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Renal artery aneurysm: Surgical indications and results
Eur J VascSurg 6, 477-486 (1992)
Renal Artery Aneurysm: Surgical Indications and Results T. Hupp 1, J. R. Allenberg 1, K. Post 2, T. Roeren 2, M. Meier ~ and J. H. Clorius 3 1Department of Surgery, Division of Vascular Surgery, 2Department of Radiodiagnostics, The University of Heidelberg, Germany, and 3Department of Radiology and Pathophysiology, The German Cancer Research Center, Heidelberg, Germany The clinical course of 23 patients with 28 renal artery aneurysms (RAAs) is reported. The RAAs were recorded over a period of 10 years. Thirty-five per cent of the RAAs (eight of 23 patients) were detected during the investigation of hypertension, whereas 26% (six of 23 patients) were discovered incidentally while imaging atherosclerotic arterial disease in the aorto-iliac region by angiography. Twenty-two aneurysms were treated surgically and primary nephrectomy was necessary in one case. The surgical technique used was excision of the aneurysm with bypass grafting in 13 cases (seven Dacron, five vein, one arterial bypass), a running suture following aneurysm excision in four cases and an end-to-end anastomosis in two cases. The results (for a period of 1-10 years) were excellent in all but three cases: two early graft occlusions (vein interposition) and one late occlusion (Dacron bypass) in the course of a re-operation which had become necessary because of a ruptured aneurysm of the gastro-epiploic artery after 3 months. Three of 23 patients were treated by embolisation of four intraparenchymal aneurysms. The follow-up of a nontreated saccular aneurysm showed a total thrombosis of the aneurysm within 4 years and fixed renal hypertension developed later in this patient. We suggest surgical repair of an RAA regardless of its size and the clinical symptoms, in order to prevent microembolism into the renal parenchyma and to avoid the development of fixed renal hypertension, h#rarenal aneurysms can be treated by embolisation to stop severe haematuria thus preserving the kidney. The resection of RAA is called for if renovascular hypertension occurs, if the renal function is impaired and if an affected solitary kidney must be maintained and~or if RAA was discovered accidentally with a simultaneous aorto-iliac vascular disease. Key Words: Renal artery aneurysm; Reconstructive surgery; Embolisation; Indication hypertension; Renovascular.
Introduction When examining the aorto-iliac region angiographically we have occasionally encountered a renal artery aneurysm (RAA). Whether diagnosed incidentally on imaging for obliterating or dilatating aortic disease or found during imaging for refractory hypertension, the diagnosis of a renal artery aneurysm is rather rare. It occurs angiographically in 0.1-0.3% of angiograms. 1'2 If angiography is symptom-related for suspected non-aneurysmal renal disease, e.g. in the case of hypertension, suspected tumour, or haematuria, the incidence, according to Stanley et al., 1 is about 50%; the incidence of RAA in angiography of obliterating or dilatating arteriopathy in the aorto-iliac region is 11%. The percentage of RAA in all visceral artery aneurysms is 15-25% 3,4 and autopsy findings show a percentage of 0.01%.5 Please address all correspondenceto: T. Hupp, Divisionof Vascular Surgery, Department of Surgery, Universityof Heidelberg, Im Neuenheimer Feld 110, D-6900Heidelberg, Germany. 0950-821X/92/050477+01 $08.00/0© 1992Grune & StrattonLtd.
Apart from a reno-vascular hypertension (7090% of all patients) and acute haemorrhage due to rupture (0.5-5% of all patients), clinical symptoms are of little or no diagnostic value. L3"6 Most renal artery aneurysms are noticed angiographically in the assessment of hypertension. Once an RAA has been confirmed, the vascular surgeon is faced with the problem of the natural history of RAA. The localisation and reconstruction procedures for RAA which sometimes involve an ex vivo revascularisation constitutes a challenge for the vascular surgeon.
Patients and Methods In the Vascular Registry of the Department of Surgery, University of Heidelberg, 24 extraparenchymal renal artery aneurysms (RAA) were identified in 20 patients and four intraparenchymal renal artery aneurysms were found in three patients during a 10-
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Table 1. Summary of findings in 23 patients with renal artery aneurysms (January 1980-January 1990)
Patient no.
Age
Sex
Extraparenchymal RAA 1 40 M
Admission blood pressure (mmHg)
Admission symptoms
Aneurysm size (cm)
Aneurysm side (R/L)
Findings/ pathology
Comments/ follow-up ( + / - )
240/120"
Covered rupture
16.5
L
Nephrectomy, aortic patch plasty
Mycotic
Death 2 months postop. (pleural empyema)
2.5
L
Vein graft interposition
FMD
Early occlusion
FMD
Early occlusion
Treatment
2
54
F
170/95
Ultrasonic incidental finding
3
26
M
190/130"
Hypertension, renal insufficiency
2.0
L
Vein graft interposition
4
72
M
230/150"
AAA II renal insufficiency
2.0
L
Dacron graft AS interposition, simultaneous bifurcation graft
5
25
F
130/80
Haematuria
1.8
R
Resection RAA, running suture - -
6
71
M
180/95"
AAA, renal insufficiency
1.5 1.3
R R
Aorto-renal AS Dacron graft Simultaneous bifurcation graft
7
56
M
220/120"
AAA, renal insufficiency
2.8
R
Aorto-renal Dacron graft Simultaneous aortic tube
8
35
F
190/90"
Hypertension, ruptured cerebral aneurysm
2.5
L
Hypogastric artery graft
AS
FMD
9
16
M
200/100"
Hypertension
1.7 0.4
R R
Vein graft interposition
FMD
+/ex situ repair
10
51
M
180/110"
Acute renal failure
1.2
R
Vein graft interposition
Dissecting RAA, solitary kidney
+/ex situ repair
11
56
F
120/90
Haematuria
3.2
R
Resection RAA, FMD, EE solitary kidney
12
47
F
240/120"
Hypertension
1.6
R
Resection RAA, AS EE
13
57
F
210/90"
Hypertension
2.5
R
Resection RAA, - running suture
14
26
F
230/150"
Hypertension
0.9
R
Aorto-renal vein graft
FMD
15
73
M
140/85"
AAA, incidental 1.8 finding 2.3
R L
Dacron graft interposition Simultaneous bifurcation graft
AS
16
58
M
180/100"
TAA, renal insufficiency
R L
Resection RAA AS Running suture
Eur J Vasc Surg Vol 6, September 1992
2.5 2.8
+/nephrectomy left (hypernephroma)
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Table 1.--contd.
Patient no.
Age
Sex
Admission blood pressure (mmHg)
17
63
M
190/80"
Hypertension
3.0
R
18
64
M
170/90"
AAA, hypertension, renal insufficiency
1,5
L
19
74
M
Rupture, haemorrhagic shock
1,0
L
20
39
F
Hypertension
2,2
R
180/80"
Admission symptoms
Aneurysm size (cm)
Aneurysm side (R/L)
Findings/ pathology
Comments/ follow-up ( + / - )
Aorto-renal Dacron graft
Multiple visceral aneurysms
Late occlusion reoperation
Aorto-renal Dacron graft Simultaneous aortic tube
AS
+/death 8 months postop. (pulmonary cancer)
Traumatic rupture
Death in diagnostic
Treatment
Conservative
Thrombosis -/severe of the hypertension aneurysm sac
Intraparenchymal RAA 21 41 M
22
48
M
23
56
M
90/70
Haematuria, haemorrhagic shock
1.1 0.6
L L
Endovascular embolisation
Solitary kidney
Haematuria anaemia
1.2
R
Endovascular embolisation
False aneurysm, solitary kidney
+/intrarenal aneurysm tumourenucleation
Haematuria, haemorrhagic shock
1.9
R
Endovascular embolisation
False aneurysm
+/intrarenal aneurysm tumourenucleation
+/intrarenal aneurysm nephrostomy
AAA: abdominal aortic aneurysms; TAA: thoracic aortic aneurysm; RAA: renal artery aneurysm; EE: end-to-side anastomosis; FMD: fibro-muscular dysplasia; AS: arteriosclerosis. * Patient on treatment with blood pressure medication.
year period (January 1980-January 1990). Before therapy, patients were selected for surgery by a committee of physicians consisting of internists, radiologists and vascular surgeons. Out of the 23 patients one died during diagnostic evaluation (case no. 19, Table 1); one patient was treated conservatively and the natural history of this patient's RAA was observed over a period of 6 years (case no. 20, Table 1). Five patients were found to have multiple RAAs: two were bilateral, and three patients had two aneurysms both located on one renal artery. Patients with small intraparenchymal aneurysms with associated systemic arteritis were not included in our set of patients. Four patients had an additional stenosis of the renal artery. At the time of diagnosis four patients had a functional solitary kidney. The male/female ratio was 15:8 and the age range 16-74 years with a median of 49.9 years. Thirteen patients (56%) were older than 50 years and four patients (20%) were younger than 30 years (Table 1). The overall follow-
up period was 28.8 months (6-72 months) and the family physicians were required to admit the patients if hypertension or renal function deteriorated.
