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THE
AMERICAN
JOURNAL
OF
ROENTGENOLOGY RADIUM THERAPY AND NUCLEAR MEDICINE
VOL.
OCTOBER,
125
THE
SPECIFICITY
OF
By CHARLES
RENAL
B. MULHERN,
WALLACE
T.
MILLER,
No.
M.D.,
PHILADELPHIA,
VEIN
2
THROMBOSIS*
M.D., PETER H. ARGER, and ARNOLD CHAIT,
M.D., M.D.
PENNSYLVANIA
ABSTRACT:
Clinical and roentgenographic features of renal authors’ experience with 17 cases is presented. The roentgenologist with a high degree of suspicion and urographic findings, make the specific diagnosis high percentage of cases.
vein
thrombosis
are
discussed.
The
O
RIGINALLY
described by Rayer in renal vein thrombosis is generally considered an uncommon event. In the past, most cases were first recognized at autopsy. However, increased clinical understanding and awareness of the condition in conjunction with improved roentgenographic techniques should allow antemortern diagnosis. Our experience with 17 cases of renal vein thrombosis is presented. Correlation of the spectra of clinical and intravenous pyelographic presentations reveals a composite picture of the condition. Once suspected, the diagnosis can be confirmed angiographically. Prompt and appropriate therapy may then be undertaken. 1840,21
BACKGROUND
Harrison *
27,
Presented
et al.”
described
at the Seventy-fifth
fundamental
Annual
Meeting
of the American
can, by correlation of clinical of renal vein thrombosis in a
varieties of renal vein obstruction: (i) thrombosis of the inferior vena cava and involvement of the renal veins secondary to extension of thrombi from pelvic and leg veins; (2) compression or invasion of the inferior vena cava and renal veins by tumor; (3) renal vein thrombosis secondary to primary renal disease; and (4) primary renal vein thrombosis. Except in the infant, primary renal vein thrombosis is thought to be rare, and this is probably related to the rapidity of blood flow in the adult. In the infant the flow rate normally tends to be low and this may pe compromised further by problems such as dehydration secondary to gastroenteritis.”7 The response of the kidney is determined both by the completeness of occlusion of the vein and by the temporal balance between the occlusion of the vein and the developRoentgen
Ray
Society,
San Francisco,
California,
September
24-
1974.
From
the Department
of Radiology,
Hospital
of the University
29!
of Pennsylvania,
Philadelphia,
Pennsylvania. Thia
One
IiIIIIII Ilfihlif IIII 1Ufl1IIIHI IIii 5iQWAB8BS
Muihern,
292
Arger,
Miller
TABLE
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ACUTE
.
Patient
Age
Sex
i.
8
M
2.
28
F
3.
6i
M
4.
64
M
5.
50
M
6.
62
M
SLEW IVC=
Systemic Inferior
.
RENAL
VEIN
..
Primary
Pancreatic carcinoma SLE
adeno-
Diabetes mellitus, hypertension ColQn carcinoma Pancreatic or coIon carcinoma Abdominal aortic aneurysm
pain,
leg edema
Flank kidney Flank
pain,
leg edema,
pain,
leg edema
Flank kidney Flank
pain,
leg edema,
pain,
leg edema pain,
pulsatile
1975
DATA
SUMMARY
Pulmonary Embolus
Migratory, palpable
None IVC,
palpable
IVC IVC,
mass
leg
None
leg
IVC
Outcome
X
Death,
renal
None
Alive,
X
Death,
pulmonary
X
Death,
renal
failure
X
Death,
renal
failure
None
Death,
renal
failure
right
failure nephrectomy embolus
lupus erythematosus. vena cava.
ment of collateral venous drainage. These factors in turn determine the clinical and roen tgenographi c presentations.7” 13,20,26,28 In the acute condition, sudden complete occlusion of the renal vein occurs. The affected kidney enlarges with consequent severe lumbar pain, and hematuria, proteinuria, and oliguria appear. Death from renal failure usually occurs if the condition is bilateral.1”3’26’28 However, if the occlusion is gradual or only partial, collateral venous drainage will be developed. The effects are Correspondingly less serious and adequate renal function may be preserved. This latter is the most common situation; a nephrotic syndrome frequently develops.8”7”9’2#{176} #{149}
CLINICAL
OcToBER,
Thrombohlebiris
Evidence
Flank
Abdominal
CLINICAL
.
Clinical
Chait
I
THROMBOSIS:
..
Condition
and
AND
UROGRAPHIC
SPECTRA
Acute renal vein thrombosis occurs with sudden complete occlusion of the vein. Six of our 17 patients presented in this fashion. Table I summarizes the clinical data of these patients. The patients were all acutely ill. Sudden persistent flank cr abdominal pain occurred in all 6 pitients. Physical examination revealed marked costovertebral angle tenderness. Occasionally, the involved kidney was palpable (, per cent). Leg edema was an almost constant finding, being present in 5 of 6 pa-
tients (83 per cent). Of particular note was the presence of thrombophiebitis and pulmonary embolism during the course of the illness; this occurred in 4 patients (67 per cent). Urinalysis in all 6 patients revealed gross hematuria and proteinuria. Of these 6 patients, only i is alive, and this patient was subjected to right nephrectomy; 4 patients died in renal failure, and i patient died from pulmonary embolus. This represents an 83 per cent mortality. Previous authors have commented on the variable spectrum of intravenous pyelographic changes.3’4”3’26’’28 They have described a variability of renal size, nephrogram density and excretory function. Generally, there is absent to poor visualization of the collecting system which frequently is distorted and stretched, mimicking polycystic kidney disease. Compression of the renal pelvis and proximal ureter by the edematous, boggy renal mass may be seen.3’4”3’’26’28 A summary of the intravenous pyelographic statistics in our 6 cases with acute renal vein thrombosis is presented in Table I,. The affected kidney was increased in size in most cases (Fig. i); width was increased to a greater degree than length. In 50 per cent of the patients, the nephrogram was decreased as expected; however, in the other 50 per cent, it was increased
VoL.
