8%
 in 2009, approximately 57,800 people will be diagnosed
 13,000 will die from RCC in the United States
 worldwide mortality exceeds 100,000 per year
 eighth most common cancer
 typically fourth to sixth decade of life
Incidence rates are rising three
times faster than mortality rates
 Survival has improved over time
Renal cell carcinoma
 Risk factors
 Smoking- two fold increase
 Occupational exposure
 cadmium, asbestos, and petroleum by-products
 Acquired cystic diseases of the kidney
 30 times greater in dialysis patients with acquired
polycystic disease
 malignancy typically after at least 8 -10 yrs of
dialysis
 After transplant
Renal cell carcinoma
 Risk factors





PCKD- RCC often bilateral
Alcohol
Cytotoxic chemotherapy/ prior radiation
Unopposed estrogen
Uncontrolled hypertension
Genetic factors: Von Hippel Lindau
 Autosomal dominant
 abnormalities in chr 3pq
 increased formation of vascular
tumours (mostly benign) called
hemangioblastomas and risk
for renal carcinomas and
pheochromocytomas
Reed syndrome
 Multiple cutaneous and uterine leiomyomatosis
syndrome
 hereditary leiomyoma and renal cell cancer syndrome
 characterized by cutaneous leiomyomas, uterine
fibroids, and renal carcinomas
 renal tumors are aggressive
 metastasize and death in patients in their 30s
Renal Cell Carcinoma
 History
 Often zero point zero clues
 Twenty-five to thirty percent of patients are asymptomatic
 found on incidental radiologic studies
 Classic triad is not common – only 10%




flank pain
hematuria
flank mass
indicative of advanced disease
Renal Cell Carcinoma
 History







Weight loss (33%)
Fever (20%)
Hypertension (20%)
Hypercalcemia (5%)
Night sweats
Malaise
Varicocele
 usually left sided, due to obstruction of the
testicular vein (2% of males)
Renal Cell Carcinoma
 Physical




Gross hematuria
Hypertension
Supraclavicular adenopathy
flank or abdominal mass with bruit
 30% present with metastatic disease
 evaluation for metastatic disease
 lung (75%)
 Varicocele and findings of paraneoplastic
syndromes raise clinical suspicion for this
diagnosis.
Differential Diagnosis of RCC




NHL
Pyelonephritis
Abscess
Angiomyolipoma benign
 Oncocytoma -benign
 Metastasis from
distant primary
 Metastatic melanoma
 Renal adenoma –
benign
 Renal cyst
 Renal infarct
 Sarcoma
 Transitional cell
carcinoma of renal
pelvis
Renal cell carcinoma
 challenging tumor because paraneoplastic
syndromes
 hypercalcemia
 erythrocytosis
 nonmetastatic hepatic dysfunction (Stauffer
syndrome)
 polyneuromyopathy
 amyloidosis
 dermatomyositis
 hypertension
Labs to consider








Urine analysis
CBC count with differential
Renal profile
Liver function tests (AST and ALT)
Calcium
Erythrocyte sedimentation rate
Prothrombin time
Activated partial thromboplastin time
Imaging – often incidentally discovered
 CT scan
 imaging procedure of choice for diagnosis and
staging
 Ultrasonography
 MRI
 PET
 mets
 Bone Scan
 Especially high alk phos
Procedures and Subtypes of RCC
 Percutaneous cyst puncture and fluid analysis
 5 histologic subtypes of rcc





clear cell (75%)
chromophilic (15%)
chromophobic (5%)
oncocytoma (3%)
collecting duct (2%)
 very aggressive,often younger pts
Staging of RCC
 Robson modification of the Flocks and
Kadesky system
 Stage I - Tumor confined within capsule of kidney
 Stage II - Tumor invading perinephric fat but still
contained within the Gerota fascia
 Stage III - Tumor invading the renal vein or inferior
vena cava (A), or regional lymph-node involvement
(B), or both (C)
 Stage IV - Tumor invading adjacent viscera
(excluding ipsilateral adrenal) or distant
metastases
Robson staging system
Treatment
 probability of cure is related directly to the
stage
 more than 50% of patients with renal cell
carcinoma are cured in early stages
Surgical treatment of RCC
 Surgery is curative in the majority of patients
without metastatic RCC
 Preferred treatment for patients with stages I, II,
and III disease
 Also used for palliation in metastatic disease
 Radical nephrectomy
 most commonly performed standard surgical procedure
today
 complete removal of the Gerota fascia and its contents,
including a resection of kidney, perirenal fat, and
ipsilateral adrenal gland, with or without ipsilateral
lymph node dissection
Surgical treatment of RCC
 Laparoscopic nephrectomy
 Advantages
 less invasive procedure, incurs less morbidity, and is
associated with shorter recovery time and less blood
loss
 Disadvantages
 concerns about spillage and technical difficulties in
defining surgical margins
Treatment of RCC
 no hormonal or chemotherapeutic regimen is accepted as
a standard of care
 options are surgery, radiation therapy, chemotherapy,
hormonal therapy, immunotherapy, or combinations of
these
 IL-2-T-cell growth factor and activator and natural killer
cells
 Interferon alpha
 Sutent-Sunitinib
 multi-kinase inhibitor
 high response rate (40% )
 Sorafenib –Nexavar

kinase and vascular endothelial growth factor (VEGF)
multireceptor kinase inhibitor

advanced renal cell carcinoma
Treatment
 For previously untreated patients
 low or intermediate risk
 sunitinib or the combination of bevacizumab
and interferon alpha
Treatment Recommendations
 Radical nephrectomy
 most widely used approach
 preferred procedure when there is evidence of invasion
into the adrenal, renal vein, or perinephric fat
 Partial nephrectomy
 for smaller tumors
 particularly valuable in patients with bilateral or multiple
lesions
 If renal dysfxn
 Elderly patients with significant comorbid disease
 increases the risk of surgery
 ablative techniques
 cryoablation, radiofrequency ablation
What happened to the patient?
 Ordered records from OSU
 Cr post op was 2.5
 Did not required sx for incercerated hernia
 Reduced at bedside
 Aggressive IVF hydration
 Cr improved daily
 Peak Cr 6.1 11/16
 5.27
3.76
3.27
3.16
Learning Points
 Stages of CKD
Renal Cell Carcinoma Learning Points
 History
 Often zero point zero clues
 Twenty-five to thirty percent of patients are asymptomatic
 found on incidental radiologic studies
 Classic triad is not common – only 10%




flank pain
hematuria
flank mass
indicative of advanced disease
Learning Points: Renal Cell Carcinoma
 About 25-30% of patients have metastatic
disease at diagnosis
 fewer than 5% have solitary metastasis
 surgical resection is recommended in
selected patients with metastatic renal
carcinoma
Thank You ;)
 Resources
 Up to date
 http://emedicine.medscape.com/article/281340treatment