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Bilateral Wilms� Tumor

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Bilateral Wilms� Tumor
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Bilateral Wilms’ Tumor

Samuel Anim MD



3/12/2010



I have nothing to disclose

Case

• CC: 13 m o F with progressive abdominal distension and

constipation for 3 weeks



• ROS: Intermittent fever, Dyspnea, vomiting, no weight

loss, no hematuria



• PMHx : Idiopathic dilated cardiomyopathy @ 4 months of

age with LVFS of 16 % and EF 30 %

• Meds : enalapril, carvidilol, digoxin

• G&D : Appropriate

• FHx : Negative for malignancy. Still birth in maternal Aunt

• Birth Hx : Normal

Examination

• T: 38.5 F, HR: 101-140, BP: 108 – 143/56-100, RR: 40,

O2: 95 %

• HEENT: No syndromic facies PERRL

• NECK : Supple without lymphadenopathy

• RESP : Slightly decreased at the bases, otherwise CTAB

• CVS: S1 + S2 no murmurs

• ABD: 12 cm mass below the right costal margin and 5

cm below the left costal margin

• CNS: grossly intact

• GEN: normal female pre pubertal external genitalia

tanner stage I. No masses/hernia in the groin

• SKIN: Intact

• EXT: normal

Blood work

• CBC:

– WBC: 19.2 (n- 59, l - 26 m 13); Hb: 12 g/dl; Plt - 606

• CMP normal except for,

– Na 134, BUN 21, Protein 5.4, albumin 2

• Mg, Phos, Ca - normal

• LDH - 650, ESR - 71

• Urinalysis:

– 2-3 + protein,

– microscopy negative for RBC,

– hyaline and granular casts present

• Ur Protein – 265, Ucr – 25.7, Urine Prot/Cr - 10

• Lipid panel normal

Imaging

• Initial US from OSH : Polycystic Kidney Disease

• US:

– Right kidney is almost entirely replaced by mass. The larger upper pole mass

measures 9.4 x 8.2 x 11.2 cm. and lower pole mass measuring 3.0 x 3.5 cm. This

mass is solid and contains multiple focal cystic areas, likely representing necrosis.

– The left lower pole renal mass measures 3.3 x 3.4 x 2.8 cm. The parenchyma of

the left kidney is otherwise normal.

• CT Abdo/Pelvis – Bilateral renal masses

• Chest CT: normal

• Pathology : Nephroblastoma with intralobular

nephrogenic rests and areas of focal necrosis bilateral

• Special tests

– DNA micro array – negative for genetic imbalance

– WT 1 mutation: transition of G>A @ position 1186 0f codon

396 associated with Denys Drash syndrome

– Karyotype – 46 XX

BILATERAL WILMS’ TUMOR

Epidemiology

• 1st described by Dr Rance in 1814 with bilateral tumors

• Max Wilms – 1899 also described bilateral presentations

• Mean age of presentation earlier than unilateral Wilms’

• Incidence

– Unilateral: 6 % of all childhood cancers = 650 new

cases /year

• Bilateral 5- 8 % of all Wilms’ tumor

• Equal sex distribution

• AA>Caucasians>Asian

• Metachronous Vrs Synchronus

Clinical features

• Abdominal mass – Commonest symptom

• +/- pain, fever N &V constipation, weight loss

• Hematuria – 30 %

• Microscopic /macroscopic

• Hypertension - 25 %

– Cardiomyopathy

• Hypereninemia and increased cathechol amines

• Other vaso-active amines involved

• Part of a syndrome - 20 %

– Genital, eyes, MR,

• Coagulopathy – 10 %

– Acquired vWF

Pathology

• 3 elements

• Blastemal, stromal, epithelial

• Anaplasia

• Polypoid nuclei, > 3 X surrounding nuclei

• Frequency of 5-7 %

• Focal of diffuse

• Marker of Resistance to chemotherapy

• Nephrogenic Rests

• Embryonal nephroblastic tissue

• Intralobar or intralobular

• Majority regress spontaneously

• Remain dormant or progress to malignancy

WT 1 Gene mutation

• WT 1

– 5-15% of all Wilms’ tumor

• located on 11p13

• 10 exons

• Encodes transcription factors with 4 zinc finger regions

• Alternative splicing may result in inclusion and exclusion of 3 amino

acids (KTS) -

• 4 main isoforms

– +KTS bind to RNA and – KTS bind to DNA

– High levels in Podocytes

• Required in ureteric budding, nephron formation, differentiation of the

podocytes

• Complex phenotypes

• In mice, involved in coronary vessels and epicarduim abnormalities

Wilms’ Tumor Genes cont

• WT 2

– 11p15.5

• Region of genetic imprinting

– BWS (5%) and IGF II expression

• WT 3

– 16 q

• WT X

- located on the X chromosome

– Tumor suppressor

– ? Role as a prognostic factor in Wilms’ tumor (15/51)