No.
125,
The
2
Specificity
of Renal
RENAL
VEIN
THROMBOSIS:
INTRAVENOUS
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(6 Cases: Renal
Size
Range Rt. Lt. Average Rt. Lt. Nephrogram Pelvocalyceal Ureters
System
4 Intravenous
Length
6.0-8.7 6.5-8.4
13.4
7.1
SUMMARY
7.4
14.5
A 64 year c. ... ..i pain. Note increase in length kidney (open arrows). I.
DATA
Pyelograms)
13.5-16.7
I
Increased Not Seen Notched
(Fig. 2, A and B). We were able to visualize all but i pelvocalyceal system; 50 per cent of these were distorted and stretched (Fig. 2B; and 3). Additional roentgenographic findings may be helpful: evidence of pulmonary embolism occurred in 50 per cent of our patients. Abdominal roentgenograms may reveal a mass such as an aneurysm or neoplasm in the region of the renal vein. Chronic renal vein thrombosis occurs with gradual or incomplete occlusion of the renal venous drainage. A nephrotic syndrome is a frequent sequela. McCarthy et al.’7 showed pain to be present in 13 of 40 patients (34 per cent). In ii patients (29 per cent) there was thrombosis
...
PYELOCRAM
Width
11.5-14.5
Decreased Stretched Displaced
293
Thrombosis
II
TABLE ACUTE
Vein
mark. and width
of left
I
Dilated from Not seen
obstruction
I
of the inferior vena cava, and in 14 cases (36 per cent), thromboembolic occlusion of a pulmonary artery. Eleven of our 17 patients presented as chronic renal vein thrombosis. Table in summarizes the clinical data. Seven of ii patients were male; the average age was 6 years. Pain was a prominent feature in only 3 cases (27 per cent);
Fio. 2. A 63 year old male with left flank pain. Note increasingly dense nephrogram between (A) i minute film and (B) hour film. Pelvocalyceal system stretched but not dilated (open arrows).
Mulhern,
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294
Arger,
Miller
VEIN
OCTOBER,
THROMBOSIS:
CLINICAL
DATA
SUMMARY
Tumor Patient
Age Sex
Primary
Condition
Clinical
Evidence
Thrombophlebitis
Nephrotic Syndrome
iM
SLE
Pain,
3. 4. 5,
70F 42M
Hypernephroma Hypernephroma Trauma Trauma
Mass Pain, mass Edema, mass Edema
6.
72M
7.
51M
Diabetes Carcinoid
Edema Edema
8.
48M
Hypertension
Pain,
so.
M 68F
Mass Edema
i i.
63F
Hypernephroma Positive coagulogram; carcinoma, certain primary Abdominal aortic aneurysm
XX (IVC occlusion) 0 0 0 0 0 X X X (IVC occlusion) 0 X X X (IVC occlusion) X X 0 0 X X
Mass
0
i.
2.
.
SLEW IVC.’.
52M
Systemic Inferior
mellitus
lupus erythematosus. vena cava.
un-
1975
III
TABLE RENAL
Chait
tumor (hypernephroma in 3, carcinoid in i, and abdominal aortic aneurysm in I). Of note is the fact that in only i of these latter patients (carcinoid) was the nephrotic syndrome present. On physical examination the most frequent abnormality was leg edema. Dilated abdominal wall veins with upward blood flow indicative of inferior vena caval obstruction was seen in only I patient. Proteinuria was the only consistently found laboratory abnormality. The urinalysis, however, may also demonstrate occasional red blood cells, white blood cells, granular or hyaline casts, and oval fat bodies. Creatinine and blood urea nitrogen levels ranged from normal to moderately elevated. As in the acute condition, various authors have described a variety of intravenous pyelographic appearances in chronic renal vein thrombosis.3’4”3’27’2628 Table IV summarizes urographic data of the JO of ii patients with available studies. Renal size was generally increased; the width, as in the acute stage, was increased to a greater degree than length (Fig. ; and ). The nephrogram was normal in 5 cases (o per cent), decreased in 4 cases (40 per cent), and increased in only i case (io
however, edema and a palpable mass were both present in 7 cases (64 per cent). As in the patients with acute renal vein thrombosis, those with chronic renal vein thrombosis demonstrated a high incidence of pulmonary embolism-4 cases (36 per cent). This is consistent with the high clinical incidence of pleuritic chest pain, pleural effusion, and congestive heart failure in our patients. Primary renal disease was the apparent underlying etiology in 3 cases (27 per cent), trauma in 2 cases (19 per cent), and carcinomatosis with a positive coagulogram in i case ( per cent). In the remaining 5 cases (45 per cent), compression of the renal venous drainage was caused by
CHRONIC
and
mass,
edema,
edema
mass
0
In
.
vasion
Compression
or
Pulmonary Embolus
0
X
X X 0 0
0 0 0 X
0 X
0 X
0 X 0
X 0 0
X
0
VOL.
