RENAL RUPTURE AFTER TRANSPLANTATION PAUL J. VAN CANGH, M.D. RICHARD ROBERT

M. EHRLICH, B. SMITH,

M.D.

M.D.

From the Department of Surgery/Urology, UCLA School of Medicine, and Wadsworth Veterans Administration Hospital, Los Angeles, California

ABSTRACT -Nine instances of spontaneous allografi rupture have been identifid in a series of 325 renal transplantations. Repair of the graft was accomplished in 4 cases. One graft functioned for five and one-half years, one kidney was removed immediately because of uncontrolled hemorrhage, and two grafts were subsequently removed because of rejection. Immediate nephrectomy was performed in 5 cases of irreversible rejection. The duration of ischemia and method of preservation appeared to have no etiologic importance. Evidence of severe acute rejection was present in all 9 cases. The recent increase in graft rupture parallels the increasing frequency of severe early acute rejection reactions.

Renal rupture is a rare but well-known complication of renal transplantation. l-l1 Recent review of our transplant experience shows increasing incidence of this potentially lethal complication. Nine graft ruptures have been identified in our series of 325 transplants at the UCLA Hospital and Wadsworth Veterans Administration Hospital from 1963 to 1975. All were associated with acute rejection reaction (Table I). An additional case that resulted from trauma is excluded from this series. One patient (Cases 3 and 8) survived the rupture of two grafts. Rupture led to death in 1 patient (Case 7). Repair of the rupture was performed in 4 cases. In one (Case 3) the bleeding could not be controlled, and the kidney had to be removed. Three grafts were successfully repaired; two were subsequently lost from rejection at three and six weeks postrepair. There was only one long-term survivor in our series (Case 1). Immediate nephrectomy was performed in 5 cases. In 4 cases the rejection episode was clearly irreversible and in 1 case, the poor condition of the patient was an additional factor.

April 28, 1975. Ischemia time was eight hours and twenty-two minutes. Immediate function was not noted. Two days postoperatively the patient was found to have an enlarging mass in the right lower abdominal quadrant. She was taken to surgery immediately where cardiovascular collapse occurred during the induction of anesthesia. Cardiac arrest ensued, but resuscitation was successful. Exploration revealed a large amount of fresh and old blood originating from multiple small tears involving the entire renal cortex. Immediate nephrectomy was performed. The kidney was markedly swollen (370 Gm.). Microscopic report revealed medullary coagulation necrosis with exudative and proliferative glomerular changes with perivascular infiltration of lymphocytes compatible with acute rejection. Death occurred two months later from a myriad of complications related to this procedure. Case 1

A thirty-seven-year-old diabetic woman received an E-match cadaveric renal transplant on

A forty-six-year-old man underwent cadaveric renal transplantation on April 9, 1968. Six days postoperatively an expanding mass was noted around the graft. Exploration revealed a 4-cm. laceration involving the outer convexity of the upper pole. The graft was grossly edematous but otherwise appeared viable. The laceration was closed with interrupted mattress sutures of

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Case Abstracts Case 7

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TABLE I. Case Number

Date

1

4/Q/68

C

?

?

2

1213169

P

D

3t

10/17/73

P

4

7112/74

5 6 7

8t 9

Clinical data in 9 cases of renal rupture*

Donor Tissue Circ. Source Type Ab. (%) LDA .

Method of Preservation

Time of Lowest Rupture Creatinine (Days) (Mg./lOO Ml.)

Ringer’s

6

1.3

2

Living

5

2.5

D

2

Living

9

1.0

C

E

1

. .

Machine

8

2.4

7125174 7127174 4128175

C C C

B D E

50 71 0

+ + -

Sack’s Sack’s Sack’s

11 10 2

1.6 8.6 N.F.

4129175 8128175

C C

E E

17 1

-

Sack’s Collins’

10 3

N.F. N.F.

*Key: Circ. Ab. = circulating antibody; LDA = lymphocyte-dependent positive; - = negative; N.F. =-nonfunction. Wase 3 and 8 are same patient.

3-O chromic catgut with the use of a fat bolster.

Postoperative course was uneventful. Serum creatinine stabilized at 1.3 mg. per 100 ml. Renal function was stable for five and one-half years until death supervened from chronic liver failure. Comment Graft rupture is a grave complication of renal transplantation. It usually occurs in the first two weeks after transplantation’-7’g but has been seen as late as I70 days following transplantation.3 Rupture occurred from two to eleven days in our series. Pain and swelling over the graft with associated vascular collapse and oliguria are the main presenting symptoms. Hematuria may also occur but is of little diagnostic significance in the early postoperative period. Acute rejection, ischemic damage, renal biopsy, air emboli secondary to perfusion, trauma, and urinary obstruction have all been implicated in the etiology of graft rupture. Heparinization necessary for post-transplant dialysis often accentuates the problem. As in our series acute rejection and ischemic damage with accompanying edema and decreased cortical blood flow account for most cases. Although graft rupture is more commonly seen in cadaveric transplants, the duration of cold and warm ischemia times does not appear to correlate with the incidence of graft rupturee4 Ischemia time in this series does not differ significantly from our general series

