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Infectious complications in ABO-incompatible living donor kidney transplantation: a single center experience
Infectious Complications in ABO-Incompatible Living Donor Kidney Transplantation: A Single Center Experience K. Tanabe, K. Takahashi, T. Tokumoto N. Ishikawa, T. Oshima, A. Kanematsu, R. Kitani, S. Fuchinoue, T. Yagisawa, K. Ota, S. Teraoka, T. Agishi, and H. Toma
W
E performed ABO-incompatible living kidney transplantations in order to expand indications for kidney transplantation.1–3 ABO-incompatible renal transplant recipients usually have a relatively heavy immunosuppression compared to ABO-compatible patients. Therefore, it was assumed that they may have many more infectious complications than ABO-compatible patients. Infection remains the leading cause of morbidity and mortality throughout the posttransplant course. Prevention and treatment of infectious disease complications of transplantation are of major importance, and the requisite immunosuppressive therapy must be judiciously administered.4,5 In this study, we reviewed infectious complications in ABO-incompatible kidney transplant recipients.
MATERIALS AND METHODS Patients Sixty-seven patients with end-stage renal failure underwent ABOincompatible living kidney transplantation at our institute between January 1989 and December 1995. The mean age was 34.9 years (range, 8 to 58 years), with 38 males and 29 females. Incompatibility in ABO-blood group antigens was as follows: A1 3 O, 23 patients; B 3 O, 19 patients; A1B 3 A1, 7 patients; B 3 A1, 8 patients; A1 3 B, 4 patients; A1B 3 B, 4 patients; A1B 3 O, 2 patients. The number of HLA-A, -B, and -DR mismatches were 1.6 6 1.1 and 0.76 6 0.6, respectively (Table 1). Background data of the ABO-compatible kidney transplant recipients are shown in Table 1.
Removal of Serum anti-A and/or anti-B Antibodies To remove anti-A and/or anti-B antibodies,2,3 recipients received one or two sessions of double-filtration plasmapheresis (DFPP) and three or four sessions of immunoadsorption, prior to transplantation, until their anti-A immunoglobulin G (IgG)/IgM titers and/or anti-B IgG/IgM titers decreased to the level of 1:16 or below. DFPP was performed 7 days before surgery, using the following plasma separators: OP-05H (Asahi Medical Co Ltd, Tokyo, Japan) and Evaflux 2A (Kuraray Co Ltd, Osaka, Japan). Immunoadsorption was performed using a Biosynsorb A and/or B immunoadsorption column (Chemobiomed Ltd, Edmonton, Alberta, Canada). Patients showing anti-A and/or anti-B antibody titers exceeding 1:64 after surgery underwent immunoadsorption or DFPP. IgM anti-A and anti-B levels were determined using the
Table 1. Patients’ Characteristics No. of patients Age (years) Sex (M/F) Donor source Parents Siblings Spouse Incompatibility A1 3 O B3O A1B 3 A1 B 3 A1 A1 3 B A1B 3 B A1B 3 O HLA-A, -B mismatch HLA-DR mismatch
n 5 67 34.9 (8 –58) 38/29 43 10 14 23 patients 19 patients 7 patients 8 patients 4 patients 4 patients 2 patients 1.6 6 1.1 0.76 6 0.6
saline and/or Bromerin agglutination technique, as specified in the protocol, and Indirect Coomb’s test was used to measure IgG titers.
Immunosuppressive Regimen In the induction phase, methylprednisolone (MP), cyclosporine (CyA), azathioprine (AZ), antilymphocyte globulin (ALG), and deoxyspergualin (DSG) were used.2,3 MP administration was started on the day of transplantation, at a dose of 125 to 500 mg/d, and reduced to a maintenance dose of 8 mg/d by the fourth month. Oral administration of CyA, 8 to 10 mg/kg per day, was started 2 days before transplantation, and drip infusion of CyA, 3 mg/kg, was administered on the day of transplantation. CyA administration was then adjusted to maintain a CyA trough level in whole blood of between 200 and 300 ng/mL for 1 or 2 months after transplantation, and between 80 and 100 ng/mL thereafter. AZ administration, 2 mg/kg per day, was started 2 days before transplantation, and continued for 1 week, after which it was reduced to 1 mg/kg per day and adjusted according to the peripheral white blood cell count. From Department of Urology, Kidney Center, Tokyo Women’s Medical College, Tokyo; Department of Urology, Niigata University, Niigata; and Department of Surgery (III), Kidney Center, Tokyo Women’s Medical College, Tokyo, Japan. Address reprint requests to Kazunari Tanabe, MD, Department of Urology, Kidney Center, Tokyo Women’s Medical College, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162 Japan.
