Nephrol Dial Transplant (2001) 16: 124-127
© 2001 European Renal Association-European Dialysis and Transplant Association
Renal allograft rupture is associated with rejection or acute tubular necrosis, but not with renal vein thrombosis
Boris Wolfgang Hochleitner,
Reinhold Kafka,
Bernard Spechtenhauser,
Claudia Bösmüller,
Wolfgang Steurer,
Alfred Königsrainer and
Raimund Margreiter
Department of Transplant Surgery, Innsbruck University Hospital, Innsbruck, Austria
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Abstract
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Background. Whereas rejection was reported to be the most
common cause of renal allograft rupture (RAR) in the pre-cyclosporin
era, renal vein thrombosis (RVT) is purported to be the main
cause of RAR in patients taking cyclosporin. The extremely low
incidence of RVT in our series (0.11%) prompted us to analyse
our collective with regard to RAR.
Method. Between 1974 and 1999, 1811 renal transplants were performed. Patients with RAR, defined as a tear of the renal capsule and parenchyma, were identified and possible underlying factors studied.
Results. RAR was diagnosed in nine male and five female recipients (0.8%) with a median age of 36 years. Immunosuppression consisted of azathioprine and prednisolone in seven patients and of cyclosporin-based therapy in the seven others. At exploration five grafts were removed immediately: three because of irreversible rejection, one because of deep wound infection, and one with a twisted renal vein. Six of the nine salvaged kidneys have been functioning after a mean observation time of 45 months. In the pre-cyclosporin era RAR was associated with acute rejection in five out of seven cases as compared with only three of the seven on cyclosporin treatment. Core biopsies might have been the cause in three cases.
Conclusion. RAR is a rare complication after renal transplantation. Acute rejection still represents the most frequent cause of RAR in the cyclosporin era.
Keywords: Cyclosporin; renal allograft rupture; acute tubular necrosis
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Introduction
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As first reported in 1968 [
1], spontaneous renal allograft rupture
(RAR) is a rare but potentially life-threatening complication
following kidney transplantation associated with high rate of
graft loss [
2–
4]. Its incidence has been reported to range
from 0.3 to 9.6% of all transplants. The majority of RAR has
been described to occur in the first 3 weeks after surgery.
In the pre-cyclosporin era acute rejection was the most common
cause, whereas under cyclosporin-based immunosuppression renal
vein thrombosis has been reported to be the main cause of RAR
[
4]. Since the incidence of renal vein thrombosis was extremely
low in our series (0.11%), we were interested in the factors
potentially involved in RAR in our patients.
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Patients and methods
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Between March 1974 and May 1999, 1811 renal transplants were
performed at Innsbruck University Hospital. Of these 1730 were
from cadaver donors, 71 from living-related and 10 from living-unrelated
(spouses in all cases) donors. Until 1980, prophylactic immunosuppression
consisted of azathioprine and high-dose steroids. Acute rejection
episodes were treated with 3
x1 g methylprednisolone, later on
with 3
x500 mg methylprednisolone and anti-thymocyte globulin
(ATG) for steroid-resistant rejection. From 1980, more and more
patients were treated with cyclosporin, either alone or in combination,
with low-dose steroids. Most of the patients in the early 1980s
were enrolled in prospective trials [
5,
6]. Since 1984 most patients
have received triple-drug therapy with cyclosporin, azathioprine
and steroids. Patients at immunological risk (more than 80%
panel-reactive HLA antibodies, loss of a previous transplant
from irreversible acute rejection) received induction therapy
with ATG. In the late 1980s some patients received various monoclonal
antibodies and from 1995 on tacrolimus (FK506) (in controlled
trials). The surgical procedure was carried out in a standardized
manner. The graft vein was anastomosed end-to-side to the external
iliac vein with a 5/0 or 6/0 Prolene running suture, or sometimes,
in re-transplants or for reasons of size to the common iliac
vein. In cadaveric kidneys the right renal vein was usually
extended with the attached vena cava. The renal artery was anastomosed
with an aortic patch end-to-side to the external iliac artery.
In some live donor transplants, the artery was anastomosed end-to-end
with the internal iliac artery, which was also done in cases
of
en-bloc transplantation of paediatric kidneys. The ureteroneocystostomy
was performed using a modified Leadbetter–Politano technique
in most patients.
RAR was defined as a tear of the renal capsule as well as the renal parenchyma associated with haemorrhage and was confirmed by exploration in all instances. Various donor, procurement as well as recipient characteristics were compared between patients who developed RAR and the entire patient population with the use of the t-test, 
2-test or Mann–Whitney U-rank sum test, as required. A logistic regression model was fitted to evaluate whether cold ischaemia, acute tubular necrosis, acute rejection, age of the recipient and CMV infection are independent risk factors. P-values <0.05 were considered statistically significant.
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Results
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RAR was diagnosed in 14 (0.8%) of the 1811 renal transplant
recipients (Table 1
). Between 1974 and 1981 the incidence was
as high as 2.8% and decreased to about 0.7% after 1982. The
average age of the nine male and five female patients was 36
(22–57) years. Eleven of the 14 transplants were first
transplants, for three patients it was their second graft. The
underlying kidney diseases were glomerulonephritis in eight
patients and pyelonephritis in four. The two remaining patients
suffered from nephroangiosclerosis. The demographics of the
14 cadaveric donors, nine of which were male, show a mean age
of 28 (0.5–69) years. For organ preservation HTK solution
was used in one, UW in five and EuroCollins in eight cases.