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Repair

Result

Functioning 5 yr., 6 mo.; died cirrhosis Yes Rejected 6 wk. later; retransplanted 815173 Attempted Failed; immediate nephrectomy; retransplanted Yes Rejected 3 wk. later; dialysis No Dialysis No Dialysis No Died 2 mo. later of complications related to rupture No Dialysis Dialysis No Yes

antibody; C = cadaveric; P = parent; + =

(Table II). Th e incidence of rupture among cadaveric organ recipients most likely correlated with the increased incidence of severe acute rejection episodes in this population. Both Murray et al.’ and Salaman et ~1.’ have reported a case in which renal biopsy was believed to be a major factor leading to rupture. One of our patients (Case 9) underwent renal biopsy at the time of transplantation. The biopsy site was noted to be intact and far removed from the site of rupture. The most common site of rupture is usually on the convex surface of the kidney along the longitudinal axis. Stresses secondary to marked graft swelling would be maximal in this area. In addition to this possible causative factor, cortical blood flow during an episode of acute tubular necrosis or acute rejection was also seen to be least in this area. Four kidneys in our series had multiple ruptures involving much of the cortical surface of the kidney (Table III). In addition to our series Fjeldborg and Kim8 have also reported multiple graft ruptures involving the entire cortical surface. These cases have always been associated with severe allograft rejection and swelling. It is of interest in our series that 7 of 9 transplant ruptures have occurred in the past two years, compared with only 2 ruptures in our previous nine years of transplant experience. We have been unable to relate this to any single factor other than a definite increase of severe acute rejection reactions during this time period.

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TABLE II.

Case Number 1 2 3 4 5 6 7 8 9

lschemia time

TABLE III.

Ischemia Time 4 hours Living Living 25 hours 21 hours 18 hours 8 hours I4 hours 37 hours

Case Number 1

30 minutes 18 minutes 13 minutes 22 minutes 22 minutes

2 3 4 5 6 7

Type ofrupture

Type of Rupture Single, 4 cm., convex upper pole Multiple, most severe outer convexity lower pole Single, 2.5 cm., upper pole medial aspect Multiple, outer convexity; (two lacerations) Complete “blow out” rupture of outer convexity Multiple stellate fractures; entire cortex Multiple smaI1 cortical ruptures; entire cortex Single, 5 cm., rupture of outer convexity Single, 3-cm. laceration outer convexity of lower pole

It is interesting to note that in Cases 5 and 6 and also in Cases 7 and 8 rupture occurred within two days of each other. All four of these grafts were perfused with Sack’s solution, and we were concerned that perhaps some abnormality related to this batch of Sack’s solution may have been responsible for these episodes of rupture. However, we were unable to find other such occurrences in and around this time in which Sack’s solution had been used. Prompt and aggressive treatment for rejection is the best prophylaxis. Routine capsulotomy appears to have no place in the prevention of this occurrence since in 2 cases in our series and in 11 cases in the literature rupture occurred despite capsulotomy.2,4,7 The management of renal rupture after transplantation takes into consideration two factors: first, the condition of the patient, and second, the quality of the graft. A patient in good general condition, with adequate coagulation parameters, can withstand a trial of repair with a good chance of success. On the other hand, a patient in shock with a bleeding diathesis is best treated with prompt nephrectomy. Similarly, one would be inclined to salvage a healthy looking kidney, from a living donor, which still has some function and cortical perfusion and does not show severe signs of rejection. In addition, an angiogram with excellent cortical flow and without severe changes or rejection would encourage us to repair the graft. A cadaveric graft, however, with signs of acute rejection would be discarded immediately. Sixteen cases from the literature ahd 3 of our own were successfully repaired. Grafts in 4 of the 16 cases from the literature were subsequently removed because of rupture (from seven to thirty-three days after repair). Two grafts in our series were removed because of rejection three and six weeks later. However, 1 patient had had persisting graft function for more than five and a half years postrupture.

1. MURRAY, J. E., et al.: Five years’ experience in renal transplantation with immunosuppressive drugs, Ann. Surg. 168: 416 (1968). 2. SALAMAN,J. R., et al.: Surgical aspects of clinical renal transplantation, Br. J. Surg. 56: 413 (1969). 3. LORD, R. S., BELZER, F. O., and KOUNTZ, S. L.: Delayed spontaneous rupture of the allografted kidney, Arch. Surg. 166: 607 (1970). 4. LORD, R. S., EFFENEY, D. J., HAYES, J. M., and TRACY, G. D.: Renal allograft rupture: cause, clinical features and management, Ann. Surg. 177: 268 (1973). 5 HAIMOV, M., GLABMAN, S., and BURROWS, L.: Spontaneous rupture of the allografted kidney, Arch. Surg. 163: 510 (1971). 6, KOOTSTRA, G., MEIJER, S., and ELEMO, J. D.: “Spontaneous” rupture of homografted kidneys, ibid. 108: 107 (1974). 7. POISSON, J., et al. : Rupture spontanee du rein allotransplantb, J. Urol. Nephrol. 79: 575 (1973). 8. FJELDBORC, O., and KIM, C. H.: Spontaneous rupture of renal transplant, Stand. J. Urol. Nephrol. 8: 31 (1974). 9. HABERAL, M. A., et al.: Late spontaneous rupture in a homografted kidney, Arch. Surg. 109: 824 (1974). 10. LIBERTINO, J. A., MERINO, M. J., ZINMAN, L., and TAKACS, F. J.: Spontaneous rupture of renal transplants, Urology 3: 75 (1974). 11. GHOSE, M. K., et al. : Spontaneous rupture of renal allotransplants, J. Urol. 109: 790 (1973).

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If a ruptured graft is left in situ, it is imperative that the patient be observed very closely for the next four to six weeks in the event rupture should recur. UCLA School of Medicine Los Angeles, California 90024 (DR. SMITH) References

JANUARY 1977 /

VOLUME IX, NUMBER 1

Renal rupture after transplantation.

RENAL RUPTURE AFTER TRANSPLANTATION PAUL J. VAN CANGH, M.D. RICHARD ROBERT M. EHRLICH, B. SMITH, M.D. M.D. From the Department of Surgery/Urology,...
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