SPONTANEOUS RUPTURE OF THE RENAL ALLOGRAFT Okay Odocha, MD, Clive 0. Callender, MD, and Vivian W. Pinn-Wiggins, MD Washington, DC
Spontaneous renal allograft rupture, an unusual complication of renal transplantation, occurred in a 35-year-old woman 10 days after transplantation. Unusual localized pain and tenderness at allograft site, oliguria, and hypotension, a triad frequently seen in renal allograft rupture, were present. Management by transplant nephrectomy was inevitable because of the patient's downhill course. Histopathologic findings diagnostic of acute allograft rejection support current thinking that spontaneous rupture may be the final outcome, although unusual, of renal allograft rejection. Key words * acute allograft rupture * acute rejection* spontaneous graft rupture
Non-traumatic spontaneous rupture of the renal allograft is an infrequent and unusual complication of human renal transplantation. Occurring in 0.8% to 9.6% of all renal transplants," 2 usually within the first 2 weeks of transplantation,"3'4 its etio-pathogenesis has remained obscure. To date, however, the most frequently identifiable factor in up to 60% of the patients has been acute From the Department of Surgery and Pathology, Howard University Hospital, Washington, DC. Requests for reprints should be addressed to Dr Clive 0. Callender, Howard University Hospital, 2041 Georgia Ave, NW, Washington, DC 20060. JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
allograft rejection.4-7 In addition, most ruptures reported have occurred in cadaveric renal allografts.13,4,6,8,9 Debate on the management of such allograft rupture has focused on allograft salvage versus transplant nephrectomy.12'5'6'8 It appears that the recent trend is toward performing transplant nephrectomy if excessive hemorrhage, allograft necrosis, and rupture compromise patient survival.1 4'10 If the patient's condition is stable, and the allograft rupture site is surgically manageable, allograft salvage should be attempted." 2'68' 10-12
CASE REPORT An otherwise healthy 33-year-old black woman with hypertension and end-stage renal disease, (hemodialysis-dependent), underwent an uneventful cadaveric renal transplant on April 18, 1987. Postoperatively, immunosuppression was with Antilymphocyte Globulin (ALG), Imuran, and Solumedrol. Development of thrombocytopenia and vaginal bleeding led to the discontinuation of ALG and Imuran, and subsequent replacement with cyclosporin (CSA) from the 3rd postoperative day (POD). On the 5th POD, the patient developed a vague abdominal pain and a temperature of up to 101.4°E Physical examination and septic workup were unremarkable. On POD 8, the patient complained of dizziness and headache. She was noted to have herpetiform eruptions in the anogluteal groove, and moderate hypertension of 170/120 mm Hg. She was seropositive (high titer) for herpes virus and cytomegalovirus (CMV). 171
RENAL ALLOGRAFT RUPTURE
14
-
1210 86 p
< z U.
Transplant Nephrectomy
4~~~~~~~
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2-
ES
L
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Figure IA. Renal allograft immediately after surgical excision with localized perirenal hemorrhage.
I_~~~~A
80
5
-
60 40 -
E
L D0
0
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4000
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Figure 1 B. Transplant nephrectomy with mottled capsular surface and localized blood clot at the superior pole.
Figure IC. Cut surface of allograft, reflecting cortical necrosis and medullary congestion. The patient was started on acyclovir cream 5% and captopril. On POD 9, she suddenly developed right
80/60), and oliguria. Renogram showed no flow in the transplant kidney and no excretion into the bladder. Consequently, the patient underwent emergency exploratory laparatomy. Intraoperatively, over 0.2 L of blood clots were evacuated. The allograft (Figures lA-C) was edematous, swollen, and congested. The surface was mottled. A jagged rupture located in the superior pole was present. The perinephric area contained a large amount of blood clot. A transplant nephrectomy was performed. Postoperatively, the patient had an uncomplicated hospital course. She was restarted on hemodialysis and discharged home on June 5, 1987.