Aetiology of renal artery aneurysms In our set of patients, arteriosclerosis was the most common cause for RAA and was seen in eight of all patients, seven of whom were male. In six of these patients an abdominal aortic aneurysm was also present. The median age of this subgroup with arteriosclerosis dependent RAA was 63 years, ranging from 51 to 73 years (Table 2). In six patients (four females, two males) fibromuscular dysplasia was found to cause the RAA (Fig. 1) and the mean age of this subgroup was 34, ranging from 16 to 54 years (Table 2). In one female patient haemangiectatic hypertrophy was also evident (case no. 8, Table 1). Eur J Vasc Surg Vol 6, September 1992
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Table 2. Renal artery aneusysms: aetiology, age and sex of the 23 patients (January 1980-January 1990)
Aetiology
No.
Age (2)
Range
Male/female
Extraparenchymal Arteriolsclerosis + simulataneous AAA
8 6
63 66
51-73 56-73
7/1 7/1
Fibroplasia
6
34
16-54
2/4
Traumatic
1
74
--
1/--
Mycotic
1
40
--
1/--
Aneurysmal disease
1
63
--
1/--
Unknown
3
40
25-57
--/3
2
52
48-56
2/--
1
41
--
1/--
Intraparenchymal Iatrogenic Traumatic
(a)
(b) ~
v~i~ ~
AAA: abdominal aortic aneurysm. In f o u r p a t i e n t s a t r a u m a t i c / i a t r o g e n i c cause for the R A A w a s noticed. T r a u m a in a p o l y t r a u m a t i s e d p a t i e n t (case no. 19, Table 1) w i t h s u b s e q u e n t r u p t u r e a n d h a e m o r r h a g e of a pre-existing R A A u l t i m a t e l y r e s u l t e d in the d e a t h of the p a t i e n t d u r i n g diagnosis. O n e p a t i e n t (case no. 21, Table 1) w h o h a d h a d a n e p h r o s t o m y for several y e a r s , d e v e l o p e d t w o intrarenal a n e u r y s m s c a u s e d b y r e c u r r e n t c a t h e t e r i s a t i o n t r a u m a . I n t w o p a t i e n t s (case nos. 22 a n d 23, Table 1) a n intrarenal, iatrogenic false a n e u r y s m o c c u r r e d p o s t o p e r a t i v e l y f o l l o w i n g e n u c l e a t i o n of a renal t u m o u r (Table 2).
Fig. 2. Arteriograms in a 39-year-old patient (case no. 1) with a large renal artery aneurysm (RAA) on the left side. (a) Displacement of the aorta by the RAA (arrow). (b) Selective renogram shows the size of the RAA with 16.5 cm in diameter (arrowheads). O n e 40-year-old p a t i e n t h a d a so-called m y c o t i c a n e u r y s m in c o n j u n c t i o n w i t h c o n c e a l e d retroperitoneal r u p t u r e (case no. 1, Tables 1, 2 a n d Fig. 2). O n e 63-year-old p a t i e n t h a d m u l t i p l e a n e u r y s m s of u n k n o w n origin w i t h a n R A A of the right renal artery, a h e p a t i c a r t e r y a n e u r y s m a n d an a n e u r y s m of the g a s t r o e p i p l o i c a r t e r y (case no. 17, Tables I a n d 2).
Fig. 1. Preoperative renogram (a), intraoperative sites (b), postoperative renogram (c) in a 16-year-old patient (case no. 9). (a) Fibromuscular dysplasia with two RAAs of the right renal artery (1.7 and 0.4cm in diameter). Clinical examination: severe hypertension; scintigraphic examination: right kidney 30% of total function. (b) Extracorporal reconstruction with vein graft interposition, distal anastomosis with running suture (arrow), after revascularisation orthotope replantation of the kidney. (c) Postoperative i.v.-DSA (1 year): proper graft and normal circulation to the kidney, no stenosis, no dilatation of the graft. Clinical examination: no hypertension, no antihypertensive medication; scintigraphic examination: right kidney 48% of total function. Eur J Vasc Surg Vol 6, September 1992
Renal Artery Aneurysm
Despite histological examination the aetiology of the aneurysm in two patients could not be determined as was the case in the only patient who did not undergo therapy (case no. 20, Table 1).
481
Aneurysm configuration The shape and configuration of the RAA was fusiform in 17 patients and saccular in eight. In three patients a false aneurysm was present; all of which were intrarenal (Fig. 3).
Localisation of the renal artery aneurysms Twelve aneurysms were located on the main renal artery with two patients developing a bilateral and one patient a double aneurysm. The average size of these aneurysms was 3.8 cm (range from 0.5 to 16.5; Fig. 3). I
No. of aneurysms
Location
[
Configuration No.
Average size (mm)
i
12
i
Fusiform Saccular
8 4 ,
58
Fusiform Saccular
6 2
23
Fusiform ~accular
2 I
17
Saccular
I
18
Main trunk
8 >,
I ° bifurcation
~j
5
Diagnostics In eight patients RAA was diagnosed while angiographically investigating hypertension, and in six others the incidental diagnosis of an RAA was established while radiographically imaging an abdominal aortic aneurysm. To diagnose an RAA, the technique of choice is conventional or intra-arterial digital subtraction angiography (DSA). A large incomplete ruptured RAA (size 16.5cm) was mistaken for an abdominal aortic aneurysm, the correct diagnosis being established intraoperatively (case no. 1, Table 1; Fig. 2). Twelve aneurysms could not be visualised by ultrasound techniques after an RAA was diagnosed angiographically. Only one RAA of the renal hilus on a recently hypertensive 54-year-old female patient (case no. 2, Table 1) was revealed by ultrasonography as an incidental finding. Calcified aneurysms of the renal artery were found in five patients on plain films in the kidneys.
I° branch
I
~ J - " ~
Symptoms of renal artery aneurysms Pole artery
Extraparenchymal RAA i E -~ --~ ~ ~-
Fusiform iSaccular ISpurious
4
I 0
12
3
_ 2 ° branch
Fig. 3. Renalartery aneurysms (28 aneurysms in 23 patients): localisation and configuration. At the hilus, or in the region of the first bifurcation, there were eight aneurysms whose average size was 2.3 cm, ranging from 1.0 to 3.0cm. Three aneurysms were located in the segmental arteries. The average size of these aneurysms was 1.7cm, range between 1.5 and 2.0 cm. One aneurysm of 1.8cm in diameter was found (case no. 5, Table 1) in a polar artery. The average size of the four intraparenchymatous aneurysms in the subsegmental arteries was 1.2 cm (range 0.6-1.9 cm) in diameter (Fig.
3).