No.
525,
The
2
Specificity
of Renal
RENAL
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(ii
Renal
VEIN
Cases,
THROMBOSIS: 10
INTRAVENOUS
Intravenous
DATA
SUMMARY
Only) Width
11.0-17.5
6.o-io.o
12.5-17.3
6.0-10.0
13.8
7.5 7.9
14.5
Normal Normal Normal
System
Decreased Stretched Not seen
2 i
ROENTGENOGRAPHIC TECHNIQUES
Retrograde dicated only
Report
Length
per cent). The pelvocalyceal system was normal in only 2 cases (20 per cent), and distorted and stretched in 6 cases (6o per cent) (Fig. ; and ). In 6 of 7 cases (86 per cent) visualized ureters were notched (Fig. ; and 6). Additional roentgenographic findings which may be helpful include the chest roentgenogram for evidence of pulmonary emboli or metastatic disease (#{231} per cent). A mass in the region of the kidney or renal vein may be evident on abdominal roentgenograms. ADDITIONAL
295
PYELOGRAM
Pyelograms:
Size
Range Rt. Lt. Average Rt. Lt. Nephrogram Pelvocalyceal Ureters
Thrombosis
IV
TABLE CHRONIC
Vein
pyelography in the face
generally of an enlarged
is inkid-
Increased Not seen Notched
6 3
i
Dilated secondary obstruction
i
6
to
ney without visualization of the collecting system on drip infusion intravenous pyelography. Weiner et al.27 recently reviewed the findings in renal vein thrombosis using retrograde pyelography. Of note was the presence of an irregular pelvic outline in association with an irregular nodularlinear mucosal pattern. Others have noted the splayed collecting system, narrowing of the ureteropelvic junction, and parenchymal back diffusion of injected contrast material-all findirgs secondary to marked renal edema.’8’28 Renal arteriography for several reasons is to be preferred as the initial confirmatory angiographic study.3’26 With this study, one may evaluate, without the danger of dislodging a clot, the state of the renal paren-
‘-
4
-
.1 FIG.
.
drome. arrows). calyceal arrows).
A
year old male with the nephrotic Note large, widened left kidney The renal outline is fuzzy. The system is distorted and stretched
40
syn(open pelvo(closed
U.
year old male with the nephrotic syndrome. Note large kidneys with stretched pelvocalyceal systems. Ureteral notching is marked on the right (open arrows).
FIG.
.
A
15
Muihern,
196
Arger,
Miller
and
Chait
thrombosis
of
OCTOBER,
the
smaller
venous
1975
rad-
ides.9”4
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DISCUSSION
Renal grave
prognosis.
clearly after
6. A 53
FIG.
drome. tem
year
Note and
old
male
mildly
notched
with
the
Stretched
ureter
nephrotic
syn-
pelvocalyceal
on the
left
(open
SyS-
arrows).
chyma and renal blood flow. Also, with delayed filming, one may visualize the renal vein and possibly the site of obstruction. Collateral renal venous drainage may be seen. Arterial changes include decreased caliber of the arteries, decreased rate of blood flow, and deviation and stretching of the interlobar arteries.’3’26’28 The nephrographic phase may reveal loss of the normal distinction between the cortical and medullary blush.3 In the chronic stage, these findings in the arterial and nephrographic stages may not be seen. Notching of the ureter secondary to collaterals may be documented.2’3 The more definitive, although somewhat hazardous, technique in doubtful cases is inferior vena cavography, with or without selective renal phlebography. Janower’4 emphasizes tion using
the role of an 18 gauge
femoral
vein
vein defined,
thrombosis
has
Treatment, can
be
a relatively although
undertaken
not only
having established a definitive diagnosis. Of particular interest is the relative infrequency with which the premortem diagnosis is definitely established. The clinical presentation of renal vein thrombosis has been described in the literature as a spectrum. Yet Pollak et al.2#{176} concluded that in a significant proportion of patients, the syndrome is characteristic enough to permit a clinical diagnosis. Despite positive urographic and ancillary roentgenographic features in most cases,
injec-
needle as a confirmatory measure. This not only reduces the hazards that occur with catheter employment but also allows clarification of the diagnosis with use of only basic equipment without specialized skills (Fig. 7). In both the acute and chronic case, renal vein thrombosis may be demonstrated by visualization of clot. The lack of wash-out in the renal veins is a suggestive finding. In selective renal phlebography, prolonged wash-out renal
time vein
branch
associated filling
with is consistent
decreased with
FIG.
“.
Right femoral vein injection shows venous obstruction with extensive collaterals.
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VOL.
125,
No.