• FWT 1- 17 q, FWT2 – 19 q, p53, 1 P

Genetic Syndrome

• Denys Drash (DDS) – 95 %

• Frazier’s syndrome – rare

• complete gonadal dysgenesis, gonadoblastoma

• Nephrotic syndrome with FSGC

• Intron 9

• WAGR – 30 %

• Wilms tumor, Aniridiae, GU abnormalities MR

• BWS and other over growth syndromes –

5%

Denys Drash Syndrome

• Pseudohemaphroditism

– With 46 XY or 46 XX

• Congenital GN (Diffuse Messangial sclerosis) with

progression to ESRD

– Presents with Proteinuria

• Wilms’ tumor

– usually bilateral

• Exon 8/9

– Part of the zinc finger encoding region

Cardiomyopathy and WT1 mutation

Wagner et al 2008



• Case report of a 4 month old F with sever HTN 220/140, FTT

oliguria, RF

• HTN unresponsive to multi drug therapy with Nicardipine, enalapril,

labetalol. Associated with cardiogenic shock and Anemia,

thrombocytopenia

• US consistent with hypertrophy and moderate signs of heart failure

and pericarditis

• Bilateral nephrectomy performed – dialysis dependent and awaiting

transplant. Required minoxidil after nephrectomies

• Pathology

– Persistence of metanephric blastema with focal calcifications. No

wilms’ tumor

– Imunno staining with antibodies against podocytes (WT1

neprine) revealed no uptake when compared to controls of

normal and wilms tumor patients

– further testing revealed complete absence of glomerulii

• Sequennce analysis of WT1 mutation revealed C-T at BP 29 of exon

9 in blood and blastema tissue

• No abnormality identified in parents – de novo mutation

Prognostic factors

Asch et al 1985 (1966-1981)

• Age at presentation

• Stage – kidney with the

highest stage

• Biologic markers –

– LOH 1p and 16 q

(NWTS - 5)

• Histology

– Favorable Vs.

unfavorable

– Anaplasia

• Synchronous Vs.

Metachronus

• Metastasis to the lungs

Prognostic factors

Treatment

• Aim

1. Eradication of neoplasm

2. Preservation of Renal function

• Synchronous – 9 % have RF

• Metachronous – 18 %

• Unilateral Wilms' – 1 %

• Recurrent or Persistent disease commonest

cause

• Treatment related – Rad, Chemo, Surg, Genetics

3. Decreasing toxicity from Chemotherapy

Treatment

• Surgery

• Timing

• Nephron sparing surgery

• Chemo therapy

• DACT, VCR. DOXO,

• IFOS, Carboplatin and Etoposide

• Radiation

• Dependent on stage

• Tumor bed Vs. whole abdominal vs. chest for metastasis

• Complications

• Recurrence – 8.2 %

• ESRD

Surgery Vs. Biopsy +Chemo

1970- 1990 @ L A Children’s





Surgery Biopsy + chemo

N- 8 N-7



Age 3.6 y +/- 2.2 2.3 y +/- 2.2





% renal mass preserved 52 +/- 12 73 +/- 16 (p – 0.03)





Survival No difference No difference





Metastasis/ Local No difference No difference

recurrence



Renal Failure 3 1

UK study

Kumar et al 1998



• Aim: Conservative treatment using initial biopsy,

chemotherapy and definite surgery compared to Surgery

up front followed by chemo therapy (1980 - 1995)

• N- 71 children with Bilateral Wilms

• 57 - biopsy, chemo and surgery

• 13 - surgery and chemo

• 1 - bilateral renal cyst Excluded

• All patients had synchronous tumors

• OS – 69 % in both groups

• Renal function normal in 80 % of both groups

• Mean preserved renal mass 45 % in conservative Vs. 35

%

Current Bilateral Wilms tumor

study

• Aims : to improve 4 y EFS to 73 %

• Prevent removal of at least 1 kidney in 50 % of patients

• Definitive surgery by 12 week of chemotherapy

• Open Biopsy discouraged

– Avoid misdiagnosis

– Detection of anaplasia

• Positive in 30 %

• Open/Needle Biopsy upstages tumor to stage III

– increased incidence of abdominal recurrence

• Intensified chemotherapy for anaplasia

Progress

• Received 12 weeks of chemotherapy with DACT and

VCR

• Doxo: Held because of Hx idiopathic dilated

Cardiomyopathy

• Cardiomyopathy resolved with LV EF – 57 % and FS – 29 %

• Good response with decrease in tumor volume of >50 %

• Proteinuria resolved

• Maintained normal renal function

• Surgery after 12 weeks of chemotherapy

• Biopsy of normal renal tissue consistent with DMS

• Will follow closely with

• scans

• renal function

Concerns

• ESRD with dialysis dependence

– Peritoneal Vrs CVVH

• Recurrence

• Will not need abdominal radiation

References

• Prognostic factors and outcome in bilateral Wilms' tumor, Morris J. Asch, Stuart Siegel, Leslie

White, Eric Fonkalsrud, Daniel Hays, Hart Isaacs, Cancer, 56 (10), Pages 2524 - 2529

• Treatment of bilateral Wilms’ tumor: Comparison of initial biopsy and chemotherapy to initial

surgical resection in the preservetion of renal mass and funcion. Journal of Pediatric Surgery,

Volume 27, Issue 8, August 1992, Pages 1009-1015

Donald B. Shaul, Myur M. Srikanth, Jorge A. Ortega, G.Hossein Mahour

• Conservative surgical management of Bilateral Wilms tumor: results of the United Kingdom

Childrens Cancer Study Group. The Journal of Urology, Volume 160, Issue 4, October 1998,

Pages 1450-1453 Rajendra Kumar, Ray Fitzgerald, Fin Breatnach

• A novel wilms tumor 1 gene mutation in a achild with severe renal dysfunction and persistent renal

blastema, Pediatric Nephrology, Sep2008, Vol. 23 Issue 9, p1445-1453. Wagner, Nicole; Wagner,

Kay-Dietrich; Afanetti, Mickael; Nevo, Fabien; Antignac, Corinne; Michiels, Jean-Francois; Schedl,

Andreas; Berard, Etienne.

Thank You


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