There are no particular signs indicating the diagnosis of RAA. Most renal artery aneurysms were detected during angiographic assessment of patients with suspected reno-vascular hypertension. Quite often the diagnosis was incidental to angiography performed for dilatating or obliterating aorto-iliac disease. A non-specific symptom in all but two patients (17/19) was hypertension. The average preoperative blood pressure was 184/98 mmHg. Eight of the 19 patients had refractory hypertension and were having angiography prior to the final diagnosis of RAA and this population's (8/19) average blood pressure was 204/ 106mmHg. In a 35-year-old female patient a hypertensive crisis resulted in a ruptured intracerebral aneurysm of the posterior communicating artery. Following neurosurgery the RAA which caused the hypertension was diagnosed and 4 weeks later it was resected (case no. 8, Table 1). Eur J Vasc Surg Vol 6, September1992
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In seven patients renal function was impaired which, in the case of three patients, led to a prerenal investigation and hence helped establish the diagnosis of the RAA. At the time of the diagnosis, one of these patients was already suffering from complete renal failure. A solitary kidney was present in this case and additional renal artery dissection was the cause of the thrombotic occlusion of the RAA (case no. 10, Table 1). The average creatinine values in this population was 3.2 mg d1-1. In two patients the RAA ruptured, in one a concealed retroperitoneal rupture was present, arising from a saccular a n e u r y s m of the left main renal artery. The large RAA (16.5 cm) led to displacement a n d constriction of the aorta (case no. 1, Table 1, Fig. 2). The second polytraumatised patient died during diagnosis from rupture of an existing small (1 cm) saccular RAA (case no. 19, Fig. 4).
at the contralateral t u m o u r free kidney (case no. 11, Table 1) was found.
Intraparenchymal RAA In all three patients the principal sign was haematuria with haemorrhagic shock. The diagnosis, namely rupture of the a n e u r y s m with bleeding into the pelvicalyceal system, was arrived at by means of angiography. Two patients with a solitary kidney h a d had a previous t u m o u r enucleation indicating that the a n e u r y s m developed for iatrogenic reasons. The development of two aneurysms in another patient was caused by a recurrent cannulation of a nephrostomy. S y m p t o m s specifically attributable to the RAA calling for immediate surgical or endovascular intervention occurred in six patients. In two with a ruptured RAA, in one with RAA and simultaneous renal artery dissection and thrombotic occlusion, and in the other three with haematuria and haemorrhagic shock from intrarenal bleeding.
Surgical treatment/technicalprocedures (extraparenchymal RAA) Table I lists the clinical data and the choice of surgical procedure for revascularisation. Twenty-two of the 24 a n e u r y s m s (20 patients) were treated surgically (Table 3). Only one primary nephrectomy was Table 3. Renal artery aneurysm: surgical therapy (January 1980January 1990)
Therapy Nephrectomy Aorto-renal bypass/renorenal interposition
n 1 13
Dacron
7
Vein
5
Hypogastric artery graft
1
Aneurysm resection
6
Running suture
4
End-to-end anastomosis
2
Fig. 4. Arteriogram in a 74-year-oldpatient (case no. 19): ruptured saccular RAA of the left renal artery after polytrauma, RAA 1.0 cm in diameter (arrowhead). Arrows show the intra-abdominal haemorrhage. The patient died from a haemorrhagic shock during diagnostic evaluation.
Embol~sation(intrarenal aneurysms)
In one patient haematuria was indirectly responsible for the diagnosis of RAA. During investigation of a p r e s u m e d renal t u m o u r the fibro-muscular dysplasia of both renal arteries with a big hilar a n e u r y s m
necessary since the a n e u r y s m of 16.5 cm diameter in this patient h a d destroyed the renal artery so that a patchplasty of the aorta after n e p h r e c t o m y was performed (case no. 1, Table 1, Fig. 2).
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(a) (b) Fig. 5. Aortogram(a) and intraoperativesitus (b) in a 57-year-oldpatient (case no. 13). (a) FusiformRAA at the firstbifurcation,2.5 cm in diameter. (b) Intraoperativesitus before resection of the RAA. In the remaining 21 RAA patients surgery was undertaken. A total of 19 revascularisations were necessary after aneurysm resection. In two patients with two aneurysms of the ipsilateral renal artery only one bypass procedure was required after resection of both aneurysms (case nos 6 and 9, Table 1). Excision of the RAA with primary closure of the artery by longitudinal suture (Fig. 5) or an end-to-end anastomosis was possible in six cases. Aorto-renal or renal interposition bypass grafting was preferred in 13 cases. A Dacron bypass was inserted in seven, a vein bypass in five and a hypogastric artery graft in one (Table 3). In one patient with multiple aneurysms (case no. 19, Table 1) and one patient with a distal hilar aneurysms and simultaneous acute thrombosis of the RAA (case no. 10, Table 1) resection of the aneurysms and revascularisation was carried out after removing the kidney using bench surgery. Six patients had to have a simultaneous aortic reconstruction and renal revascularisation because of simultaneous renal and aortic aneurysms. In one patient (case no. 17, Table 1) a simultaneous reconstruction of an RAA, an hepatic artery aneurysm and an iliac artery aneurysm was performed.
Results Extraparenchymal R A A
There was no mortality in the 18 patients on w h o m
we operated. Primary patency rate in the 19 reconstructions in 17 patients was 89.5%. There were two early occlusions which occurred in one patient (case no. 2, Table 1) in conjunction with a triple-vein bypass following resection of a peripheral hilar aneurysm, and in another patient (case no. 3, Table 1) in conjunction with vein interposition following resection of a segmental artery aneurysm. As the residual kidney functioned well and the hypertension was stabilised by medication there was no need to reoperate. The early bypass occlusions in these patients were probably caused by technical problems. Today, one would have performed an ex vivo vascular reconstruction 7 in these two cases. The postoperative blood pressure returned to normal in seven of 17 (41%) patients and the remaining 10 patients showed a considerably improved blood pressure after medication. The average postoperative blood pressure of all patients was 148/ 81 mmHg. Renal insufficiency was improved in three of seven patients (serum creatinine K1.4mgd1-1) and three patients had a marked improvement in their creatinine and urea values. The creatinine level of one patient remained unchanged. In this subgroup of patients with renal insufficiency (7/17 patients) the average postoperative creatinine level was 1.6mgd1-1 (range: 1.4 to 2.2mgdl-1). Two patients died during the follow-up period, one of them (case no. 1, Table 1) within 2 months of Eur J Vasc Surg Vol 6, September1992
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surgery from a pleural empyema and the other (case no. 18, Table 1) died within 8 months of a lung carcinoma. In the patient with multiple visceral aneurysms (case no. 17, Table 1) a delayed occlusion occurred 3 months later during re-operation; w h i c h was necessary because of haemorrhagic shock from upper gastro-intestinal bleeding caused by rupture of an aneurysm of the right gastro-epiploic artery. In this case it was not possible to do another bypass.
IntraparenchymaI RAA The ruptured aneurysms and the subsequent haemorrhage into the pelvicalyceal system, present in four intrarenal aneurysms, required immediate embolisation. After superselective imaging of the intrarenal vascular lesions by i.a. DSA two patients had embolisation performed using Ethibloc (case nos 22 and 23, Table 1). One patient (case no. 21, Table 1) did not respond to embolisation using Ethibloc but fibringluten emboli stopped the bleeding. All haemorrhages were successfully stopped by embolisation with maintenance of renal function. Considering that two of the three patients had solitary kidneys after contralateral nephrectomy for tumour (Table 1) the result was excellent.