PATHOLOGICAL STUDIES Figure 2 shows a composite chart illustrating the
172
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
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daily changes seen in the patient's blood urea nitrogen (BUN), creatinine clearance, plasma creatinine level, urinary output, and fraction of excretion of sodium. All indicate the progressive loss of function in the allograft. The renal allograft measured 15.5 cm X 9 cm X 6 cm and weighed 434 gm. A 4-cm X 3-cm capsular hemorrhage was present in the superior pole and extended well into the cortex. The cut surface was edematous. The medullary region appeared congested and the cortex mottled, with pale areas of necrosis. Extensive cortical necrosis with focal superior pole hemorrhagic necrosis and capsular hemorrhage were seen. Focal changes of vascular rejection were present, as well as moderately severe acute tubulointerstitial cellular rejection (Figures 3A-C). Ultrastructural studies of two glomeruli showed acute ischemic necrosis consistent with cortical necrosis. No deposits or basement membrane changes were identified. Many mononuclear cells were present in the interstitium. No evidence of significant immunoglobulin, complement or fibriogen deposition in the allograft was seen with immunofluorescent studies.
'1 Figure 3A. Interstitial hemorrhage extending into pericapsular tissue.
V I
DISCUSSION Reports of the incidence of nontraumatic, spontaneous renal allograft rupture have ranged from 0.8% to 9.61%1,2,9 and might be higher, as some ruptures might go undetected.3 Most ruptures (Figures lA-C) are seen in cadaveric renal allografts and tend to occur within the first 2 weeks.1'3'4'6'9 In a recent literature review of 149 renal allograft ruptures, 125 of the grafts (83.9%) were from cadavers.3 Mode of preservation, storage time, and the composition of the cold perfusate did not correlate with the tendency to rupture.4 It seems, however, that acute rejection and swelling may lead to rupture.4-7 Clinical presentations of graft rupture include localized pain and tenderness at the transplant site, oliguria, and hypotension. These findings, as well as the biochemical derangements (Figure 1) noted in our
patient, prompted surgical exploration. Interestingly, other workers consider that the combination of pain, hypotension, and oliguria occur sufficiently in renal allograft rupture to constitute a diagnostic triad.3'4 In the management of renal allograft rupture, serious consideration is given to the clinical condition of the patient and the findings at operation. Transplant nephrectomy is indicated when the combination of rupture, with its attendant hemodynamic derangements, compromises the patient.",4"10 In the stable patient with JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
Figure 3B. Vascular (humoral) rejection with surrounding acute interstitial cellular rejection.
Figure 3C. Unremarkable glomerulus with ad. jacent acute interstitial cellular rejection. 173
RENAL ALLOGRAFT RUPTURE
a less compromised allograft, a salvage operation should be attempted.1'2'6'8"0-12 Literature Cited 1. Susan LP, Braun WE, Banowsky LH, Straffon RA, Valenzuela R. Rupture human renal allograft. Urology. 1978;1 1(1):53-57. 2. Dryburgh P, Porter KA, From RAF, et al. Should the ruptured renal allograft be removed? Arch Surg. 1979;1 14:850852. 3. Thukral R, Mir AR, Jacobson MP. Renal allograft rupture: a report of three cases and review of the literature. Am J Nephrol. 1982;2:15-27. 4. Lord RSA, Effeney D, Hayes JM, Tracy GD. Renal allograft rupture. Ann Surg. 1973;177(3):268-273. 5. Ajao OG, Callender CO, Stevens J, Sampson C. Spontaneous renal allograft rupture four years after transplantation. Urol Int. 1984;39:49-51. 6. Serrallach N, Gutierrez R, Serrate R, et al. Renal allograft rupture: surgical treatment by renal corsetage with
174
lyophilized human dura. J Urol. 1985;133(3):452-455. 7. Homan WP, Cheigh JS, Kim SJ, et al. Renal allograft fracture: clinicopathological study of 21 cases. Ann Surg. 1977; 1 86(6):700-703. 8. Anderson B, Sampson C, Callender CO. Spontaneous renal allograft rupture without rejection: a case report. J Urol. 1976;1 1 5:745-746. 9. Schwartz A, Podzimek A, Valenta J, et al. Spontaneous renal allograft rupture clinical and pathological patterns. Int Urol Nephrol. 1986;18(1):105-1 10. 10. Ngheim DD, Corry RJ. Long-term result of conservative surgical management of the ruptured renal transplant. Am Surg. 1 983;49(7):392-395. 11. Goldman M, De Pauw L, Kinnaert P, et al. Renal allograft rupture: possible causes and results of surgical conservative management. Transplantation. 1981;32(2):153-156. 12. Yadav RVS, Sinha R, Chugh KS, et al. Renal allograft rupture and its management. Urol Int. 1985;40:230-232.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