Prophylactic immunosuppression consisted of azathioprine and
prednisolone in seven patients, and of cyclosporin, azathioprine
and prednisolone in the remaining seven patients. RAR occurred
on day 11 (3–21), post-transplant. Clinical presentation
was similar in all patients: sudden pain and swelling over the
graft with a drop in haematocrit and in blood pressure accompanied
by oliguria. When RAR was suspected, diagnosis was confirmed
in most but not all patients by ultrasound examination. At emergency
exploration, a huge haematoma surrounding the convexity of the
graft was found in 13 patients. In one patient the haematoma
was ruptured into the abdominal cavity. Most of the RAR had
occurred along the convex border of the graft, others at either
renal pole. In one patient who had received two paediatric kidneys
en-bloc, twisting of the left renal vein occurred as a result
of poor placement of the graft. This outflow problem appeared
to be the cause of the RAR. In all other grafts, vessels were
found to be patent. Five grafts were removed immediately: three
because of irreversible concomitant rejection, one because of
deep wound infection, and the one with the twisted renal vein.
In the remaining nine grafts, haemostasis was achieved with
careful suturing, and/or the use of haemostyptic material as
well as infrared or laser coagulation and fibrin glue. In two
cases with deep extended scars, repair was achieved by wrapping
the graft with a mesh of absorbable material. In one case RAR
occurred on day 6 and was repaired successfully. A second RAR,
however, on day 39 prompted nephrectomy. All patients survived
RAR. Six of the nine repaired kidneys are currently functioning
after a mean observation time of 45 (1–111) months. Figure
1
depicts the possible aetiologies. In the pre-cyclosporin era
RAR was associated with acute rejection in five out of seven
cases, whereas under cyclosporin only three of seven RAR were
caused by rejection. Cyclosporin levels of these three patients
on the day of or the day before RAR were 213, 91, and 188 ng/ml.
Core biopsies seem to have been the cause of RAR in three cases,
since all of them occurred within 6 h following biopsy. When
comparing the incidence of cold ischaemia, acute tubular necrosis,
acute rejection, age of the recipient and CMV infection between
patients with and without RAR, only acute tubular necrosis and
rejection were found to be significantly different between the
two cohorts and may therefore be considered a possible risk
factors of RAR (Fig. 2
).
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Fig. 1. Graft ruptures show temporal associations with acute rejection, closed-needle biopsies and acute tubular necrosis. Of our 14 patients who underwent renal allograft rupture, seven received conventional prophylactic immunosuppression with azathioprine+cortisone (Aza/Cort). The other seven patients were treated with cyclosporine-based triple therapy.
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Fig. 2. The frequency of acute tubular necrosis and acute rejection in patients with and without RAR, being significantly different.
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Discussion
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In a series of 885 consecutive renal transplants, performed
in Oxford between 1975 and 1990 renal vein thrombosis (RVT)
with consecutive RAR was observed in eight cases (0.9%), all
of which were receiving cyclosporin-based triple drug therapy
as prophylactic immunosuppression [
4]. In another series of
75 consecutive renal transplants in Riyadh, RAR was encountered
in three male patients; two of these cases were associated with
steroid-resistant rejection and one with RVT [
7]. Our experience
does not confirm the association of RAR with venous thrombosis
since the incidence of venous thrombosis in our series was 0.11%
in contrast to 0.8% for RAR. Furthermore, RAR was associated
with renal vein thrombosis in only one out of seven patients
with RAR taking cyclosporin, azathioprine and prednisolone for
immunosuppression. In the remaining seven patients with RAR
immunosuppression consisted of azathioprine and prednisolone,
and no renal vein thrombosis was seen.
Our data revealed an association between RAR and rejection as well as ATN. Cold ischaemia, preservation conditions, age of the recipient and CMV infection were not found to be risk factors. In a similar analysis of 12 patients sustaining RAR in a series of 331 consecutive renal transplants recipient age, the white-to-black donor-recipient race mismatch and the need for dialysis were identified as risk factors [8]. A recent case report concludes that renal allograft rupture results from interstitial edema due to acute tubular necrosis [9].
In most but not all of our RAR patients ultrasound was a valuable aid in establishing the diagnosis. Soler et al. found in six out of 18 cases of RAR a disruption of the white linear echo of the graft capsule [10].
Transplant nephrectomy is a definite treatment for RAR, but some authors argue that transplant nephrectomy is justified only in patients who would otherwise die [11]. The salvage rate varies between 40 and 100% and was 64% in our series, which would indicate that it is well worth trying to salvage spontaneously ruptured renal allografts [2–4].
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Notes
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Correspondence and offprint requests to: B. W. Hochleitner,
Department of Transplant Surgery, Innsbruck University Hospital,
Anichstraße 35, A-6020 Innsbruck, Austria.
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References
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Received for publication: 24. 2.00
Revision received 10. 7.00.
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Abstract
Introduction