KIDNEY TUMOURS

BY

DR. I. O. MBAH (MB;BS, FWACP)

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WHAT IS A KIDNEY TUMOUR?

A growth or a mass inside our kidneys

Some of these growths are cancerous but many are not (GOODNEWS)

Introduction 1: PURPOSE OF OUR KIDNEYS

• Detoxify (clean) our blood
• Balance fluids
• Electrolyte balance (Na+, K+, Ca2+, Mg+, HCO3- etc)
• Make hormones that stabilize our BP
• Make RBCs
• Keep our bones strong. How?

MORE on A KIDNEY MASS

• A tumour is an abnormal growth in the body
• A kidney tumour is an abnormal growth in the kidney
• 1 in 4 of kidney masses are benign (non cancerous)
• Smaller masses are more likely to be benign
• Larger ones more likely to be malignant (Ca)
• Some tumours grow slowly, others aggressive and spread very quickly

• Most kidney growths (40%) are small and localized
• Localized means tumour has not spread from where it started
• The main classes of kidney tumours are:
• RCC
• Benign tumours
• Wilms tumours (rare in adults)

INTRODUCTION 2

• Renal Cell Ca (RCC) is the most frequently occurring solid lesion within the kidney
• Followed by WILM’S TUMOUR (mostly in children)
• Urothelial tumors of the Calyces and Renal pelvis (adenocarcinoma)- Hypernephroma
• Bcos it resembles tumour from adrenal cortex

EPIDEMIOLOGY

• Kidney tumours account for 2-3% of all cancers
• Male preponderance 1.5:1
• Peak incidence 60-70 years
• Highest incidence in developed countries (10 most common Cas in the USA, 76,000 new cases yearly)- Non Caucasians
• Worldwide annual increase in incidence 2%

AETIOLOGY

• There is no known cause for developing a kidney mass;
• But there are a number of things that can increase the risk for kidney tumours

RISK FACTORS

• A number of different risk factors have been studied
• some of which are modifiable (creating an opportunity for primary prevention).
• The risk factors for kidney cancer have been categorized as:
• Life style risk factors—
• tobacco smoking, excess body weight, alcohol consumption, physical activity and diet

PAST MEDICAL HISTORY

• Medical history—

hypertension,

chronic kidney diseases,

kidney stones,

dialysis-related cystic disease,

treatment with cyclophosphamide (chemotherapy agent),

post renal transplant 

 and diabetes mellitus

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GENETIC & ENVIRONMENTAL

• Environmental and occupational exposures—
• trichloroethylene and aristolochic acid
• Genetic risk factors and others

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PREDISPOSING FACTORS

• Cigarette smoking
• Obesity, poor diet
• HT / Prolonged intake of antihypertensive
• Workplace exposure to chlorinated chemicals
• Being on Renal dialysis
• Genetic Predisposition : von Hippel-Lindau (VHL) protein loss (4-6%)

• von Hippel-Lindau is protective

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• VLH protein fxns as a tumour suppressor and inhibits hypoxia induced genes
• These genes encode VEGF (vascular endothelial growth factor), TGF-ᾳ creating conditions favouring epithelial proliferation

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CLINICAL FEATURES

• 50% MAY BE ASYMPTOMATIC : NO symptoms in the early stages. Incidental finding using non-invasive imaging (like?)
• When symptomatic the classic triad are:
• Flank pain (bw the ribs and hips)
• Low back pain (refuses to go away)-Not traumatic
• Abd mass
• Gross haematuria

BASICALLY TRIAD of

• Presentation is classically described as the triad of:
• Macroscopic haematuria: 60%
• Flank pain: 40%
• Palpable flank mass: 30-40%^[1]
• This triad is however only found in 10-15% of patients

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OTHER SYMPTOMS

• The 3 “A”
• Fever (not inf related, PPP or does not go away)
• Due to metastases (30%)- depending on organ
• Stauffer’s syndr (paraneoplastic cholestatic jaundice)
• Hypertension
• Erythrocytosis
• Hypercalcemia

• About 25-30% of patients have metastatic disease at the time of diagnosis. 
•  Renal cancer most often spreads to the lungs (75%),
• regional lymph nodes (65%),
• bones (40%), and
• liver (40%).   The patient may complain of a cough or bone pain secondary to metastasis to the lungs or bone, respectively.