2
The
Specificity
of Renal
few authors have appreciated a characteristic roentgenographic picture of this entity. An analysis of our experience with 17 cases reveals on the contrary a significant degree of diagnostic specificity if particular attention is paid to the historical data, physical findings, and laboratory data in conjunction with the urographic observations. The acute episode of renal vein thrombosis presents a rather classical picture. The outstanding features are: (i) pain in the lower back or flank usually radiating to the groin area; (2) frequently a palpable mass; (,) associated edema in the lower extremities; (.) hematuria; (,) proteinuria; and (6) frequently extrarenal thromboembolic episodes. Urographically, the kidney appears congested, with increased dimensions. There may be no renal contrast medium excretion on the involved side (or sides). More commonly, a nephrogram is seen and, although faintly visualized, the collecting system is stretched. At this point, utilizing available clinical and roentgenographic information considerably narrows the diagnosis. Obstructive uropathy secondary to a urinary tract calculus is a frequent consideration but should not produce proteinuria, peripheral edema, or thromboembolic episodes if these are present. A stretched pelvocalyceal system, when visible, is also inconsistent with this diagnosis. Other diagnostic considerations such as renal artery occlusion or pennephric abscess are also unlikely to present with a clinical and roentgenographic appearance which might be confused with renal vein thrombosis. When this disease is suspected, inferior vena cavography or arteriography will easily confirm the diagnosis. In chronic renal vein thrombosis associated with the nephrotic syndrome, the diagnosis is usually less clear-cut and the differential diagnosis includes essentially all the causes of the nephrotic syndrome. Typically the patient presents with a previous history of flank pain or thromboembolic episodes. Physical evidence of inferior
Vein
Thrombosis
297
TABLE REPORTED WITH
I.
V
CONDITIONS RENAL
VEIN
ASSOCIATED THROMBOSIS
Infectious Pyelonephritis
Ascending
phlebitis
Ileocolitis
2.
Phycomycosis leukemia) Neoplasm Hypernephroma Transitional
(particularly
cell carcinoma,
with
lymphoma,
renal pelvis
Primary carcinoma elsewhere (bronchogenic cinoma, breast carcinoma, hepatoma) 3. Circulatory Disorder MI; CHF Cyanotic and polycythemic conditions Sickle cell anemia 4.
Systemic
.
Aniyloidosis Diabetic glomerulosclerosis Renal hypertension Trauma
6. Surgery Splenorenal Transplant Indwelling 7. Other
car-
Disorders
shunt catheter
in IVC
Idiopathic Papillary necrosis Post partum
Consumptive
coagulopathy
Glomerulonephritis, MI= CHF= IVC=
membranous
Myocardial infarct. Congestive heart failure. Inferior vena cava.
vena caval obstruction, such as collateral abdominal veins or lower trunk and leg edema, may be observed. The presence of an underlying disorder associated with increased incidence of renal vein thrombosis is supportive evidence (Table v). Urographically, the involved kidney may demonstrate the following: (i) slight increase in size; (2) normal or slightly decreased concentration of contrast material by the kidney; (3) a stretched collecting system; and () ureteral notching. It is important to emphasize that these findings may be minimal. It is not feasible in the present framework to list all possible causes of the nephrotic syndrome and its corresponding
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298
Mulhern,
Arger,
clinical and urographic picture to differentiate it from that seen in chronic renal vein thrombosis. However, using a modification of the etiologic scheme of the nephrotic syndrome as proposed by Schreincr,24 one can eliminate several categories rather simply. For example, historical data should reveal exposure to nephrotoxins, allergens, or harmful drugs. The clinical history and laboratory data should expose an infectious etiology of the nephrotic syndrome. Various metabolic diseases presenting with a nephrotic syndrome, such as diabetic glomerulosclerosis, will generally have associated abnormal laboratory values, such as an abnormal glucose tolerance test. Urography will commonly exhibit small shrunken kidneys bilaterally. Amyloidosis may be a very difficult diagnosis to exclude. The physical examination rarely reveals evidence of amyloid deposition elsewhere. Rectal biopsy is a safe confirmatory procedure. Symmetrical urographic changes are likely and ureteral notching is not seen. Various other systemic diseases noted by Schreiner24 may also cause the nephrotic syndrome. By virtue of the fact that they are systemic diseases, evidence of the pathologic process should be clinically present elsewhere. Sickle cell anemia, for example, will present in a young Black with a positive sickle cell preparation. Essential hypertension can be suspected on the basis of severe hypertension and other evidence of systemic vascular disease, such as eyeground changes. Glomerular disease, one of the most frequent causes of the nephrotic syndrome, must also be excluded. Recent sore throat with fever or a positive ASO titer is consistent with glomerulonephnitis. Hematuna, the hallmark of glomerulonephnitis, is a prominent finding in renal vein occlusion only during the acute stage. The urographic findings of acute renal vein thrombosis are not present in glomerulonephnitis. In those patients with chronic renal vein thrombosis not associated with a nephrotic syndrome, tumor is the most likely etiologic
Miller
and
Chait
OcrosEa,
1975
factor. Hypernephroma or renal pelvic carcinoma, the most frequent neoplasms to invade the renal vein, should be recognized roentgenographically. Compression or invasion of the renal vein or vena cava by tumor may be suspected on the urogram with ureteral notching. As is the case in many other diseases, the clinical and urographic picture of renal vein thrombosis is sufficiently characteristic to establish the diagnosis. A high index of suspicion on the part of the clinician or the radiologist will lead to the diagnosis in most instances. Confirmatory studies, particularly modified inferior vena cavography, may be undertaken immediately. Arteniography will yield further confirmatory information. Charles
Muihern,
B.
M.D.