Discussion
Despite the very low incidence of RAAs (0.01% according to statistical data from autopsies) its diagnosis is increasing because of more frequent angiographic investigation of the renal arteries. 3"5"7"8 The incidental diagnosis of RAA occurs in this way up to 11% of patients having an angiogram for obliterating or dilatating disease of the aortoiliac region. 1"3"4 In the period of our study, we found in our patient population 28 renal artery aneurysms in 23 patients, which amounts to 0.18% of all vascular surgical patients. We were able to record the spontaneous development of one RAA over a period of 6 years (case no. 20, Table 1). This patient's diagnosis was established when an angiogram was performed because of hypertension. Apart from the 2 cm saccular RAA next to the hilus of the kidney, contralateral renal agenesis was noticed. As the operative risk was considered too high at the time of diagnosis and since the renin values remained constantly low and the hypertension was easily controlled by medication, the aneurysm was treated conservatively. Two years later angiography showed partial thrombosis of the aneurysm Eur J Vasc Surg Vol 6, September1992
which eventually thrombosed completely suggesting apparent spontaneous healing (Fig. 6). In the meantime, however, hypertension developed possibly due to recurrent thrombo-embolism. Fixed hypertension developed and parts of the lower pole of the kidney were lost because of recurrent microembolism 9-11 (Fig. 6). The fact that all but two patients had preoperative hypertension suggests that reno-vascular hypertension develops without significant renal artery stenosis. A possible cause could be microembolism from the renal artery aneurysms. Because of this possibility in our patients normalisation of blood pressure following aneurysm resection and revascularisation was achieved in only seven of 17 (41%) patients. N e w diagnostic methods are able to identify patients with fixed renal hypertension. 3,10-12 Recently published data using stress renography have suggested that surgical cure of reno-vascular hypertension can be predicted. 6"10,12 In patients with stress-mediated bilateral disturbance of renal hippuran transport during preoperative scintigraphic examination, postoperative cure of high blood pressure can not be expected. Although hypertension was cured by surgical therapy in only 41% of these patients there was no surgical or technical reason for these poor results. As a result we postulate that hypertension can be caused by recurrent intrarenal thrombo-embolism or by late injury to the intrarenal blood vessels because of long-term hypertension. 10,11 From this we can say that the presence of associated renal hypertension is an indication for surgical therapy. Apart from the treatment of hypertension, another major indication for surgical therapy of RAAs is organ preservation.13 By removing the RAA which is a suspected source of embolism the remaining organ function will be preserved. The most common causes of RAA are arteriosclerosis (AS) and fibro-muscular dysplasia (FMD). 1'6"8'14 From the histological findings there was no difference in the frequency of rupture. In our own series a traumatic aetiology with a ruptured aneurysm was present only once and must be considered as a rare cause of rupture of the aneurysm.15 Whether the shape of the aneurysm gives some indication to the potential rupture risk remains uncertain. In our patient population only two of the extrarenal RAAs ruptured and these were saccular. Contrary to the observations of other authors we observed that the fusiform shape (61%) was the most common aneurysm shape. 1,6, 9 Because of the relatively small number of patients evaluated, we cannot judge the influence of aneurysm size on the risk of rupture. Other auth-
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Fig. 6. Arteriograms in a 39-year-old woman (case no. 20) with unilateral aneurysm of the right renal artery and its natural history (no surgical therapy). (a) Size (2.2cm) and configuration (saccular) of the RAA. (b) After 2 years: partial thrombosis of the RAA. (c) After 3 years: increase of the partial thrombosis. (d) After 4 years: complete thrombosis of the aneurysm sac, rarification of the parenchymal circulation in the lower pole of the kidney due' to recurrent microembolisations out of the aneurysm. Now the patient suffers from a severe hypertension with a necessary multi-drug therapy. ors 1, 3, 6, 9,14 h a v e related the n e e d for o p e r a t i o n to the size of the a n e u r y s m . If the a n e u r y s m is smaller t h a n 2 c m t h e r e is n o risk of r u p t u r e a n d t h e r e f o r e n o indication for o p e r a t i o n . 1 T h e overall r u p t u r e rate of a n R A A is 5% b u t the r u p t u r e risk w i t h y o u n g p r e g n a n t w o m e n is increased. 16"17 In o u r p a t i e n t s o n l y t w o extrarenal a n e u r y s m s r u p t u r e d , o n e w a s the b i g g e s t a n e u r y s m (16.5 c m in diameter) a n d the o t h e r w a s the smallest a n e u r y s m (1 c m in diameter). W h e t h e r the o c c u r r e n c e of t h e s e t w o r u p t u r e s of extrarenal R A A ,
in a n overall p a t i e n t g r o u p of 24, indicates a g e n e r a l r u p t u r e risk or a so-called " b e n i g n s p o n t a n e o u s c o u r s e " of the small a n e u r y s m s , r e m a i n s to be determ i n e d . 5"6 A c c o r d i n g to H e n r i k s s o n et al., is the r u p t u r e rate of all e x t r a p a r e n c h y m a l R A A s is 7 % , j u d g i n g f r o m a n g i o g r a p h i c l o n g - t e r m studies. A n e p h r e c t o m y w a s r e q u i r e d in all cases of r u p t u r e d R A A . U n f o r t u n a t e l y t h e r e are n o d a t a o n the d e v e l o p m e n t of h y p e r t e n s i o n in t h o s e p a t i e n t s t r e a t e d c o n s e r v a tively.g, 18 Eur J Vasc Surg Vol 6, September 1992
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Owing to their aetiology, intraparenchymal aneurysms form a separate entity and, according to their traumatic pattern, are false aneurysms. It is noteworthy that, contrary to observations with extraparenchymal RAAs, all of the intraparenchymal aneurysms ruptured into the pelvi-calyceal system. By means of endovascular therapy the haematuria was stopped in all cases saving the kidneys. 19'2° All intraparenchymal aneurysms in our patient population were of iatrogenic or traumatic origin. Some authors 4"21 have reported cases of aneurysms following fine needle biopsy.
3 4 5 6
7 8 9
Conclusion
Controversy exists as to the indications for surgery for RAAs. The major argument for the surgical resection of an RAA is to remove the source of thromboembolism and through this to avoid the later vessel injuries which lead to fixed renal hypertension and loss of kidney function. Resection and revascularisation of extrarenal aneurysms is particularly called for if renD-vascular hypertension is present, if impaired kidney function had been confirmed by scinfigraphy, if an acute thrombosis of the RAA with simultaneous occlusion of the renal artery must be prevented, and if a solitary kidney with a prerenal RAA must be preserved. The comparatively low operative risk and the high therapeutic efficiency regarding surgical removal of the suspected source of embolism justifies surgery (especially in young patients). Endovascular therapy with embolisation of the ruptured intraparenchymal aneurysm ensures, by controlling the haemorrhage, preservation of the affected kidney.
10 11 12
13 14 15 16 17
18 19 20
References 21 1 STANLEYJC, RHODESEL, GEWERTZBL, CHANGCY, WALTERJF, FRY WJ. Renal artery aneurysms. Arch Surg 1975; 110: 13271333. 2 HAGEMANJH, SMITHRE, SZILAGYIDE, ELLIOTTJP.Aneurysms of
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the renal artery: problems of prognosis and surgical management. Surgery 1978; 10: 563-572. THAMG, EKELUNDL, HERRLINK, LINDSTEDTE, OLIN T, BERGENTZ SE. Renal artery aneurysms, natural history and prognosis. Ann Surg 1982; 197: 348-352. DETERLINGR. Aneurysms of the visceral arteries. J Cardiovasc Surg 1971; 12: 309-322. HEBERER G, SACHWEH D, DENECKE H. Das Aneurysma der Nierenarterie. Mfinch Med Wschr 1973; 115: 217-224. MARTIN RS, MEACHAM PW, DIETSHEIM JA, MULHERIN JL JR, EDWARDS WH. Renal artery aneurysm: selective treatment for hypertension and prevention of rupture. J Vasc Surg 1989; 9: 2634. NovicK AC. Surgical management of branch renal artery disease. Value of in situ and extracorporeal technique. Nephron 1986; 44 (suppl. 1): 40-44. MCKIEL, CF JR, GRAF EC, CALLAHANDH. Renal artery aneurysms: a report of 16 cases. J. Urol 1966; 96: 593-599. POUTASSEEF. Renal artery aneurysms: their natural history and surgery. J Urol 1966; 95: 297-307. HuPP T, CLORIUSJH, ALLENEERGJR. Renovascular hypertension. Predicting surgical cure with exercise renography. J Vasc Surg 1991; 14: 200-207. STANSBYGP, HILSON AJW, HAMILTONG. Renovascular hypertension secondary to renal artery aneurysm detected by Captopril-renography. Eur J Vasc Surg 1991; 5: 343-346. CLORIOSJH, ALLENBERGJR, HuPP T, STRAUSSLG, SCHMIDLINP, IRNGARTINGER G, WAGNER R, MUKHOPADHYAYC. Predictive value of exercise renography for presurgical evaluation of nephrogenic hypertension. Hypertension 1987; 10: 280-286. BERGENTZSE, BERGQUISTD, WEIBULLH. Changing concepts in renovascular surgery. Br J Surg 1989; 76: 429-430. DE BAKEYME, LEFRAKEA,GARCIA-RINALDIR,NOONGP. Aneurysm of the renal artery. A vascular reconstructive approach. Arch Surg 1973; 106: 438-443. BROWNMF, GRAHAMJM, MATTOXKL, FELICIANODV, DE BAKEY ME. Renovascular trauma. Am I Surg 1980; 140: 802-805. SCHOONIM, SEEMANT, NIEMANDD, LINDELLD, ANDERSCHB, BJOI(EROD S. Rupture of renal arterial aneurysm in pregnancy: case report. Acta Chir Scand 1988; 154: 593-597. DAYTONB, HELGERSONRB, SOLLINGERHW, ACHER CW. Ruptured renal artery aneurysm in a pregnant uninephric patient: successful ex vivo repair and autotransplantation. Surgery 1990; 107: 708-712. HENRIKSSONC, LURESP, NILSON AE, PETTERSSONS. Angiographically discovered, non operated renal artery aneurysms. Scand J Urol Nephrol 1984; 18: 59-62. COHEN AM, FISHERMF, YOON YS. Total therapeutic embolisation of the kidney for hypertension in a child with a mycotic aneurysm. Cardiovasc Intervent Radiol 1983; 6: 121-124. POST K, HIJPP T, ROERENT, BRAMBSHJ, ALLENBERGJR, KAUF~MANN GW. Nierenarterienaneurysmen. Radiologe 1991; 31: 5661. WEISSMANJ, GIYANANIVL, LANDRENEAIdMD, KILPATRICKJS. Postbiopsy arterial pseudoaneurysm in a renal allograft. Detection by Duplex Sonography. J Ultrasound Med 1988; 7: 515-518.
