TUMORS OF KIDNEY
The kidney tumors exist more frequent in children and men 40-60 years. From data of
statistics, the kidney tumor in the adult people is 2-3 % of population. Men are ill almost
in the 2 times more frequent, than women. The concerning frequency of defeat of right
and left kidney is the same. More often an illness is bilateral, but on the occasion a
second kidney is struck later (sometimes in 15 years), that eliminates possibility of
metastasis. Probably, the tumor develops independently in it.
Ethiology. In the genesis of kidney tumor, it grows due to of hormone violations,
influencing an ionizing radiation and chemical matters. Some authors abide by the viral
theory of origin of new formations of kidney. In origin of kidney tumor the smoking
assists. A prognosis and tactic of medical treatment at tumors is built on the basis of
results of morphological and histological researches of remote new formation. Malignant
tumors, about 90 % malignant tumors of kidney make a cancer. In 1883 Grawitz
described in details a cancer tumor of kidney which named for a long time after the
author’s name. Later they began to name it as a hypernephroma (for similarity to fabrics
of adrenal gland), and as a cancer. Now, they name this tumor as kidney “cancer”
(synonyms are “a lightcellular cancer”, “kidney-cellular cancer”). The kidney cancer
makes 5-6 % of all urology diseases and 2-3 % of new formations. It arises up mainly in
age 40-70 years, at men - in the 2,5-3 times more frequent. It develops from epithelium
of different path of nephron and collective tubes: ball capsule epithelium, kidney tubulla
(descending part of loop of nephron, distal part of tubulla loop of nephron). As a rule,
the united histological forms of tumor exist.
A frequency of defeat of right and left kidney is identical; the bilateral process exists
in 0,5-1,5 % cases. A tumor is localized in the different part of kidney. Their sizes are
from a few millimeters to 20-30 centimetres and more in diameters. Their form is round
or oval, surface is often hilly, rarely smooth and brilliant, the consistency is soft, elastic,
sometimes dense.
The pathomorphology. They distinguish ferrous, papillary and solid-cellular forms of
kidney cancer after the morphological structure.
As the great number of various morphological forms of kidney cancer exists, that’s
why it is very difficult to clear up the nature of new formation – a primary tumor or a
metastasis.
The kidney sarcoma seldom exists, in 3,3 % cases. The source of its origin can be
connecting of tissue, kidney capsule, remains of muscles and kidney, wall of kidney
vessels. The tumor’s consistency is soft (liposarcoma) or dense (fibrosarcoma); it is
grey, grey-rouse or yellow on section. The areas of necrosis and hemorrhages often
appear.
Classification.
Clinical staging is important in order to decide on a therapeutical approach but
surgical and anatomopathological staging is equally important for our knowledge about
prognosis.
The staging system for renal cell carcinoma was described by Flocks and Kadesky in
1958 and later modified by Robson in 1963. Robson’s classification was in the widespread use by the urological community. In 1978 RCC was for the first time staged
according to TNM staging system proposed by International Union Againts Cancer
(UICC).
Multiple revisions to the TNM system for RCC have been made during the last years
by American Joint Commission on Cancer (AJCC) and UICC. The TNM classification
was revised in 1987 and recently in 1997.
System by Floks and Kadesky, modified by Robson:
Stage I – tumor confined to the kidney
Stage II – extension of the tumor to perirenal fat (not beyond the Gerota’s fascia)
Stage III – local extension
a. to renal or inferior vena cava
b. locoregional lymph nodes are involved
c. venous and lymph nodal involvement
Stage IV – advanced disease
a. infiltration of adjacent organs except adrenal gland
b. distant metastases
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The UICC present TNM classification of RCC is following:
Т- a primary tumor;
Тх – it’s impossible to set a presence and tumor diffusion degree. This category can be
used for histological or citological confirmed metastases in the region lymphatic knots
or remote organs;
Т1 – tumor ≤ 7cm. in greatest dimension limited to the kidney;
T2 – tumor by size over 7 cm. in greatest dimension limited to the kidney;
T3 - tumor extends into major veins or involve adrenal or perinephric tissues but not
beyond Gerota’s fascia
T3a – tumor invades adrenal gland or perinephric tissues but not beyond Gerota’s
fascia
T3b – tumor grossly extends into renal vein or vena cava
T3c – tumor grossly extends vena cava above the diaphragma
Т4 - tumor invades beyond Gerota’s fascia
N-region lymphatic knots;
Nx- it is impossible to set the presence of metastases in the region of the lymphatic
knots;
N0 – no regional lymph node metastasis
N1 – metastasis to a single regional lymph node
N2 – metastasis in more than one regional lymph node
Мх- the defining of remote metastases is impossible
М0 – no distant metastasis
М1 – distant metastasis
In 1997 TNM classification of renal cell carcinoma the cutoff between T1 andT2
tumors was increased to 7 cm.