Department of Radiology Hospital of the University 3400 Spruce Street Philadelphia, Pennsylvania
of Pennsylvania 19104
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THE
AMERICAN
JOURNAL
OF
ROENTGENOLOGY RADIUM THERAPY AND NUCLEAR MEDICINE
VOL.
OCTOBER,
125
THE
SPECIFICITY
OF
By CHARLES
RENAL
B. MULHERN,
WALLACE
T.
MILLER,
No.
M.D.,
PHILADELPHIA,
VEIN
2
THROMBOSIS*
M.D., PETER H. ARGER, and ARNOLD CHAIT,
M.D., M.D.
PENNSYLVANIA
ABSTRACT:
Clinical and roentgenographic features of renal authors’ experience with 17 cases is presented. The roentgenologist with a high degree of suspicion and urographic findings, make the specific diagnosis high percentage of cases.
vein
thrombosis
are
discussed.
The
O
RIGINALLY
described by Rayer in renal vein thrombosis is generally considered an uncommon event. In the past, most cases were first recognized at autopsy. However, increased clinical understanding and awareness of the condition in conjunction with improved roentgenographic techniques should allow antemortern diagnosis. Our experience with 17 cases of renal vein thrombosis is presented. Correlation of the spectra of clinical and intravenous pyelographic presentations reveals a composite picture of the condition. Once suspected, the diagnosis can be confirmed angiographically. Prompt and appropriate therapy may then be undertaken. 1840,21
BACKGROUND
Harrison *
27,
Presented
et al.”
described
at the Seventy-fifth
fundamental
Annual
Meeting
of the American
can, by correlation of clinical of renal vein thrombosis in a
varieties of renal vein obstruction: (i) thrombosis of the inferior vena cava and involvement of the renal veins secondary to extension of thrombi from pelvic and leg veins; (2) compression or invasion of the inferior vena cava and renal veins by tumor; (3) renal vein thrombosis secondary to primary renal disease; and (4) primary renal vein thrombosis. Except in the infant, primary renal vein thrombosis is thought to be rare, and this is probably related to the rapidity of blood flow in the adult. In the infant the flow rate normally tends to be low and this may pe compromised further by problems such as dehydration secondary to gastroenteritis.”7 The response of the kidney is determined both by the completeness of occlusion of the vein and by the temporal balance between the occlusion of the vein and the developRoentgen
Ray
Society,
San Francisco,
California,
September
24-
1974.
From
the Department
of Radiology,
Hospital
of the University
29!
of Pennsylvania,
Philadelphia,
Pennsylvania. Thia
One
IiIIIIII Ilfihlif IIII 1Ufl1IIIHI IIii 5iQWAB8BS
Muihern,
292
Arger,
Miller
TABLE
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ACUTE
.
Patient
Age
Sex
i.
8
M
2.
28
F
3.
6i
M
4.
64
M
5.
50
M
6.
62
M
SLEW IVC=
Systemic Inferior
.
RENAL
VEIN
..
Primary
Pancreatic carcinoma SLE
adeno-
Diabetes mellitus, hypertension ColQn carcinoma Pancreatic or coIon carcinoma Abdominal aortic aneurysm
pain,
leg edema
Flank kidney Flank
pain,
leg edema,
pain,
leg edema
Flank kidney Flank
pain,
leg edema,
pain,
leg edema pain,
pulsatile
1975
DATA
SUMMARY
Pulmonary Embolus
Migratory, palpable
None IVC,
palpable
IVC IVC,
mass
leg
None
leg
IVC
Outcome
X
Death,
renal
None
Alive,
X
Death,
pulmonary
X
Death,
renal
failure
X
Death,
renal
failure
None
Death,
renal
failure
right
failure nephrectomy embolus
lupus erythematosus. vena cava.
ment of collateral venous drainage. These factors in turn determine the clinical and roen tgenographi c presentations.7” 13,20,26,28 In the acute condition, sudden complete occlusion of the renal vein occurs. The affected kidney enlarges with consequent severe lumbar pain, and hematuria, proteinuria, and oliguria appear. Death from renal failure usually occurs if the condition is bilateral.1”3’26’28 However, if the occlusion is gradual or only partial, collateral venous drainage will be developed. The effects are Correspondingly less serious and adequate renal function may be preserved. This latter is the most common situation; a nephrotic syndrome frequently develops.8”7”9’2#{176} #{149}
CLINICAL
OcToBER,
Thrombohlebiris
Evidence
Flank
Abdominal
CLINICAL
.
Clinical
Chait
I
THROMBOSIS:
..
Condition
and
AND
UROGRAPHIC
SPECTRA
Acute renal vein thrombosis occurs with sudden complete occlusion of the vein. Six of our 17 patients presented in this fashion. Table I summarizes the clinical data of these patients. The patients were all acutely ill. Sudden persistent flank cr abdominal pain occurred in all 6 pitients. Physical examination revealed marked costovertebral angle tenderness. Occasionally, the involved kidney was palpable (, per cent). Leg edema was an almost constant finding, being present in 5 of 6 pa-
tients (83 per cent). Of particular note was the presence of thrombophiebitis and pulmonary embolism during the course of the illness; this occurred in 4 patients (67 per cent). Urinalysis in all 6 patients revealed gross hematuria and proteinuria. Of these 6 patients, only i is alive, and this patient was subjected to right nephrectomy; 4 patients died in renal failure, and i patient died from pulmonary embolus. This represents an 83 per cent mortality. Previous authors have commented on the variable spectrum of intravenous pyelographic changes.3’4”3’26’’28 They have described a variability of renal size, nephrogram density and excretory function. Generally, there is absent to poor visualization of the collecting system which frequently is distorted and stretched, mimicking polycystic kidney disease. Compression of the renal pelvis and proximal ureter by the edematous, boggy renal mass may be seen.3’4”3’’26’28 A summary of the intravenous pyelographic statistics in our 6 cases with acute renal vein thrombosis is presented in Table I,. The affected kidney was increased in size in most cases (Fig. i); width was increased to a greater degree than length. In 50 per cent of the patients, the nephrogram was decreased as expected; however, in the other 50 per cent, it was increased
VoL.