PHYSICAL EXAM

• Asthenia
• Cervical Lymphadenopathy
• Bil pitting oedema of the LLs
• Jaundice
• Abd mass
• Non-reducing varicocele

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INVESTIGATION

• Initiate imaging : >50% (Incidental findings)
• USS
• CT Scan of Abd & chest with contrast (metastases, intrabd & pulmonary)
• MRI of abd & chest (for those with renal impairment & allergic to contrast)
• Percutaneous bx (usually if secondaries are suspected)

OTHERS

• SEUCr & calculate eGFR
• FBC
• LFT
• Bone profile (Bone scan, CXR, for metastases)
• Renogram (if there’s concern about relative fxn of the contralateral kd)
• Urinalysis
• Kidney bx (for type of tumour)

GRADING & STAGING

• A TUMOUR GRADE TELLS HOW AGGRESSIVE the Ca cells are in your body
• A tumour stage tells how much the Ca has spread
• Grades 1-4 shows increasing severity with “1” the least & “4”, the highest
• A higher grade and advanced stage are seen in large tumours & has poor prognosis

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FUHRMAN NUCLEAR GRADE

• The most widely used and most predictive grading system for renal cell cancer is:
• The "Fuhrman nuclear grade“
• which is on a scale of I-IV,
• where grade I carries the best prognosis and grade IV the worst.

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STAGING : TNM Classification

• T = Primary tumour
• N = Regional Lymph nodes
• M = distant Metastases

• T1a = ≤4cm in greatest dimension restricted to the kd
• T1b = >4cm ≤ 7cm
• T2 = >7cm limited to the kd
• T3a = invasion of adrenal or perinephric tissues but not beyond
• T3b = extension to renal vein/ branches or IVC below the diaphragm
• T3c = IVC above the diaphragm
• T4 = Tumor invades beyond Gerota’s fascia

• N0 = No regional LN
• N1 – One regional LN
• N2 = More than one regional LN

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• M0 = No distant Metastases
• M1 = Distant metastases

STAGE 2

METASTASES

TREATMENT

• Patients with renal cell cancer may work with a team of health care professionals to coordinate their care. Eg
•  Urologist, Surgeon,
• Urologic Oncologists,
• Medical Oncologists,
• Radiation Oncologists,
• Oncology Nurse,
• Registered Dietician

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• There are different types of treatment for patients with renal cell cancer. Five types of standard treatment are used:

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1. Surgery
2. Radiation therapy
3. Chemotherapy
4. Immunotherapy
5. Targeted therapy

1. ^]

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RCC is primarily treated by surgical interventions.

Although aggressive, a radical nephrectomy is the preferred method of treatment for both localized and metastasized diseased.

• This consists of the removal of:
• Kidney
• Gerota’s fascia : (fibroareolar tissue surrounding the kidney and perirenal fat)
• Adrenal gland
• Regional lymph nodes

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TREATMENT

• If localized you can do any of the following in radical nephron sparing nephrectomy (T1a in the presence of normal contralateral kd)
• 1. OPN (Open partial)
• 2. LPN (Laparoscopic Partial)
• 3. In T3b & T3c do radical nephrectomy & thrombectomy
• Lymph node dissection not routinely done

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LOCAL RECURRENCE RATE

• 3-6 YEARS FOLLOW UP after OPN = 0-4%
• LPN more complicated than OPN usually done for pts with T1-2 (papillary type 1 RCCs) are indolent compared to Type 2 which is more aggressive

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Other modalities of therapy

• Cryotherapy or Radiofrequency probes placed either laparoscopically or percutaneously depending on tumour position
• 5yr local recurrence rate following Cryoabalation is 6-10%
• Treatment of mRCC Tumor nephrectomy + INF-ᾳ improves survival
• INF-ᾳ or IL-2
• Angiogenesis inhibitors /(Sorafenib & Sunitinib) ie
• Multikinase inhibitors; Temsirolimus (mTOR) (Mammalian…) better as monotherapy

Kidney cancer is rarely curable once it has spread to other organs at the time of diagnosis.

Targeted agents are currently considered as the standard treatment for advanced kidney cancer that has spread to other organs. ^[9]

• Targeted therapies, which work by targeting the cancer at a cellular level, have expanded the options for the treatment of kidney cancer.
• Targeted treatments block specific abnormal signals present in kidney cancer cells that allow them to grow.
• These medications have shown promise in treating kidney cancer that has spread to other areas of the body.

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• The targeted medications Axitinib (Inlyta), Bevacizumab (Avastin), Pazopanib (Votrient), Sorafenib (Nexavar) and Sunitinib (Sutent)
• block signals that play a role in the growth of blood vessels that provide nutrients to cancer cells and allow cancer cells to spread.

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• Temsirolimus (Torisel) and Everolimus (Afinitor) are targeted medications that block a signal that allows cancer cells to grow and survive.

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PROGNOSTIC INFO

• TNM Stage
• RCC sub type
• Histological features carrying poor prognosis (papillary 2 instead of 1)
• Coagulative necrosis in clear cell RCC
• Microvascular invasion

OTHERS

• Collecting Duct Ca is frequently metastatic at diagnosis
• Renal medullary Ca has some morphological overlap (papillary 1 & 2)and occurs in younger patients and asso with SCD
• Renal Oncocytoma are almost invariably benign but rare hybrid tumours with chromophobe RCC exist
• Current WHO (2004)Histological grading is based on Heidelberg classification