Accepted 17 April 1992
Renal Artery Aneurysm: Surgical Indications and Results T. Hupp 1, J. R. Allenberg 1, K. Post 2, T. Roeren 2, M. Meier ~ and J. H. Clorius 3 1Department of Surgery, Division of Vascular Surgery, 2Department of Radiodiagnostics, The University of Heidelberg, Germany, and 3Department of Radiology and Pathophysiology, The German Cancer Research Center, Heidelberg, Germany The clinical course of 23 patients with 28 renal artery aneurysms (RAAs) is reported. The RAAs were recorded over a period of 10 years. Thirty-five per cent of the RAAs (eight of 23 patients) were detected during the investigation of hypertension, whereas 26% (six of 23 patients) were discovered incidentally while imaging atherosclerotic arterial disease in the aorto-iliac region by angiography. Twenty-two aneurysms were treated surgically and primary nephrectomy was necessary in one case. The surgical technique used was excision of the aneurysm with bypass grafting in 13 cases (seven Dacron, five vein, one arterial bypass), a running suture following aneurysm excision in four cases and an end-to-end anastomosis in two cases. The results (for a period of 1-10 years) were excellent in all but three cases: two early graft occlusions (vein interposition) and one late occlusion (Dacron bypass) in the course of a re-operation which had become necessary because of a ruptured aneurysm of the gastro-epiploic artery after 3 months. Three of 23 patients were treated by embolisation of four intraparenchymal aneurysms. The follow-up of a nontreated saccular aneurysm showed a total thrombosis of the aneurysm within 4 years and fixed renal hypertension developed later in this patient. We suggest surgical repair of an RAA regardless of its size and the clinical symptoms, in order to prevent microembolism into the renal parenchyma and to avoid the development of fixed renal hypertension, h#rarenal aneurysms can be treated by embolisation to stop severe haematuria thus preserving the kidney. The resection of RAA is called for if renovascular hypertension occurs, if the renal function is impaired and if an affected solitary kidney must be maintained and~or if RAA was discovered accidentally with a simultaneous aorto-iliac vascular disease. Key Words: Renal artery aneurysm; Reconstructive surgery; Embolisation; Indication hypertension; Renovascular.
Introduction When examining the aorto-iliac region angiographically we have occasionally encountered a renal artery aneurysm (RAA). Whether diagnosed incidentally on imaging for obliterating or dilatating aortic disease or found during imaging for refractory hypertension, the diagnosis of a renal artery aneurysm is rather rare. It occurs angiographically in 0.1-0.3% of angiograms. 1'2 If angiography is symptom-related for suspected non-aneurysmal renal disease, e.g. in the case of hypertension, suspected tumour, or haematuria, the incidence, according to Stanley et al., 1 is about 50%; the incidence of RAA in angiography of obliterating or dilatating arteriopathy in the aorto-iliac region is 11%. The percentage of RAA in all visceral artery aneurysms is 15-25% 3,4 and autopsy findings show a percentage of 0.01%.5 Please address all correspondenceto: T. Hupp, Divisionof Vascular Surgery, Department of Surgery, Universityof Heidelberg, Im Neuenheimer Feld 110, D-6900Heidelberg, Germany. 0950-821X/92/050477+01 $08.00/0© 1992Grune & StrattonLtd.
Apart from a reno-vascular hypertension (7090% of all patients) and acute haemorrhage due to rupture (0.5-5% of all patients), clinical symptoms are of little or no diagnostic value. L3"6 Most renal artery aneurysms are noticed angiographically in the assessment of hypertension. Once an RAA has been confirmed, the vascular surgeon is faced with the problem of the natural history of RAA. The localisation and reconstruction procedures for RAA which sometimes involve an ex vivo revascularisation constitutes a challenge for the vascular surgeon.
Patients and Methods In the Vascular Registry of the Department of Surgery, University of Heidelberg, 24 extraparenchymal renal artery aneurysms (RAA) were identified in 20 patients and four intraparenchymal renal artery aneurysms were found in three patients during a 10-
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Table 1. Summary of findings in 23 patients with renal artery aneurysms (January 1980-January 1990)
Patient no.
Age
Sex
Extraparenchymal RAA 1 40 M
Admission blood pressure (mmHg)
Admission symptoms
Aneurysm size (cm)
Aneurysm side (R/L)
Findings/ pathology
Comments/ follow-up ( + / - )
240/120"
Covered rupture
16.5
L
Nephrectomy, aortic patch plasty
Mycotic
Death 2 months postop. (pleural empyema)
2.5
L
Vein graft interposition
FMD
Early occlusion
FMD
Early occlusion
Treatment
2
54
F
170/95
Ultrasonic incidental finding
3
26
M
190/130"
Hypertension, renal insufficiency
2.0
L
Vein graft interposition
4
72
M
230/150"
AAA II renal insufficiency
2.0
L
Dacron graft AS interposition, simultaneous bifurcation graft
5
25
F
130/80
Haematuria
1.8
R
Resection RAA, running suture - -
6
71
M
180/95"
AAA, renal insufficiency
1.5 1.3
R R
Aorto-renal AS Dacron graft Simultaneous bifurcation graft
7
56
M
220/120"
AAA, renal insufficiency
2.8
R
Aorto-renal Dacron graft Simultaneous aortic tube
8
35
F
190/90"
Hypertension, ruptured cerebral aneurysm
2.5
L
Hypogastric artery graft
AS
FMD
9
16
M
200/100"
Hypertension
1.7 0.4
R R
Vein graft interposition
FMD
+/ex situ repair
10
51
M
180/110"
Acute renal failure
1.2
R
Vein graft interposition
Dissecting RAA, solitary kidney
+/ex situ repair
11
56
F
120/90
Haematuria
3.2
R
Resection RAA, FMD, EE solitary kidney
12
47
F
240/120"
Hypertension
1.6
R
Resection RAA, AS EE
13
57
F
210/90"
Hypertension
2.5
R
Resection RAA, - running suture
14
26
F
230/150"
Hypertension
0.9
R
Aorto-renal vein graft
FMD
15
73
M
140/85"
AAA, incidental 1.8 finding 2.3
R L
Dacron graft interposition Simultaneous bifurcation graft
AS
16
58
M
180/100"
TAA, renal insufficiency
R L
Resection RAA AS Running suture
Eur J Vasc Surg Vol 6, September 1992
2.5 2.8
+/nephrectomy left (hypernephroma)
Renal Artery Aneurysm
479
Table 1.--contd.