No.
125,
The
2
Specificity
of Renal
RENAL
VEIN
THROMBOSIS:
INTRAVENOUS
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(6 Cases: Renal
Size
Range Rt. Lt. Average Rt. Lt. Nephrogram Pelvocalyceal Ureters
System
4 Intravenous
Length
6.0-8.7 6.5-8.4
13.4
7.1
SUMMARY
7.4
14.5
A 64 year c. ... ..i pain. Note increase in length kidney (open arrows). I.
DATA
Pyelograms)
13.5-16.7
I
Increased Not Seen Notched
(Fig. 2, A and B). We were able to visualize all but i pelvocalyceal system; 50 per cent of these were distorted and stretched (Fig. 2B; and 3). Additional roentgenographic findings may be helpful: evidence of pulmonary embolism occurred in 50 per cent of our patients. Abdominal roentgenograms may reveal a mass such as an aneurysm or neoplasm in the region of the renal vein. Chronic renal vein thrombosis occurs with gradual or incomplete occlusion of the renal venous drainage. A nephrotic syndrome is a frequent sequela. McCarthy et al.’7 showed pain to be present in 13 of 40 patients (34 per cent). In ii patients (29 per cent) there was thrombosis
...
PYELOCRAM
Width
11.5-14.5
Decreased Stretched Displaced
293
Thrombosis
II
TABLE ACUTE
Vein
mark. and width
of left
I
Dilated from Not seen
obstruction
I
of the inferior vena cava, and in 14 cases (36 per cent), thromboembolic occlusion of a pulmonary artery. Eleven of our 17 patients presented as chronic renal vein thrombosis. Table in summarizes the clinical data. Seven of ii patients were male; the average age was 6 years. Pain was a prominent feature in only 3 cases (27 per cent);
Fio. 2. A 63 year old male with left flank pain. Note increasingly dense nephrogram between (A) i minute film and (B) hour film. Pelvocalyceal system stretched but not dilated (open arrows).
Mulhern,
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294
Arger,
Miller
VEIN
OCTOBER,
THROMBOSIS:
CLINICAL
DATA
SUMMARY
Tumor Patient
Age Sex
Primary
Condition
Clinical
Evidence
Thrombophlebitis
Nephrotic Syndrome
iM
SLE
Pain,
3. 4. 5,
70F 42M
Hypernephroma Hypernephroma Trauma Trauma
Mass Pain, mass Edema, mass Edema
6.
72M
7.
51M
Diabetes Carcinoid
Edema Edema
8.
48M
Hypertension
Pain,
so.
M 68F
Mass Edema
i i.
63F
Hypernephroma Positive coagulogram; carcinoma, certain primary Abdominal aortic aneurysm
XX (IVC occlusion) 0 0 0 0 0 X X X (IVC occlusion) 0 X X X (IVC occlusion) X X 0 0 X X
Mass
0
i.
2.
.
SLEW IVC.’.
52M
Systemic Inferior
mellitus
lupus erythematosus. vena cava.
un-
1975
III
TABLE RENAL
Chait
tumor (hypernephroma in 3, carcinoid in i, and abdominal aortic aneurysm in I). Of note is the fact that in only i of these latter patients (carcinoid) was the nephrotic syndrome present. On physical examination the most frequent abnormality was leg edema. Dilated abdominal wall veins with upward blood flow indicative of inferior vena caval obstruction was seen in only I patient. Proteinuria was the only consistently found laboratory abnormality. The urinalysis, however, may also demonstrate occasional red blood cells, white blood cells, granular or hyaline casts, and oval fat bodies. Creatinine and blood urea nitrogen levels ranged from normal to moderately elevated. As in the acute condition, various authors have described a variety of intravenous pyelographic appearances in chronic renal vein thrombosis.3’4”3’27’2628 Table IV summarizes urographic data of the JO of ii patients with available studies. Renal size was generally increased; the width, as in the acute stage, was increased to a greater degree than length (Fig. ; and ). The nephrogram was normal in 5 cases (o per cent), decreased in 4 cases (40 per cent), and increased in only i case (io
however, edema and a palpable mass were both present in 7 cases (64 per cent). As in the patients with acute renal vein thrombosis, those with chronic renal vein thrombosis demonstrated a high incidence of pulmonary embolism-4 cases (36 per cent). This is consistent with the high clinical incidence of pleuritic chest pain, pleural effusion, and congestive heart failure in our patients. Primary renal disease was the apparent underlying etiology in 3 cases (27 per cent), trauma in 2 cases (19 per cent), and carcinomatosis with a positive coagulogram in i case ( per cent). In the remaining 5 cases (45 per cent), compression of the renal venous drainage was caused by
CHRONIC
and
mass,
edema,
edema
mass
0
In
.
vasion
Compression
or
Pulmonary Embolus
0
X
X X 0 0
0 0 0 X
0 X
0 X
0 X 0
X 0 0
X
0
VOL.