Heidelberg Classification of Renal Cell Tumors
I. Benign tumor Metnephric adenoma
Papillary adenoma
Oncocytoma
II. Malignant tumor Conventional RCC
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Papillary RCC
Chromophobic RCC
Ductal cell carcinoma
Non-classified RCC
Kidney cancer metastases in lung are accompanied by the rise of body temperature, by
cough with sputum, sometimes with the blood admixtures, by pain in side or behind
sternum. Multiple new formations appear. Sometimes the metastasis in lung has a type
of solitarry (single) node, which is not clinically shown for a long time. In such case it is
possible to delete a metastatic tumor.
The clinical feature of metastases in the central nervous system depends upon
localization of pathological cell.
The clinical picture of tumors of kidney is extraordinary various. In some cases tumors
are not accompanied by the subjective feeling for a long time. A diagnosis is putting in
case of inspection of patients concerning other disease, most frequently in the tie with
appearance of metastases in lungs, bones and others like that. However in majority of
patients in case of tumor appearance the general state of body become worse as a result
of intoxication by products of exchange in the tumular fabric. A patient complains of a
general weakness, rapid fatigue, decrease or loss of appetite, he is becoming thin,
increase body temperature (sometimes about 38-39 С), chill, and anemia.
In most cases of tumor kidney total haematuria (60-88 %) is shown. It appears
suddenly or bach pain background in area of kidney. Sometimes after haematuria there
is the typical attack of kidney colic that is halted together with out development of blood
clots (4-10 cm). Haematuria exists at one-two urination or a few hours proceed or days,
and then it is suddenly disappear. The next bleeding can appear in a few days, months
and even years.
So far as haematuria at the kidney tumors often has a profuse nature, it can cause the
tamponade
urinary
bladder
and
the
sharp
delay
of
urine.
Then there is a pain after the value symptom of kidney tumor. It exists in 50 % sick, it
can be dull and sharp, permanent and periodic.
4
A third symptom of kidney tumor is palpation of new formation. It exists in 50-75%
patients.
The kidney tumor symptoms often haven’t a urology nature, proceed during a few
months, and sometimes the years. It is a firm (“causeless”) rising of body temperature
(20-30% patient), general weakness (20-40%), a patient is becoming thin (20-30%), loss
of appetite, nausea, vomiting (10-15 %), neuropatia, miositis (4-6 %) and etc. About 30
% patients enter to a permanent establishment with the undiagnosed tumor.
The temperature of body is quickly normalized after a nefrectomii. If it isn’t, it is needed
to search in organism the metastases.
Hypertension is due to segmental artery occlusion or to elaboration of renin or reninlike substances. The most dramatic syndrome is associated with nonmetastatic hepatic
dysfunction and referred to as hepato-renal syndrome. Hepatic functions return to
normal by majority of patients after nephrectomy.
The varicocele belongs to the important symptoms, it is determined in the neglected
stages of disease. The causes of its appearance are: a) clench or germination by tumor of
left kidney venues; b) clench by tumor or metastases in the lymphatic vessels of lower
hollow venes; c) tumular thrombosis of lower hollow venes or kidney venes. Sometimes
there are remote metastases at first display of kidney tumor.
A diagnostics of kidney tumors at presence of the characteristic signs is simple. It is
based on the clinical displays of disease, data of laboratory and roentgenologic research
of patient.
In case of research of blood and urine the changes are exposed that are characteristic
not only for the kidney tumor. In case of general analysis of blood the ESR growths,
they mark anemia, at biochemical rising of activity of alkaline phosphatasa, level of
globulin, decline of albumin, maintenance in whey of blood and growth of its enzymin
activity and etc. The erytrocit-, protein- and leucocyturia are exposed in urine. The
tumor can calcificate. On urogram a calcification has a various structure. Give the
clearer image of contours of kidney tomographia and pneumoperutoneum.