Patient no.
Age
Sex
Admission blood pressure (mmHg)
17
63
M
190/80"
Hypertension
3.0
R
18
64
M
170/90"
AAA, hypertension, renal insufficiency
1,5
L
19
74
M
Rupture, haemorrhagic shock
1,0
L
20
39
F
Hypertension
2,2
R
180/80"
Admission symptoms
Aneurysm size (cm)
Aneurysm side (R/L)
Findings/ pathology
Comments/ follow-up ( + / - )
Aorto-renal Dacron graft
Multiple visceral aneurysms
Late occlusion reoperation
Aorto-renal Dacron graft Simultaneous aortic tube
AS
+/death 8 months postop. (pulmonary cancer)
Traumatic rupture
Death in diagnostic
Treatment
Conservative
Thrombosis -/severe of the hypertension aneurysm sac
Intraparenchymal RAA 21 41 M
22
48
M
23
56
M
90/70
Haematuria, haemorrhagic shock
1.1 0.6
L L
Endovascular embolisation
Solitary kidney
Haematuria anaemia
1.2
R
Endovascular embolisation
False aneurysm, solitary kidney
+/intrarenal aneurysm tumourenucleation
Haematuria, haemorrhagic shock
1.9
R
Endovascular embolisation
False aneurysm
+/intrarenal aneurysm tumourenucleation
+/intrarenal aneurysm nephrostomy
AAA: abdominal aortic aneurysms; TAA: thoracic aortic aneurysm; RAA: renal artery aneurysm; EE: end-to-side anastomosis; FMD: fibro-muscular dysplasia; AS: arteriosclerosis. * Patient on treatment with blood pressure medication.
year period (January 1980-January 1990). Before therapy, patients were selected for surgery by a committee of physicians consisting of internists, radiologists and vascular surgeons. Out of the 23 patients one died during diagnostic evaluation (case no. 19, Table 1); one patient was treated conservatively and the natural history of this patient's RAA was observed over a period of 6 years (case no. 20, Table 1). Five patients were found to have multiple RAAs: two were bilateral, and three patients had two aneurysms both located on one renal artery. Patients with small intraparenchymal aneurysms with associated systemic arteritis were not included in our set of patients. Four patients had an additional stenosis of the renal artery. At the time of diagnosis four patients had a functional solitary kidney. The male/female ratio was 15:8 and the age range 16-74 years with a median of 49.9 years. Thirteen patients (56%) were older than 50 years and four patients (20%) were younger than 30 years (Table 1). The overall follow-
up period was 28.8 months (6-72 months) and the family physicians were required to admit the patients if hypertension or renal function deteriorated.
Aetiology of renal artery aneurysms In our set of patients, arteriosclerosis was the most common cause for RAA and was seen in eight of all patients, seven of whom were male. In six of these patients an abdominal aortic aneurysm was also present. The median age of this subgroup with arteriosclerosis dependent RAA was 63 years, ranging from 51 to 73 years (Table 2). In six patients (four females, two males) fibromuscular dysplasia was found to cause the RAA (Fig. 1) and the mean age of this subgroup was 34, ranging from 16 to 54 years (Table 2). In one female patient haemangiectatic hypertrophy was also evident (case no. 8, Table 1). Eur J Vasc Surg Vol 6, September 1992
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Table 2. Renal artery aneusysms: aetiology, age and sex of the 23 patients (January 1980-January 1990)
Aetiology
No.
Age (2)
Range
Male/female
Extraparenchymal Arteriolsclerosis + simulataneous AAA
8 6
63 66
51-73 56-73
7/1 7/1
Fibroplasia
6
34
16-54
2/4
Traumatic
1
74
--
1/--
Mycotic
1
40
--
1/--
Aneurysmal disease
1
63
--
1/--
Unknown
3
40
25-57
--/3
2
52
48-56
2/--
1
41
--
1/--
Intraparenchymal Iatrogenic Traumatic
(a)
(b) ~
v~i~ ~
AAA: abdominal aortic aneurysm. In f o u r p a t i e n t s a t r a u m a t i c / i a t r o g e n i c cause for the R A A w a s noticed. T r a u m a in a p o l y t r a u m a t i s e d p a t i e n t (case no. 19, Table 1) w i t h s u b s e q u e n t r u p t u r e a n d h a e m o r r h a g e of a pre-existing R A A u l t i m a t e l y r e s u l t e d in the d e a t h of the p a t i e n t d u r i n g diagnosis. O n e p a t i e n t (case no. 21, Table 1) w h o h a d h a d a n e p h r o s t o m y for several y e a r s , d e v e l o p e d t w o intrarenal a n e u r y s m s c a u s e d b y r e c u r r e n t c a t h e t e r i s a t i o n t r a u m a . I n t w o p a t i e n t s (case nos. 22 a n d 23, Table 1) a n intrarenal, iatrogenic false a n e u r y s m o c c u r r e d p o s t o p e r a t i v e l y f o l l o w i n g e n u c l e a t i o n of a renal t u m o u r (Table 2).
Fig. 2. Arteriograms in a 39-year-old patient (case no. 1) with a large renal artery aneurysm (RAA) on the left side. (a) Displacement of the aorta by the RAA (arrow). (b) Selective renogram shows the size of the RAA with 16.5 cm in diameter (arrowheads). O n e 40-year-old p a t i e n t h a d a so-called m y c o t i c a n e u r y s m in c o n j u n c t i o n w i t h c o n c e a l e d retroperitoneal r u p t u r e (case no. 1, Tables 1, 2 a n d Fig. 2). O n e 63-year-old p a t i e n t h a d m u l t i p l e a n e u r y s m s of u n k n o w n origin w i t h a n R A A of the right renal artery, a h e p a t i c a r t e r y a n e u r y s m a n d an a n e u r y s m of the g a s t r o e p i p l o i c a r t e r y (case no. 17, Tables I a n d 2).
Fig. 1. Preoperative renogram (a), intraoperative sites (b), postoperative renogram (c) in a 16-year-old patient (case no. 9). (a) Fibromuscular dysplasia with two RAAs of the right renal artery (1.7 and 0.4cm in diameter). Clinical examination: severe hypertension; scintigraphic examination: right kidney 30% of total function. (b) Extracorporal reconstruction with vein graft interposition, distal anastomosis with running suture (arrow), after revascularisation orthotope replantation of the kidney. (c) Postoperative i.v.-DSA (1 year): proper graft and normal circulation to the kidney, no stenosis, no dilatation of the graft. Clinical examination: no hypertension, no antihypertensive medication; scintigraphic examination: right kidney 48% of total function. Eur J Vasc Surg Vol 6, September 1992
Renal Artery Aneurysm
Despite histological examination the aetiology of the aneurysm in two patients could not be determined as was the case in the only patient who did not undergo therapy (case no. 20, Table 1).
481
Aneurysm configuration The shape and configuration of the RAA was fusiform in 17 patients and saccular in eight. In three patients a false aneurysm was present; all of which were intrarenal (Fig. 3).
Localisation of the renal artery aneurysms Twelve aneurysms were located on the main renal artery with two patients developing a bilateral and one patient a double aneurysm. The average size of these aneurysms was 3.8 cm (range from 0.5 to 16.5; Fig. 3). I
No. of aneurysms
Location
[
Configuration No.