No.
525,
The
2
Specificity
of Renal
RENAL
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(ii
Renal
VEIN
Cases,
THROMBOSIS: 10
INTRAVENOUS
Intravenous
DATA
SUMMARY
Only) Width
11.0-17.5
6.o-io.o
12.5-17.3
6.0-10.0
13.8
7.5 7.9
14.5
Normal Normal Normal
System
Decreased Stretched Not seen
2 i
ROENTGENOGRAPHIC TECHNIQUES
Retrograde dicated only
Report
Length
per cent). The pelvocalyceal system was normal in only 2 cases (20 per cent), and distorted and stretched in 6 cases (6o per cent) (Fig. ; and ). In 6 of 7 cases (86 per cent) visualized ureters were notched (Fig. ; and 6). Additional roentgenographic findings which may be helpful include the chest roentgenogram for evidence of pulmonary emboli or metastatic disease (#{231} per cent). A mass in the region of the kidney or renal vein may be evident on abdominal roentgenograms. ADDITIONAL
295
PYELOGRAM
Pyelograms:
Size
Range Rt. Lt. Average Rt. Lt. Nephrogram Pelvocalyceal Ureters
Thrombosis
IV
TABLE CHRONIC
Vein
pyelography in the face
generally of an enlarged
is inkid-
Increased Not seen Notched
6 3
i
Dilated secondary obstruction
i
6
to
ney without visualization of the collecting system on drip infusion intravenous pyelography. Weiner et al.27 recently reviewed the findings in renal vein thrombosis using retrograde pyelography. Of note was the presence of an irregular pelvic outline in association with an irregular nodularlinear mucosal pattern. Others have noted the splayed collecting system, narrowing of the ureteropelvic junction, and parenchymal back diffusion of injected contrast material-all findirgs secondary to marked renal edema.’8’28 Renal arteriography for several reasons is to be preferred as the initial confirmatory angiographic study.3’26 With this study, one may evaluate, without the danger of dislodging a clot, the state of the renal paren-
‘-
4
-
.1 FIG.
.
drome. arrows). calyceal arrows).
A
year old male with the nephrotic Note large, widened left kidney The renal outline is fuzzy. The system is distorted and stretched
40
syn(open pelvo(closed
U.
year old male with the nephrotic syndrome. Note large kidneys with stretched pelvocalyceal systems. Ureteral notching is marked on the right (open arrows).
FIG.
.
A
15
Muihern,
196
Arger,
Miller
and
Chait
thrombosis
of
OCTOBER,
the
smaller
venous
1975
rad-
ides.9”4
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DISCUSSION
Renal grave
prognosis.
clearly after
6. A 53
FIG.
drome. tem
year
Note and
old
male
mildly
notched
with
the
Stretched
ureter
nephrotic
syn-
pelvocalyceal
on the
left
(open
SyS-
arrows).
chyma and renal blood flow. Also, with delayed filming, one may visualize the renal vein and possibly the site of obstruction. Collateral renal venous drainage may be seen. Arterial changes include decreased caliber of the arteries, decreased rate of blood flow, and deviation and stretching of the interlobar arteries.’3’26’28 The nephrographic phase may reveal loss of the normal distinction between the cortical and medullary blush.3 In the chronic stage, these findings in the arterial and nephrographic stages may not be seen. Notching of the ureter secondary to collaterals may be documented.2’3 The more definitive, although somewhat hazardous, technique in doubtful cases is inferior vena cavography, with or without selective renal phlebography. Janower’4 emphasizes tion using
the role of an 18 gauge
femoral
vein
vein defined,
thrombosis
has
Treatment, can
be
a relatively although
undertaken
not only
having established a definitive diagnosis. Of particular interest is the relative infrequency with which the premortem diagnosis is definitely established. The clinical presentation of renal vein thrombosis has been described in the literature as a spectrum. Yet Pollak et al.2#{176} concluded that in a significant proportion of patients, the syndrome is characteristic enough to permit a clinical diagnosis. Despite positive urographic and ancillary roentgenographic features in most cases,
injec-
needle as a confirmatory measure. This not only reduces the hazards that occur with catheter employment but also allows clarification of the diagnosis with use of only basic equipment without specialized skills (Fig. 7). In both the acute and chronic case, renal vein thrombosis may be demonstrated by visualization of clot. The lack of wash-out in the renal veins is a suggestive finding. In selective renal phlebography, prolonged wash-out renal
time vein
branch
associated filling
with is consistent
decreased with
FIG.
“.
Right femoral vein injection shows venous obstruction with extensive collaterals.
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VOL.
125,
No.