Spontaneous renal allograft rupture, an unusual complication of renal transplantation, occurred in a 35-year-old woman 10 days after transplantation. Unusual localized pain and tenderness at allograft site, oliguria, and hypotension, a triad frequently seen in renal allograft rupture, were present. Management by transplant nephrectomy was inevitable because of the patient's downhill course. Histopathologic findings diagnostic of acute allograft rejection support current thinking that spontaneous rupture may be the final outcome, although unusual, of renal allograft rejection. Key words * acute allograft rupture * acute rejection* spontaneous graft rupture
Non-traumatic spontaneous rupture of the renal allograft is an infrequent and unusual complication of human renal transplantation. Occurring in 0.8% to 9.6% of all renal transplants," 2 usually within the first 2 weeks of transplantation,"3'4 its etio-pathogenesis has remained obscure. To date, however, the most frequently identifiable factor in up to 60% of the patients has been acute From the Department of Surgery and Pathology, Howard University Hospital, Washington, DC. Requests for reprints should be addressed to Dr Clive 0. Callender, Howard University Hospital, 2041 Georgia Ave, NW, Washington, DC 20060. JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
allograft rejection.4-7 In addition, most ruptures reported have occurred in cadaveric renal allografts.13,4,6,8,9 Debate on the management of such allograft rupture has focused on allograft salvage versus transplant nephrectomy.12'5'6'8 It appears that the recent trend is toward performing transplant nephrectomy if excessive hemorrhage, allograft necrosis, and rupture compromise patient survival.1 4'10 If the patient's condition is stable, and the allograft rupture site is surgically manageable, allograft salvage should be attempted." 2'68' 10-12
CASE REPORT An otherwise healthy 33-year-old black woman with hypertension and end-stage renal disease, (hemodialysis-dependent), underwent an uneventful cadaveric renal transplant on April 18, 1987. Postoperatively, immunosuppression was with Antilymphocyte Globulin (ALG), Imuran, and Solumedrol. Development of thrombocytopenia and vaginal bleeding led to the discontinuation of ALG and Imuran, and subsequent replacement with cyclosporin (CSA) from the 3rd postoperative day (POD). On the 5th POD, the patient developed a vague abdominal pain and a temperature of up to 101.4°E Physical examination and septic workup were unremarkable. On POD 8, the patient complained of dizziness and headache. She was noted to have herpetiform eruptions in the anogluteal groove, and moderate hypertension of 170/120 mm Hg. She was seropositive (high titer) for herpes virus and cytomegalovirus (CMV). 171
RENAL ALLOGRAFT RUPTURE
14
-
1210 86 p
< z U.
Transplant Nephrectomy
4~~~~~~~
2_ 0
2-
ES
L
co
Figure IA. Renal allograft immediately after surgical excision with localized perirenal hemorrhage.
I_~~~~A
80
5
-
60 40 -
E
L D0
0
E 500 20 _
4000
co
50 -8
t 0
loe qudrn panadtnens,hptnIo(B
100_x
2000-
4 000-
Fiu eCu42. Dal-iceiclcags E 00 2-
8
1
Figure 1 B. Transplant nephrectomy with mottled capsular surface and localized blood clot at the superior pole.
Figure IC. Cut surface of allograft, reflecting cortical necrosis and medullary congestion. The patient was started on acyclovir cream 5% and captopril. On POD 9, she suddenly developed right
80/60), and oliguria. Renogram showed no flow in the transplant kidney and no excretion into the bladder. Consequently, the patient underwent emergency exploratory laparatomy. Intraoperatively, over 0.2 L of blood clots were evacuated. The allograft (Figures lA-C) was edematous, swollen, and congested. The surface was mottled. A jagged rupture located in the superior pole was present. The perinephric area contained a large amount of blood clot. A transplant nephrectomy was performed. Postoperatively, the patient had an uncomplicated hospital course. She was restarted on hemodialysis and discharged home on June 5, 1987.