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Plain film
Anterio-posterio film must precede any contrast study of the urinary tract.
T The film should include the entire area from the diaphragm to the pubic symphisis.
Plain film allows in many cases to suspect the presence of the tumor by:
-Enlargement of whole or part of the kidney
-Changing of the shape of kidney, abnormal position of the organ
-Presence of calcifications
Excretory Urography (IVP)
This examination is sometimes required by clinicians to complete the diagnosis of
renal neoplasm. IVP is the type of dynamic examination, which allows to evaluate
excretory functions of kidneys. In this examination we can observe all kinds of must be
done during so-called nephrographic phase. This is the period when pacification of the
renal parenchyma is at its best. Simple cysts or tumours may be diagnosed by this
method with 90 % accuracy. Polar enlargement of a kidney is one of the most frequent
pyelographic changes. The renal outline may be altered and markedly irregular.
Calcification of renal carcinoma is not common but may occur and may simulate renal
lithiasis or calcification of a renal cyst. The architecture of the collecting system varies
from simple deformity of a calyx to outright destruction of one or more calyces with
their amputation.
Computed tomography.
Over the past decade, CT has become the most widely used technique for diagnosis
and staging renal tumours, partially due to the very high overall accuracy up to 90 %,
that has been achieved.
CT should further evaluate indeterminate masses in US. A large variability in the
range of attenuation values exists because of necrosis, hemorrhage, calcification,
variable protein content and vascularity. Typically renal tumors are solid in density, that
is greater than a typical cyst. The margins of the mass are usually irregular. The density
of the mass may be homogeneous or non-homogeneous. The tumours can demonstrate
local invasion into the fat within Gerota’s fascia and to the adjacent organs.
The reported accuracy rate for CT in staging renal tumours ranges between 72 % and
98 %.
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Magnetic Resonance Imaging.
Due to its high tissue contrast and Multiplan imaging capabilities, MRI provides a
detailed display of renal anatomy. Recent technical developments overcoming the
problem of respiration motion artefacts and the use of paramagnetic contrast agents have
further improved the performance of MRI which is now an alternative or complementary
imaging modality to US, excretory urography and CT. On plain MR images solid as well
as cystic renal and pararenal masses often presents the same signal intensity as the
adjacent renal tissue. Therefore detection of such tumours is based only on the visible
displacement or alteration of organ contours.
Renal arteriography; aortography; phlebography an inferior vena cavography.
Visualization of the renal arteries and renal veins may be accomplished by:
- translumbar aortography
- percutaneous aortography
- selective renal arteriography
- percutaneous phlebography
It is dynamic study of arterial blood supply of the kidney and the tumours and allows
showing the pathology as well as anatomy. Visualization of the renal veins has
become very important in the diagnosis of invasive malignancies of the kidneys and
their prognostic evaluation. During these examinations we can provide embolisation of
the tumours in nonoperative tumours or before the surgery.
Ultrasonography.
This procedure should be initial in diagnosis of the urinary tract. This examination is
safe for the patient, noninvasive, repeatable and very efficient. Ultrasonography allows
distinguishing solid mass from the cyst. Probability of detection of 3-cm tumours is 95
%. The diagnostic capabilities of sonographic Doppler analysis of blood flow allow
noninvasive recognition of the vascular pathology. The Multiplan capability of US
demonstrates the extent of the tumours. Although US is extensively used in the
detection of renal neoplasm, it is less accurate than CT or MRI in the staging of
tumours. In 50 % of patients the retroperitoneal region may not be adequately
visualized. US is also unable to detect invasion.
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Differential diagnostics.
Frequently it has to differentiate a kidney tumor with the solitary and cyst, polycistosi,
by the kidney carbuncle, tuberculosis, hydronephros, the urostones illness, paranephritis.
Kidney tumor that solitarry cyst have many of general clinic-roentgenologic signs. At
that rate important diagnostic value have data of x-ray examination, computer
thomographia,
kidney
angiography,
echography,
punction
cystography,
and
nephrotomography.
Surgical treatment of renal tumours
The basic form of the renal tumor treatment is surgery. In the present time various
modalities of surgical treatment are used: radical surgery – radical nephrectomy,
nephron – sparing surgery and palliative surgery.
