Nephrology Case Presentation Staci Smith DO November 20, 2009.

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 1.5-1.82. 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

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 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

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%-

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

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 solid-

appearing 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/281340-

treatment