PATHOLOGICAL STUDIES Figure 2 shows a composite chart illustrating the
172
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
RENAL ALLOGRAFT RUPTURE
daily changes seen in the patient's blood urea nitrogen (BUN), creatinine clearance, plasma creatinine level, urinary output, and fraction of excretion of sodium. All indicate the progressive loss of function in the allograft. The renal allograft measured 15.5 cm X 9 cm X 6 cm and weighed 434 gm. A 4-cm X 3-cm capsular hemorrhage was present in the superior pole and extended well into the cortex. The cut surface was edematous. The medullary region appeared congested and the cortex mottled, with pale areas of necrosis. Extensive cortical necrosis with focal superior pole hemorrhagic necrosis and capsular hemorrhage were seen. Focal changes of vascular rejection were present, as well as moderately severe acute tubulointerstitial cellular rejection (Figures 3A-C). Ultrastructural studies of two glomeruli showed acute ischemic necrosis consistent with cortical necrosis. No deposits or basement membrane changes were identified. Many mononuclear cells were present in the interstitium. No evidence of significant immunoglobulin, complement or fibriogen deposition in the allograft was seen with immunofluorescent studies.
'1 Figure 3A. Interstitial hemorrhage extending into pericapsular tissue.
V I
DISCUSSION Reports of the incidence of nontraumatic, spontaneous renal allograft rupture have ranged from 0.8% to 9.61%1,2,9 and might be higher, as some ruptures might go undetected.3 Most ruptures (Figures lA-C) are seen in cadaveric renal allografts and tend to occur within the first 2 weeks.1'3'4'6'9 In a recent literature review of 149 renal allograft ruptures, 125 of the grafts (83.9%) were from cadavers.3 Mode of preservation, storage time, and the composition of the cold perfusate did not correlate with the tendency to rupture.4 It seems, however, that acute rejection and swelling may lead to rupture.4-7 Clinical presentations of graft rupture include localized pain and tenderness at the transplant site, oliguria, and hypotension. These findings, as well as the biochemical derangements (Figure 1) noted in our
patient, prompted surgical exploration. Interestingly, other workers consider that the combination of pain, hypotension, and oliguria occur sufficiently in renal allograft rupture to constitute a diagnostic triad.3'4 In the management of renal allograft rupture, serious consideration is given to the clinical condition of the patient and the findings at operation. Transplant nephrectomy is indicated when the combination of rupture, with its attendant hemodynamic derangements, compromises the patient.",4"10 In the stable patient with JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
Figure 3B. Vascular (humoral) rejection with surrounding acute interstitial cellular rejection.
Figure 3C. Unremarkable glomerulus with ad. jacent acute interstitial cellular rejection. 173
RENAL ALLOGRAFT RUPTURE
a less compromised allograft, a salvage operation should be attempted.1'2'6'8"0-12 Literature Cited 1. Susan LP, Braun WE, Banowsky LH, Straffon RA, Valenzuela R. Rupture human renal allograft. Urology. 1978;1 1(1):53-57. 2. Dryburgh P, Porter KA, From RAF, et al. Should the ruptured renal allograft be removed? Arch Surg. 1979;1 14:850852. 3. Thukral R, Mir AR, Jacobson MP. Renal allograft rupture: a report of three cases and review of the literature. Am J Nephrol. 1982;2:15-27. 4. Lord RSA, Effeney D, Hayes JM, Tracy GD. Renal allograft rupture. Ann Surg. 1973;177(3):268-273. 5. Ajao OG, Callender CO, Stevens J, Sampson C. Spontaneous renal allograft rupture four years after transplantation. Urol Int. 1984;39:49-51. 6. Serrallach N, Gutierrez R, Serrate R, et al. Renal allograft rupture: surgical treatment by renal corsetage with
174
lyophilized human dura. J Urol. 1985;133(3):452-455. 7. Homan WP, Cheigh JS, Kim SJ, et al. Renal allograft fracture: clinicopathological study of 21 cases. Ann Surg. 1977; 1 86(6):700-703. 8. Anderson B, Sampson C, Callender CO. Spontaneous renal allograft rupture without rejection: a case report. J Urol. 1976;1 1 5:745-746. 9. Schwartz A, Podzimek A, Valenta J, et al. Spontaneous renal allograft rupture clinical and pathological patterns. Int Urol Nephrol. 1986;18(1):105-1 10. 10. Ngheim DD, Corry RJ. Long-term result of conservative surgical management of the ruptured renal transplant. Am Surg. 1 983;49(7):392-395. 11. Goldman M, De Pauw L, Kinnaert P, et al. Renal allograft rupture: possible causes and results of surgical conservative management. Transplantation. 1981;32(2):153-156. 12. Yadav RVS, Sinha R, Chugh KS, et al. Renal allograft rupture and its management. Urol Int. 1985;40:230-232.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 83, NO. 2