0041-1345/98/$19.00 PII S0041-1345(98)00965-8
© 1998 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
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Transplantation Proceedings, 30, 3130–3132 (1998)
COMPLICATIONS IN KIDNEY TRANSPLANT
3131 Table 3. CMV Infection
Table 2. Infectious Complications Infection
No. of Patients
CMV disease UTI Herpes zoster infection Acute hemorrhagic cystitis
10 2 2 3
ALG, 20 to 30 mg/kg per day, was begun 2 days before transplantation and continued for 14 days in general. ALG was discontinued when the platelet count decreased to 50,000/mm3 or less. DSG, 5 mg/kg per day, was administered for 5 days starting from the day of transplantation. Local irradiation of the graft was performed at a dose of 150 rad on the first, third, and fifth days after transplantation. Splenectomy was done at the time of kidney transplantation in all cases.2,3 For the treatment of acute rejection episodes, a basic dose of 500 mg MP was administered for 2 days. When rejection was not improved, muromonab CD3 (OKT3) was administered at a dose of 5 mg/d for 10 days or DSG (5 mg/kg per day) for 5 days.
Monitoring of Cytomegalovirus (CMV) Infections Antigenemia Assay of CMV Infection. The immunocytochemical detection of the pp65 antigen was performed, as previously described. Briefly, 1.5 3 105 leukocytes were centrifuged onto glass slides, fixed in acetone/methanol (1:1) for 10 minutes at 4°C, and then incubated with a mixture of the mouse monoclonal antibodies, C10 and C11 (Clonab CMV, Biotest, Germany), directed against the lower matrix protein, pp65. After reaction with alkalinephosphatase-labeled goat anti-mouse immunoglobulin antiserum, the slides were read microscopically, and pp65-positive cells were counted.
Prophylactic Administration of Trimethoprim-Sulfamethoxazole Trimethoprim-sulfamethoxazole (440 mg/80 mg) was administered, three times a day, every other day to prevent both urinary tract infection (UTI) and Pneumocystis carinii infection up to 4 months after renal transplantation.
RESULTS Patient and Graft Survival
Patient survival was 91% at 1 year and 89% at 6 years. Graft survival was 83% at 1 year and 78% at 6 years. Both patient and graft survival rates were not significantly different from those of ABO-compatible patients.3 Infectious Complications
Of 67 patients 17 recipients (25%) had 19 infectious complications after surgery (Table 2). Cytomegalovirus (CMV) infection was the most frequent infection and occurred in 10 patients (15%). No patients had a serious tissue-invasive CMV disease. Three patients had very mild tissue-invasive disease, including hepatitis, pneumonitis, and retinitis (Table 3). All CMV infections were successfully treated by ganciclovir. Nine of 10 patients with CMV disease were treated with both MP pulse and OKT3 monoclonal antibody (MAb) before onset of CMV disease.
Patients
Duration of Tx and CMV Infection (days)
Symptoms
ALG
OKT3
MP Pulse
1 2 3 4* 5† 6 7 8‡ 9 10
30 40 50 40 50 30 40 30 20 80
Fever Fever Fever Fever Fever Fever Fever Fever Fever Fever
1 1 1 1 1 1 1 1 1 1
1 1 1 1 1 1 1 2 1 1
1 1 1 1 1 1 1 1 1 1
*CMV retinitis occurred at 6 months after transplantation. † CMV pneumonitis, which was very mild, occurred. ‡ CMV hepatitis, which was very mild, occurred.
Herpes zoster infection occurred in two patients and was successfully treated by acyclovir. Three patients had adenovirus-induced hemorrhagic cystitis. Pyelonephritis occurred in two patients. There was no fatal infection after ABOincompatible renal transplantation. DISCUSSION
There are two major barriers to successful transplantation, namely infection and rejection. Any intervention that decreases the risk of rejection and permits the use of lessintensive immunosuppressive therapy will result in a decreased risk of life-threatening infection; any intervention that decreases the risk of infection and permits the safe use of more intensive immunosuppressive therapy will decrease the risk of allograft loss from rejection.5 Although immunosuppression in ABO-incompatible renal transplantation is relatively heavier than that of ABOcompatible cases, our overall incidence of infectious complications seemed to be relatively low (25%) compared to those of other reports.5 Recent progress in the control of infectious complications have helped to reduce these complications. Viral infections are the single greatest cause of infectious disease morbidity and mortality in transplant recipients.6 The most frequent virus infection in this series was CMV infection, which occurred in 10 recipients (15%). All CMV infections were non-tissue-invasive disease or very mild tissue-invasive disease, which occurred within 90 days after surgery, and were successfully treated by ganciclovir. Nine of 10 patients with CMV disease received MP pulse therapy and OKT3 treatment. As mentioned previously,4 antilymphocyte antibody seemed to be a risk factor of CMV disease. Active CMV infection is an important cause of morbidity and mortality in renal transplant recipients and has a negative influence on graft survival. Because the intensity of immunosuppression influences the incidence and severity of CMV infection, infections usually occur during the first 4 months following transplantation and are exceedingly rare after 4 months. Therefore, intense moni-
