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Nephrology Case Presentation

Staci Smith DO November 20, 2009. Nephrology Case Presentation. Case Presentation.

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Nephrology Case Presentation

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  1. Staci Smith DO November 20, 2009 Nephrology Case Presentation

  2. 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.

  3. 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

  4. 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

  5. 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. Hypercholesterolemia 6. MI 7. Peripheral vascular disease 8. Diabetes mellitus, type 2, insulin requiring 9. Tobacco abuse

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. Stages of AKI

  14. AKI – RIFLE Criteria

  15. 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

  16. 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

  17. Renal cell carcinoma

  18. 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

  19. Incidence rates are rising three times faster than mortality rates • Survival has improved over time

  20. 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

  21. Renal cell carcinoma • Risk factors • PCKD- RCC often bilateral • Alcohol • Cytotoxic chemotherapy/ prior radiation • Unopposed estrogen • Uncontrolled hypertension

  22. 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

  23. 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

  24. 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

  25. 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)

  26. 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.

  27. 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 Differential Diagnosis of RCC

  28. Renal cell carcinoma • challenging tumor because paraneoplastic syndromes • hypercalcemia • erythrocytosis • nonmetastatic hepatic dysfunction (Stauffer syndrome) • polyneuromyopathy • amyloidosis • dermatomyositis • hypertension

  29. 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

  30. Imaging – often incidentally discovered • CT scan • imaging procedure of choice for diagnosis and staging • Ultrasonography • MRI • PET • mets • Bone Scan • Especially high alk phos

  31. 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

  32. 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

  33. Robson staging system

  34. Treatment • probability of cure is related directly to the stage • more than 50% of patients with renal cell carcinoma are cured in early stages

  35. 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

  36. 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

  37. 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

  38. Treatment • For previously untreated patients • low or intermediate risk • sunitinib or the combination of bevacizumab and interferon alpha

  39. 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

  40. 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

  41. Learning Points • Stages of CKD

  42. 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

  43. 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

  44. Thank You ;)

  45. Resources • Up to date • http://emedicine.medscape.com/article/281340-treatment

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