The fundamental principles of radical surgery are following:
- choice of the best incision
- preliminary ligation of the renal artery
- lymphadenectomy
- complete excision of the tumor
- control and the tumor extending into the inferior vena cava
- excision of resectable distant metastases
The most popular parietal incision for radical nephrectomy are: xiphoumbilicus
epigastric subcostal incision, transverse abdominal incision and thoraco-phrenolaparotomic incision.
Two last incisions give optimal exposure of inferior vena cava and are the best
approaches for right renal tumours (RCC) extending into the inferior vena cava.
Optimal parietal incisions allow to expose the main vessels: the vena cava inferior, the
abdominal aorta and allow to reach the renal artery at its origin. The most important
step of the radical nephrectomy is initial ligation of the renal artery and then ligation
of the renal vein. This procedure prevents the spread of the tumor cells. The next steps
are: the mobilization of the kidney, the division of the ureter and exenteration of the
renal lodge by “en bloc” removal of the kidney, adrenal and perirenal fat with Gerota’s
8
fascia. During radical nephrectomy hilar, pericaval or periaortal lymphadenectomy is
also performed.
The role of lymphadenectomy in renal cell carcinoma is controversial in the context
of oncological urology. The reported incidence of retropences in the frequency of
nodal involvement may be explained by the extent of lymphadenectomy. Recently the
incidence of nodal metastases is minor because the diagnosis of RCC often occurs in
the early stage. However in 7 % of patients with tumor confined to the kidney (T1,
T2,M0) nodal metastases were seen.
Cumulative
overall
survival
after
radical
nephrectomy
and
extended
lymphadenectomy was appreciated on 46% and 25 % at 5 and 10 years respectively.
In-patients with tumor stage pT1 N0 M0 survival rates at 5 and 10 years of 80 %
and 50 % respectively were noted, while in-patients with tumor stage pT2 N0 M0
survival rates were 68 % at 59 % at 5 and 10 years respectively.
Patients with tumor extending to perirenal fat (T3) have shown a 70 % survival rate
at 5 years after radical nephrectomy. It is a significant improvement compared to the
14 % survival rate at 5 years after simple nephrectomy.
In-patients with lymph node metastases survival rates of 52 % and 26 % at 5 and 10
years respectively were observed.
Lymphadenectomy, an integrating part of radical nephrectomy does not increase
operative mortality and morbidity, allows for improved surgical staging of the tumor
and lower frequency of local recurrences.
In the last years there have been some reports, which indicate that almost all patients
with lymphatic spread of RCC have additional distant metastases. Therefore, the
therapeutic effect of extensive retroperitoneal lymphadenectomy in association with
radical nephrectomy seems to be low.
However, limitedlymph node dissection may be useful as a staging procedure. Thus it
seems rational that radical nephrectomy with lymphadenectomy (extended or limited)
is indicated in T2, T3 and in some T4 cases of RCC tumours.
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Conservative surgery of renal tumours.
Renal cell carcinoma may develop synchronously in both kidneys in about 1,8 to 3 %
of cases.
Frequency of renal cancer in solitary kidney is not well known. The classic indications
for nephron sparing surgery are bilateral renal tumours, tumor in solitary kidney and in
the case when radical nephrectomy would result in renal insufficiency necessitating
dialysis or transplantation.
Conservative surgery for RCC may be identified with two types of procedures:
enucleating of the tumor (tumourectomy) and partial nephrectomy.
Both these
techniques may be performed in situ or ex situ. Usually, clamping of the renal artery is
unnecessary but if it was indicated regional hypothermia should be considered.
The classic indications for conservative surgery of RCC are justifiable. In the last
years there has been a tendency toward wider application of kidney sparing surgery.
Elective kidney sparing surgery means that this form of conservative treatment is used
when the contrlateral kidney is normal.
The arguments against elective nephron sparing surgery are following: radical
nephrectomy for T1 and T2 RCC will probably be curative in 100 %, the chance of
developing contrlateral tumor is small, higher complications rate for conservative
surgery, the possibility of tumor recurrence, the possibility of multifocal RCC in the
kidney. An argument favoring nephron-sparing surgery for RCC is its efficacy in
providing for cure of cancer in series of electively treated patients. The criteria for the
indications of elective nephron sparing surgery are following: the tumor should be
solitary, well demarcated on CT, the tumor should be well localized and easily
resectable, the tumor size should not exceed 4 cm. in diameter (3-5).
Elective kidney sparing surgery in the case of small, low grade, well-localized RCC
may be usually curative.
