Nephrology Case Presentation Staci Smith DO November 20, 2009.
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Transcript of Nephrology Case Presentation Staci Smith DO November 20, 2009.
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Nephrology Case Presentation
Staci Smith DO
November 20, 2009
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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.
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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
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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
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Past Medical History
1. CKD 3 - baseline Cr 1.5-1.82. Bilateral renal masses, worrisome for renal cell carcinoma3. Hypertension 4. Coronary artery disease5. Hypercholesterolemia6. MI 7. Peripheral vascular disease8. Diabetes mellitus, type 2, insulin requiring 9. Tobacco abuse
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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
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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
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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
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ER Initial Labs
134 88 49 172 3.5 34 6.1
No Ca, Mg, Phos, UA
20.5 15.0 474 46.3
Cr back in Oct 2009 = 1.5
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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
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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
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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
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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%-
300% from baseline
<0.5ml/kg/hr for >12
hrs
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
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AKI – RIFLE Criteria
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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 solid-
appearing mass at the superior pole of the left kidney with vascular flow
no hydronephrosis
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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
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Renal cell carcinoma
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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
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Incidence rates are rising three times faster than mortality rates
Survival has improved over time
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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
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Renal cell carcinoma
Risk factors PCKD- RCC often bilateral Alcohol Cytotoxic chemotherapy/ prior radiation Unopposed estrogen Uncontrolled hypertension
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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
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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
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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
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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)
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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.
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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
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Renal cell carcinoma
challenging tumor because paraneoplastic syndromes hypercalcemia erythrocytosis nonmetastatic hepatic dysfunction (Stauffer
syndrome) polyneuromyopathy amyloidosis dermatomyositis hypertension
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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
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Imaging – often incidentally discovered
CT scan imaging procedure of choice for diagnosis and
staging
Ultrasonography MRI PET
mets
Bone Scan Especially high alk phos
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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
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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
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Robson staging system
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Treatment
probability of cure is related directly to the stage
more than 50% of patients with renal cell carcinoma are cured in early stages
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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
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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
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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
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Treatment
For previously untreated patients low or intermediate risk sunitinib or the combination of bevacizumab
and interferon alpha
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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
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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
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Learning Points
Stages of CKD
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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
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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
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Thank You ;)
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Resources Up to date http://emedicine.medscape.com/article/281340-
treatment