2
The
Specificity
of Renal
few authors have appreciated a characteristic roentgenographic picture of this entity. An analysis of our experience with 17 cases reveals on the contrary a significant degree of diagnostic specificity if particular attention is paid to the historical data, physical findings, and laboratory data in conjunction with the urographic observations. The acute episode of renal vein thrombosis presents a rather classical picture. The outstanding features are: (i) pain in the lower back or flank usually radiating to the groin area; (2) frequently a palpable mass; (,) associated edema in the lower extremities; (.) hematuria; (,) proteinuria; and (6) frequently extrarenal thromboembolic episodes. Urographically, the kidney appears congested, with increased dimensions. There may be no renal contrast medium excretion on the involved side (or sides). More commonly, a nephrogram is seen and, although faintly visualized, the collecting system is stretched. At this point, utilizing available clinical and roentgenographic information considerably narrows the diagnosis. Obstructive uropathy secondary to a urinary tract calculus is a frequent consideration but should not produce proteinuria, peripheral edema, or thromboembolic episodes if these are present. A stretched pelvocalyceal system, when visible, is also inconsistent with this diagnosis. Other diagnostic considerations such as renal artery occlusion or pennephric abscess are also unlikely to present with a clinical and roentgenographic appearance which might be confused with renal vein thrombosis. When this disease is suspected, inferior vena cavography or arteriography will easily confirm the diagnosis. In chronic renal vein thrombosis associated with the nephrotic syndrome, the diagnosis is usually less clear-cut and the differential diagnosis includes essentially all the causes of the nephrotic syndrome. Typically the patient presents with a previous history of flank pain or thromboembolic episodes. Physical evidence of inferior
Vein
Thrombosis
297
TABLE REPORTED WITH
I.
V
CONDITIONS RENAL
VEIN
ASSOCIATED THROMBOSIS
Infectious Pyelonephritis
Ascending
phlebitis
Ileocolitis
2.
Phycomycosis leukemia) Neoplasm Hypernephroma Transitional
(particularly
cell carcinoma,
with
lymphoma,
renal pelvis
Primary carcinoma elsewhere (bronchogenic cinoma, breast carcinoma, hepatoma) 3. Circulatory Disorder MI; CHF Cyanotic and polycythemic conditions Sickle cell anemia 4.
Systemic
.
Aniyloidosis Diabetic glomerulosclerosis Renal hypertension Trauma
6. Surgery Splenorenal Transplant Indwelling 7. Other
car-
Disorders
shunt catheter
in IVC
Idiopathic Papillary necrosis Post partum
Consumptive
coagulopathy
Glomerulonephritis, MI= CHF= IVC=
membranous
Myocardial infarct. Congestive heart failure. Inferior vena cava.
vena caval obstruction, such as collateral abdominal veins or lower trunk and leg edema, may be observed. The presence of an underlying disorder associated with increased incidence of renal vein thrombosis is supportive evidence (Table v). Urographically, the involved kidney may demonstrate the following: (i) slight increase in size; (2) normal or slightly decreased concentration of contrast material by the kidney; (3) a stretched collecting system; and () ureteral notching. It is important to emphasize that these findings may be minimal. It is not feasible in the present framework to list all possible causes of the nephrotic syndrome and its corresponding
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298
Mulhern,
Arger,
clinical and urographic picture to differentiate it from that seen in chronic renal vein thrombosis. However, using a modification of the etiologic scheme of the nephrotic syndrome as proposed by Schreincr,24 one can eliminate several categories rather simply. For example, historical data should reveal exposure to nephrotoxins, allergens, or harmful drugs. The clinical history and laboratory data should expose an infectious etiology of the nephrotic syndrome. Various metabolic diseases presenting with a nephrotic syndrome, such as diabetic glomerulosclerosis, will generally have associated abnormal laboratory values, such as an abnormal glucose tolerance test. Urography will commonly exhibit small shrunken kidneys bilaterally. Amyloidosis may be a very difficult diagnosis to exclude. The physical examination rarely reveals evidence of amyloid deposition elsewhere. Rectal biopsy is a safe confirmatory procedure. Symmetrical urographic changes are likely and ureteral notching is not seen. Various other systemic diseases noted by Schreiner24 may also cause the nephrotic syndrome. By virtue of the fact that they are systemic diseases, evidence of the pathologic process should be clinically present elsewhere. Sickle cell anemia, for example, will present in a young Black with a positive sickle cell preparation. Essential hypertension can be suspected on the basis of severe hypertension and other evidence of systemic vascular disease, such as eyeground changes. Glomerular disease, one of the most frequent causes of the nephrotic syndrome, must also be excluded. Recent sore throat with fever or a positive ASO titer is consistent with glomerulonephnitis. Hematuna, the hallmark of glomerulonephnitis, is a prominent finding in renal vein occlusion only during the acute stage. The urographic findings of acute renal vein thrombosis are not present in glomerulonephnitis. In those patients with chronic renal vein thrombosis not associated with a nephrotic syndrome, tumor is the most likely etiologic
Miller
and
Chait
OcrosEa,
1975
factor. Hypernephroma or renal pelvic carcinoma, the most frequent neoplasms to invade the renal vein, should be recognized roentgenographically. Compression or invasion of the renal vein or vena cava by tumor may be suspected on the urogram with ureteral notching. As is the case in many other diseases, the clinical and urographic picture of renal vein thrombosis is sufficiently characteristic to establish the diagnosis. A high index of suspicion on the part of the clinician or the radiologist will lead to the diagnosis in most instances. Confirmatory studies, particularly modified inferior vena cavography, may be undertaken immediately. Arteniography will yield further confirmatory information. Charles
Muihern,
B.
M.D.
Department of Radiology Hospital of the University 3400 Spruce Street Philadelphia, Pennsylvania
of Pennsylvania 19104
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