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Surgery of metastatic renal cancer.
Approximately one third of patients with RCC have distant metastases at diagnosis.
In-patients with multiple metastases survival are not positively affected by their
complete excision. In these cases surgical treatment of metastases has only a palliative
role. In the case of solitary synchronous or metachronous metastasis the complete
removal of metastatic foci would significantly improve the probability of longer
survival. The patient with synchronous metastasis has worse prognosis if compared to
this with metachronous disease. The beneficial effects of excision of metastatic renal
cell carcinoma are limited and the cure of patients with metastatic disease is relatively
uncommon.
Non–surgical treatment of renal tumours
Non-surgical treatment of renal cell carcinoma comprises irradiation, transfemoral
catheter embolisation of inoperable and symptomatic tumours, cytostatic treatment of
metastatic disease, hormonotherapy and imunotherapy.
Embolisation of the kidney.
Transfemoral catheter embolisation of the kidney has the following applications:
1. Curative superselective embolization in non malignant renal diseases
2. Radiologic nephrectomy as the form of palliative embolisation of renal tumors
(bleeding, pain, paraneoplastic syndromes)
3. Preoperative embolisation of renal tumors
Embolisation of the kidney is in the majority of case only palliative procedure and
very seldom gives a curative effect.
Radiotherapy.
In 1923 Waters observed that radiation could reduce the tumor mass of renal cell
carcinoma. For a long time it was thought that RCC is radioresistent. The value of preor postoperative radiotherapy for the prognosis of the patient with RCC is still
discussed. Postoperative radiotherapy locally advanced renal tumors are used in some
oncological centers. More often is indicated palliative radiotherapy of metastases.
Bone pain from metastases is well palliated in this way.
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Hormonal therapy.
Many repots from the 70’s have indicated good response in patients with RCC
receiving progesterone or androgens. The gestagens: medroxyprogesterone and
hydroxyprogesterone as well as testosterone were applied. The first optimistic results
in prospective studies have not been confirmed. On the other hand high dose of
progesterone treatment is non-toxic anabolic therapy which offers the improvement of
patient’s general condition.
Chemotherapy.
Many cytostatic drugs were used in the treatment of metastatic RCC. Positive results
of such treatment were observed in 10 % patients. In many studies vinblastine (VB) as
a single drug or in combination with lomustine (LM, CCNU) was the most effective
with response rate from 15-30 %. The continous infusional chemotherapy with 5fluoro-2-deoxyuridine (FUOR) gives a response rate of 20-33 % in patients with
metastatic RCC.
In general results of combined chemotherapy are not superior to those obtained by
single drug treatment.
Immunotherapy.
The biology of renal cell carcinoma is considered to be influenced by immune system
of the tumor host. Occasional spontaneous
regressions of metastases are arguments
for this assumption.
Multiple modalities for active or passive immunotherapy were described. In
conventional immunotherapy of RCC were used following agents: BCG, transfer
factor (TF), polymerised tumor cells, tumor cells + Corynebacterium parvum, immune
RNA (I- mRNA), tumor necrosis factor (TNF), thymosine factor 5.
In the current opinion use these agents was largely unsuccessful.
The forms of adoptive immunotherapy are LAK and TIL treatment in solid renal
tumors.
Lymphokine activated killer cells (LAK) treatment gives a 31 % response rate (CR +
PR) in RCC.
12
An alternative to the use of LAK cells generated from peripheral blood lymphocytes is
using the lymphocytes, which infiltrate the tumor (TIL). LAK and TIL adoptive
immunotherapy has been criticized mainly on account of the toxicity and expence.
In the present time the most often form of immunotherapy is the use of biological
response modifiers such as interferons and interleukins.
A large number of patients have been treated with interferons for advanced RCC
(interferon alpha, interferon beta and interferon gamma). Doses of interferons ranged
from 1 MIU daily to 16 MIU daily although the majority of patients were treated with
3 MIU daily or the same dose 3 times each week. Observed responses rates ranged
from 5 to 29 %. There is no evidence that larger doses than 5-10 MIU daily produce
higher response rates.
The toxicity of IFN with increasing doses and prolonged treatment is higher.
Interleukin-2 (Il-2) is produced by activated T cells. Some authors reported the clinical
results with Il-2 in RCC. It was used in intravenous infusions but toxicity of such
treatment was high.