Average size (mm)
i
12
i
Fusiform Saccular
8 4 ,
58
Fusiform Saccular
6 2
23
Fusiform ~accular
2 I
17
Saccular
I
18
Main trunk
8 >,
I ° bifurcation
~j
5
Diagnostics In eight patients RAA was diagnosed while angiographically investigating hypertension, and in six others the incidental diagnosis of an RAA was established while radiographically imaging an abdominal aortic aneurysm. To diagnose an RAA, the technique of choice is conventional or intra-arterial digital subtraction angiography (DSA). A large incomplete ruptured RAA (size 16.5cm) was mistaken for an abdominal aortic aneurysm, the correct diagnosis being established intraoperatively (case no. 1, Table 1; Fig. 2). Twelve aneurysms could not be visualised by ultrasound techniques after an RAA was diagnosed angiographically. Only one RAA of the renal hilus on a recently hypertensive 54-year-old female patient (case no. 2, Table 1) was revealed by ultrasonography as an incidental finding. Calcified aneurysms of the renal artery were found in five patients on plain films in the kidneys.
I° branch
I
~ J - " ~
Symptoms of renal artery aneurysms Pole artery
Extraparenchymal RAA i E -~ --~ ~ ~-
Fusiform iSaccular ISpurious
4
I 0
12
3
_ 2 ° branch
Fig. 3. Renalartery aneurysms (28 aneurysms in 23 patients): localisation and configuration. At the hilus, or in the region of the first bifurcation, there were eight aneurysms whose average size was 2.3 cm, ranging from 1.0 to 3.0cm. Three aneurysms were located in the segmental arteries. The average size of these aneurysms was 1.7cm, range between 1.5 and 2.0 cm. One aneurysm of 1.8cm in diameter was found (case no. 5, Table 1) in a polar artery. The average size of the four intraparenchymatous aneurysms in the subsegmental arteries was 1.2 cm (range 0.6-1.9 cm) in diameter (Fig.
3).
There are no particular signs indicating the diagnosis of RAA. Most renal artery aneurysms were detected during angiographic assessment of patients with suspected reno-vascular hypertension. Quite often the diagnosis was incidental to angiography performed for dilatating or obliterating aorto-iliac disease. A non-specific symptom in all but two patients (17/19) was hypertension. The average preoperative blood pressure was 184/98 mmHg. Eight of the 19 patients had refractory hypertension and were having angiography prior to the final diagnosis of RAA and this population's (8/19) average blood pressure was 204/ 106mmHg. In a 35-year-old female patient a hypertensive crisis resulted in a ruptured intracerebral aneurysm of the posterior communicating artery. Following neurosurgery the RAA which caused the hypertension was diagnosed and 4 weeks later it was resected (case no. 8, Table 1). Eur J Vasc Surg Vol 6, September1992
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In seven patients renal function was impaired which, in the case of three patients, led to a prerenal investigation and hence helped establish the diagnosis of the RAA. At the time of the diagnosis, one of these patients was already suffering from complete renal failure. A solitary kidney was present in this case and additional renal artery dissection was the cause of the thrombotic occlusion of the RAA (case no. 10, Table 1). The average creatinine values in this population was 3.2 mg d1-1. In two patients the RAA ruptured, in one a concealed retroperitoneal rupture was present, arising from a saccular a n e u r y s m of the left main renal artery. The large RAA (16.5 cm) led to displacement a n d constriction of the aorta (case no. 1, Table 1, Fig. 2). The second polytraumatised patient died during diagnosis from rupture of an existing small (1 cm) saccular RAA (case no. 19, Fig. 4).
at the contralateral t u m o u r free kidney (case no. 11, Table 1) was found.
Intraparenchymal RAA In all three patients the principal sign was haematuria with haemorrhagic shock. The diagnosis, namely rupture of the a n e u r y s m with bleeding into the pelvicalyceal system, was arrived at by means of angiography. Two patients with a solitary kidney h a d had a previous t u m o u r enucleation indicating that the a n e u r y s m developed for iatrogenic reasons. The development of two aneurysms in another patient was caused by a recurrent cannulation of a nephrostomy. S y m p t o m s specifically attributable to the RAA calling for immediate surgical or endovascular intervention occurred in six patients. In two with a ruptured RAA, in one with RAA and simultaneous renal artery dissection and thrombotic occlusion, and in the other three with haematuria and haemorrhagic shock from intrarenal bleeding.
Surgical treatment/technicalprocedures (extraparenchymal RAA) Table I lists the clinical data and the choice of surgical procedure for revascularisation. Twenty-two of the 24 a n e u r y s m s (20 patients) were treated surgically (Table 3). Only one primary nephrectomy was Table 3. Renal artery aneurysm: surgical therapy (January 1980January 1990)
Therapy Nephrectomy Aorto-renal bypass/renorenal interposition
n 1 13
Dacron
7
Vein
5
Hypogastric artery graft
1
Aneurysm resection
6
Running suture
4
End-to-end anastomosis
2
Fig. 4. Arteriogram in a 74-year-oldpatient (case no. 19): ruptured saccular RAA of the left renal artery after polytrauma, RAA 1.0 cm in diameter (arrowhead). Arrows show the intra-abdominal haemorrhage. The patient died from a haemorrhagic shock during diagnostic evaluation.
Embol~sation(intrarenal aneurysms)
In one patient haematuria was indirectly responsible for the diagnosis of RAA. During investigation of a p r e s u m e d renal t u m o u r the fibro-muscular dysplasia of both renal arteries with a big hilar a n e u r y s m
necessary since the a n e u r y s m of 16.5 cm diameter in this patient h a d destroyed the renal artery so that a patchplasty of the aorta after n e p h r e c t o m y was performed (case no. 1, Table 1, Fig. 2).
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488
(a) (b) Fig. 5. Aortogram(a) and intraoperativesitus (b) in a 57-year-oldpatient (case no. 13). (a) FusiformRAA at the firstbifurcation,2.5 cm in diameter. (b) Intraoperativesitus before resection of the RAA. In the remaining 21 RAA patients surgery was undertaken. A total of 19 revascularisations were necessary after aneurysm resection. In two patients with two aneurysms of the ipsilateral renal artery only one bypass procedure was required after resection of both aneurysms (case nos 6 and 9, Table 1). Excision of the RAA with primary closure of the artery by longitudinal suture (Fig. 5) or an end-to-end anastomosis was possible in six cases. Aorto-renal or renal interposition bypass grafting was preferred in 13 cases. A Dacron bypass was inserted in seven, a vein bypass in five and a hypogastric artery graft in one (Table 3). In one patient with multiple aneurysms (case no. 19, Table 1) and one patient with a distal hilar aneurysms and simultaneous acute thrombosis of the RAA (case no. 10, Table 1) resection of the aneurysms and revascularisation was carried out after removing the kidney using bench surgery. Six patients had to have a simultaneous aortic reconstruction and renal revascularisation because of simultaneous renal and aortic aneurysms. In one patient (case no. 17, Table 1) a simultaneous reconstruction of an RAA, an hepatic artery aneurysm and an iliac artery aneurysm was performed.
Results Extraparenchymal R A A
There was no mortality in the 18 patients on w h o m
we operated. Primary patency rate in the 19 reconstructions in 17 patients was 89.5%. There were two early occlusions which occurred in one patient (case no. 2, Table 1) in conjunction with a triple-vein bypass following resection of a peripheral hilar aneurysm, and in another patient (case no. 3, Table 1) in conjunction with vein interposition following resection of a segmental artery aneurysm. As the residual kidney functioned well and the hypertension was stabilised by medication there was no need to reoperate. The early bypass occlusions in these patients were probably caused by technical problems. Today, one would have performed an ex vivo vascular reconstruction 7 in these two cases. The postoperative blood pressure returned to normal in seven of 17 (41%) patients and the remaining 10 patients showed a considerably improved blood pressure after medication. The average postoperative blood pressure of all patients was 148/ 81 mmHg. Renal insufficiency was improved in three of seven patients (serum creatinine K1.4mgd1-1) and three patients had a marked improvement in their creatinine and urea values. The creatinine level of one patient remained unchanged. In this subgroup of patients with renal insufficiency (7/17 patients) the average postoperative creatinine level was 1.6mgd1-1 (range: 1.4 to 2.2mgdl-1). Two patients died during the follow-up period, one of them (case no. 1, Table 1) within 2 months of Eur J Vasc Surg Vol 6, September1992
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surgery from a pleural empyema and the other (case no. 18, Table 1) died within 8 months of a lung carcinoma. In the patient with multiple visceral aneurysms (case no. 17, Table 1) a delayed occlusion occurred 3 months later during re-operation; w h i c h was necessary because of haemorrhagic shock from upper gastro-intestinal bleeding caused by rupture of an aneurysm of the right gastro-epiploic artery. In this case it was not possible to do another bypass.