Recently systemic imunotherapy with interleukin 2 (Il-2), interferon alpha (INF alpha)
and 5-fluorouracyl gives promising results with response rate about 40-48 %.
However, systemic immunotherapy is limited by severe side effects. Lond-lasting
response is rare but only systemic combined immunotherapy is the most efficient in
the treatment of metastatic RCC.
TUMORS OF THE RENAL PELVIS
Malignant tumors arising from the renal calices or pelves comprise approximately
7 % of all renal neoplasm but represent fewer then 1 % of all genitourinary tumors.
They are seen approximately 3 times more frequently in men then in women. These
Tumors show no predilection for side, but they occur bilaterally in only 2-4 % of
patients.
Tumor Staging
In the absence of accurate clinical staging procedures, classification of renal pelvic
13
tumors has been based, on pathologic findings. Grabstalb, Whitmore, and Melamed
( 1971 ) and Batata et al ( 1975 ) evolved the following staging system for transitional
cell tumors of the renal pelvis and ureter:
Stage 0: Neoplasms confined to the mucosa.
Stage A: Submucosal infiltration only.
Stage B: Muscular invasion without extension through the muscle wall of the
calyx, pelvis, or ureter.
Stage C: Invasion of the renal parenchyma or the peripelvic or periureteral fat.
Stage D: Extension outside the kidney or ureter into adjacent organs, regional
Lymph nodes, or distant metastases.
Clinical Findings
A. Symptoms: Gross painless hematuria, the most common complaint, is noted
in 70-95 % of patients with renal pelvic tumors. Flank pain has been reported in
8-40 % patients and may result from tumor obstructing the ureteropelvic junction,
Ureteral colic from passage of blood clots or tumor fragments, or local extension
of the tumor to involve retroperitoneal structures. Symptoms of bladder irritation
are present in 5-10 % of patients. Constitutional symptoms (anorexia, weight loss,
and lethargy ) cause about 5 % of patients to seek medical attention.
B. Signs: There may be tenderness over the kidney, particularly if ureteral
obstruction has occurred or if infection has supervened. A flank mass
secondary to the tumor or an associated hydronephrosis is present in 10-20 %
of patients.
C. Laboratory Findings: Anemia can be marked if bleeding is profuse. Gross or
microscopic hematuria is to be expected, but at intervals the urine may be free
of red cells. Renal infection can resalt from obstruction or can be associated
with the primary tumor; in either case, pus and bacteria are present in the
urine.
D. X-Ray Findings: The diagnosis is usually suspected on the basis of an
excretory urogram, which almost always reveals abnormal findings in patients
with renal pelvic carcinoma. The most common pyelographic finding is a
14
filling defect in the renal pelvis, demonstrable in 50-75 % of the urograms.
Other radiographic findings include ureteropelvic or infundibular stenosis,
hydronephrosis, or splaying of the calices, which may suggest a renal mass.
Nonvisualization of the affected renal unit occurs in over 10 % of patients.
Although several investigators have described a distinctive appearance of renal
pelvic carcinoma on angiogramms, false-positive interpretations have exceeded
40%. The most common error is mistaking inflammatory disease for the cancer.
Selective angiogramms may demonstrate one or more of the following
features:(1) arterial encasement or amputation; (2) fine neovascularity and tumor
staining; (3) enlarged prominent pelvic ureteral arteries; and (4) irregular
diminished nephrogramms, suggesting tumor invading the renal parenchyma.
Angiographya is most useful in demonstrating other pathologic conditions (renal
artery aneurysms, vascular impression, etc) that can cause a negative defect on
urograms and mimic a renal pelvic tumor.
E. Ultrasonography: Ultrasonography may help define the nature the lethion and
distinguish a tumor from nonopaque calculi and blood clots.
F. Instrumental Examination: Cystoscopy should be done immediately when
gross bleeding is present. Blood may be seen spurting from one ureteral
orifice, which localizes the source of bleeding. During cystoscopy, the
physician should search for other urothelial tumors on the bladder or urethral
walls.
G. Cytologic Examination: Routine cytologic analysis of urine from a voided or
catheterized bladder specimen is usually of limited value, since at least 30 %
of specimens are negative for malignant cells. Collecting a urine specimen
after barbotage through a ureteral catheter greatly increases the chance for a
positive diagnosis. A retrograde brush biopsy provides specimens for both
histologic and cytologic studies leading to an accurate preoperative diagnosis.
Differential Diagnosis
Adenocarcinoma of the kidney also causes hematuria. Such a tumor, however, is
apt to be palpable or may be visible on a plain film of the abdomen as an
15
expansion of a portion of the kidney. Urograms show the intrarenal nature of the
growth. However, blood clots in the renal pelvis can mimic pelvic tumor. If
transitional cell tumor invades the parenchyma, it simulates adenocarcinoma.
Cytologic tests and angiography may make the differentiation.
A nonopaque renal stone may cause hematuria and renal pain. A mass may be
palpable if hydronephrosis develops. Urograms show a spaceoccupying lesion of
the pelvis, but the outline of the negative (black) shadow (representing the stone)
tends to be smoothly round or oval for stone and irregular (papillary) for tumor.
When the mass is a tumor, cytologic studies usually yield positive results.
Ultrasonography or CT scanning can help in differentiation.
Renal tuberculosis may also mimic a pelvis neoplasm. The urogram may show
irregularity of the pelvic outline causes by ulceration, which might suggest tumor.
The patient with urinary tract tuberculosis usually complains of vesical irritability
and has “sterile” pyuria. Acid-fast organisms can be demonstrated in the urine.
Hemangioma, an occasional cause of hematuria involving the renal pelvis or
submucosal parenchyma, is usually too small to be seen on the urogram as a
spaceoccupying lesion of the pelvis. Renal angiography establishes the diagnosis.
Treatment In the absence of demonstrable metastases, the optimal treatment is
radical nefrectomy, which includes removal of the kidney and all perinephric
tissue, keeping Gerota`s capsule intact; removal of the ipsilateral adrenal gland;
and complete excision of the ureter and adjacent vesical mucosa. When the distal
ureter has not been completely excised, subsequent recurrent disease has been
documented in one-third of the patients.
The value of lymphadenectomy in treating this disease remains undetermined.
Today, no improved rate of survival has been reported for patients with renal
pelvic tumors who have been subjected to systematic en bloc lymphadenectomy.
The age of many of these patients and the presence of atherosclerosis do not
appear to justify the increased risk of additional surgery.
The role of radiotherapy in this disease has been inadequately studied. The
unsuccessful attempts to improve survival rates of patients with renal cell
16
carcinoma by either pre- or postoperative irradiation. The risk of radiation
injuries to the liver and bowel, and the belief that lymph node involvement
represents systemic disease have contributed to a lack of enthusiasm for using
radiotherapy as an adjunct to surgery for treatment of renal pelvic tumors.
Prognosis. The prognosis for patients with benign tumors is excellent. For
patients with low-grade transitional cell carcinoma, the outlook is excellent
(approaches 100%), but when the disease is poorly differentiated, fewer than 20%
of patients are alive at 5 years. Similarly, the outlook for patients with low-stage
malignant tumors is good but becomes fair to poor as the stage increases; few
survivors are alive at 5 years if distant metastases occur. The prognosis is poor for
patients with either adenocarcinoma or squamous cell carcinoma.
References:
1. Donald R. Smith, M.D. General Urology, 11-th edition, 1984.
2. O.F.Vozianov, O.V.Lyulko. Urinology.- Kyiv: Vischa shkola, 1993.
3. Urinology edited by N.A.Lopatkin, Moscow, 1982.
4. Scientific Foundations of Urology. Third Edition 1990. Edited by Geoffrey D.
Chisholm and William R. Fair, MD. Heinemann Medical Books, Oxford.
5. Kono N, Tanahashi T, Suzawa N, Azuma C: Effects of sex hormones on oncogenesis
in rat urinary bladder by N-butyl-N-(4-hydroxybutyl)-nitrosamine. Int J Clin Phar-macol
1977;15:101-105.
6. Reid LM, Leav I, Kwan PWL, Russell P, Merk FB: Characterization of a human, sex
steroid-responsive transitional cell carcinoma maintained as a tumor line (RI98) in
athymic nude mice. Cancer Res 1984:44:4560-4573.
7 Levi F, La-Vecchia C, Randimbison L, Franceschi S: Incidence of infiltrating cancer
following superficial bladder carcinoma. Int J Cancer 1993:55:419-421.
8. Spruck CS, Ohneseit PF, Gonzalez-Zulueta M, Esrig D, Miyao N, Tsai YC, Lerner
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