IntraparenchymaI RAA The ruptured aneurysms and the subsequent haemorrhage into the pelvicalyceal system, present in four intrarenal aneurysms, required immediate embolisation. After superselective imaging of the intrarenal vascular lesions by i.a. DSA two patients had embolisation performed using Ethibloc (case nos 22 and 23, Table 1). One patient (case no. 21, Table 1) did not respond to embolisation using Ethibloc but fibringluten emboli stopped the bleeding. All haemorrhages were successfully stopped by embolisation with maintenance of renal function. Considering that two of the three patients had solitary kidneys after contralateral nephrectomy for tumour (Table 1) the result was excellent.
Discussion
Despite the very low incidence of RAAs (0.01% according to statistical data from autopsies) its diagnosis is increasing because of more frequent angiographic investigation of the renal arteries. 3"5"7"8 The incidental diagnosis of RAA occurs in this way up to 11% of patients having an angiogram for obliterating or dilatating disease of the aortoiliac region. 1"3"4 In the period of our study, we found in our patient population 28 renal artery aneurysms in 23 patients, which amounts to 0.18% of all vascular surgical patients. We were able to record the spontaneous development of one RAA over a period of 6 years (case no. 20, Table 1). This patient's diagnosis was established when an angiogram was performed because of hypertension. Apart from the 2 cm saccular RAA next to the hilus of the kidney, contralateral renal agenesis was noticed. As the operative risk was considered too high at the time of diagnosis and since the renin values remained constantly low and the hypertension was easily controlled by medication, the aneurysm was treated conservatively. Two years later angiography showed partial thrombosis of the aneurysm Eur J Vasc Surg Vol 6, September1992
which eventually thrombosed completely suggesting apparent spontaneous healing (Fig. 6). In the meantime, however, hypertension developed possibly due to recurrent thrombo-embolism. Fixed hypertension developed and parts of the lower pole of the kidney were lost because of recurrent microembolism 9-11 (Fig. 6). The fact that all but two patients had preoperative hypertension suggests that reno-vascular hypertension develops without significant renal artery stenosis. A possible cause could be microembolism from the renal artery aneurysms. Because of this possibility in our patients normalisation of blood pressure following aneurysm resection and revascularisation was achieved in only seven of 17 (41%) patients. N e w diagnostic methods are able to identify patients with fixed renal hypertension. 3,10-12 Recently published data using stress renography have suggested that surgical cure of reno-vascular hypertension can be predicted. 6"10,12 In patients with stress-mediated bilateral disturbance of renal hippuran transport during preoperative scintigraphic examination, postoperative cure of high blood pressure can not be expected. Although hypertension was cured by surgical therapy in only 41% of these patients there was no surgical or technical reason for these poor results. As a result we postulate that hypertension can be caused by recurrent intrarenal thrombo-embolism or by late injury to the intrarenal blood vessels because of long-term hypertension. 10,11 From this we can say that the presence of associated renal hypertension is an indication for surgical therapy. Apart from the treatment of hypertension, another major indication for surgical therapy of RAAs is organ preservation.13 By removing the RAA which is a suspected source of embolism the remaining organ function will be preserved. The most common causes of RAA are arteriosclerosis (AS) and fibro-muscular dysplasia (FMD). 1'6"8'14 From the histological findings there was no difference in the frequency of rupture. In our own series a traumatic aetiology with a ruptured aneurysm was present only once and must be considered as a rare cause of rupture of the aneurysm.15 Whether the shape of the aneurysm gives some indication to the potential rupture risk remains uncertain. In our patient population only two of the extrarenal RAAs ruptured and these were saccular. Contrary to the observations of other authors we observed that the fusiform shape (61%) was the most common aneurysm shape. 1,6, 9 Because of the relatively small number of patients evaluated, we cannot judge the influence of aneurysm size on the risk of rupture. Other auth-
Renal Artery Aneurysm
485
Fig. 6. Arteriograms in a 39-year-old woman (case no. 20) with unilateral aneurysm of the right renal artery and its natural history (no surgical therapy). (a) Size (2.2cm) and configuration (saccular) of the RAA. (b) After 2 years: partial thrombosis of the RAA. (c) After 3 years: increase of the partial thrombosis. (d) After 4 years: complete thrombosis of the aneurysm sac, rarification of the parenchymal circulation in the lower pole of the kidney due' to recurrent microembolisations out of the aneurysm. Now the patient suffers from a severe hypertension with a necessary multi-drug therapy. ors 1, 3, 6, 9,14 h a v e related the n e e d for o p e r a t i o n to the size of the a n e u r y s m . If the a n e u r y s m is smaller t h a n 2 c m t h e r e is n o risk of r u p t u r e a n d t h e r e f o r e n o indication for o p e r a t i o n . 1 T h e overall r u p t u r e rate of a n R A A is 5% b u t the r u p t u r e risk w i t h y o u n g p r e g n a n t w o m e n is increased. 16"17 In o u r p a t i e n t s o n l y t w o extrarenal a n e u r y s m s r u p t u r e d , o n e w a s the b i g g e s t a n e u r y s m (16.5 c m in diameter) a n d the o t h e r w a s the smallest a n e u r y s m (1 c m in diameter). W h e t h e r the o c c u r r e n c e of t h e s e t w o r u p t u r e s of extrarenal R A A ,
in a n overall p a t i e n t g r o u p of 24, indicates a g e n e r a l r u p t u r e risk or a so-called " b e n i g n s p o n t a n e o u s c o u r s e " of the small a n e u r y s m s , r e m a i n s to be determ i n e d . 5"6 A c c o r d i n g to H e n r i k s s o n et al., is the r u p t u r e rate of all e x t r a p a r e n c h y m a l R A A s is 7 % , j u d g i n g f r o m a n g i o g r a p h i c l o n g - t e r m studies. A n e p h r e c t o m y w a s r e q u i r e d in all cases of r u p t u r e d R A A . U n f o r t u n a t e l y t h e r e are n o d a t a o n the d e v e l o p m e n t of h y p e r t e n s i o n in t h o s e p a t i e n t s t r e a t e d c o n s e r v a tively.g, 18 Eur J Vasc Surg Vol 6, September 1992
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T. Hupp et al.
Owing to their aetiology, intraparenchymal aneurysms form a separate entity and, according to their traumatic pattern, are false aneurysms. It is noteworthy that, contrary to observations with extraparenchymal RAAs, all of the intraparenchymal aneurysms ruptured into the pelvi-calyceal system. By means of endovascular therapy the haematuria was stopped in all cases saving the kidneys. 19'2° All intraparenchymal aneurysms in our patient population were of iatrogenic or traumatic origin. Some authors 4"21 have reported cases of aneurysms following fine needle biopsy.
3 4 5 6
7 8 9
Conclusion
Controversy exists as to the indications for surgery for RAAs. The major argument for the surgical resection of an RAA is to remove the source of thromboembolism and through this to avoid the later vessel injuries which lead to fixed renal hypertension and loss of kidney function. Resection and revascularisation of extrarenal aneurysms is particularly called for if renD-vascular hypertension is present, if impaired kidney function had been confirmed by scinfigraphy, if an acute thrombosis of the RAA with simultaneous occlusion of the renal artery must be prevented, and if a solitary kidney with a prerenal RAA must be preserved. The comparatively low operative risk and the high therapeutic efficiency regarding surgical removal of the suspected source of embolism justifies surgery (especially in young patients). Endovascular therapy with embolisation of the ruptured intraparenchymal aneurysm ensures, by controlling the haemorrhage, preservation of the affected kidney.
10 11 12
13 14 15 16 17
18 19 20
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Accepted 17 April 1992