3132
toring of infectious complications within 4 months after renal transplantation is very important to reduce morbidity and mortality. The most severe CMV infectious complication after renal transplantation is interstitial pneumonitis, which frequently has a fatal outcome. However, such a severe tissue-invasive disease does not occur suddenly without other symptoms. It is well known that fever almost always precedes a severe tissue-invasive disease, such as CMV pneumonitis. Therefore, early diagnosis of CMV infection/disease and a correct differentiation from allograft rejection remains of great importance, especially since the antiviral drug, ganciclovir, is now available. The correct diagnosis of CMV infection should be done no later than at the onset of fever, which is a very early symptom of CMV infection. Eventually, early treatment of CMV infection should significantly reduce the risk of severe CMV disease. Thus, it is reported that new and rapid diagnostic methods, such as the CMV antigenemia assay, which detects antigen in peripheral blood leukocytes, are very important for early diagnosis and successful treatment.4 Close monitoring of CMV infection greatly contributed to reducing CMV infection and eliminating fatal CMV infection even in ABO-incompatible renal transplantation. We did not encounter any serious CMV complications as early diagnosis of CMV infection can be done by CMV antigenemia assay and since ganciclovir became available.4 Two cases of herpes-zoster infection occurred in this series; however, these infections were successfully treated by acyclovir as reported by other authors.5 Adenovirusinduced hemorrhagic cystitis is known to be a self-limiting disease, and all cases in this series spontaneously subsided. Because those viral infections are very popular and usually not serious, we do not believe we need to pay special attention for them. The most common form of bacterial infection in renal transplant recipients is urinary tract infection (UTI), which is reported to occur in 35% to 80% of renal transplant recipients.5 UTI, which occurred more than 4 months’
TANABE, TAKAHASHI, TOKUMOTO ET AL
posttransplant, can be successfully managed with conventional antibiotics. However, UTI presenting in the first few months after transplantation frequently is associated with overt pyelonephritis and bacteremia. A regimen of low-dose trimethoprim-sulfamethoxazole for 16 weeks after transplantation, which we employed these 8 years, virtually eliminated urosepsis. The incidence of UTI in this series was only 3%, which was very low compared to other reports.5 Obviously a prophylactic administration of lowdose trimethoprim-sulfamethoxazole contributes to this low incidence of UTI. It is known that a low-dose trimethoprimsulfamethoxazole regimen has the added benefit of providing effective prophylaxis against Pneumocystis carinii, Nocardia asteroides, and Listeria monocytogenes as well.5 No Pneumocystis carinii pneumonitis was encountered in our institution since we employed a regimen of low-dose trimethoprim-sulfamethoxazole administration. CONCLUSIONS
A relatively higher incidence of infectious complications was noted after ABO-incompatible living kidney transplantation compared to compatible patients; however, there was no fatal infection. ABO-incompatible living kidney transplantation offers an excellent outcome without any serious infectious complications. REFERENCES 1. Alexandre GPJ, Squifflet JP, DeBruyere M, et al: Transplant Proc 17:138, 1985 2. Takahashi K, Tanabe K, Ooba S, et al: Transplant Proc 23:1078, 1991 3. Tanabe K, Takahashi K, Sonda, et al: Transplantation 65:224, 1998 4. Tanabe K, Tokumoto T, Ishikawa N, et al: Transplantation (in press) 5. Rubin RH: Kidney Int 44:221, 1993 6. Rubin RH, Wolfson JS, Cosimi AB, et al: Am J Med 70:405, 1981
W
E performed ABO-incompatible living kidney transplantations in order to expand indications for kidney transplantation.1–3 ABO-incompatible renal transplant recipients usually have a relatively heavy immunosuppression compared to ABO-compatible patients. Therefore, it was assumed that they may have many more infectious complications than ABO-compatible patients. Infection remains the leading cause of morbidity and mortality throughout the posttransplant course. Prevention and treatment of infectious disease complications of transplantation are of major importance, and the requisite immunosuppressive therapy must be judiciously administered.4,5 In this study, we reviewed infectious complications in ABO-incompatible kidney transplant recipients.
MATERIALS AND METHODS Patients Sixty-seven patients with end-stage renal failure underwent ABOincompatible living kidney transplantation at our institute between January 1989 and December 1995. The mean age was 34.9 years (range, 8 to 58 years), with 38 males and 29 females. Incompatibility in ABO-blood group antigens was as follows: A1 3 O, 23 patients; B 3 O, 19 patients; A1B 3 A1, 7 patients; B 3 A1, 8 patients; A1 3 B, 4 patients; A1B 3 B, 4 patients; A1B 3 O, 2 patients. The number of HLA-A, -B, and -DR mismatches were 1.6 6 1.1 and 0.76 6 0.6, respectively (Table 1). Background data of the ABO-compatible kidney transplant recipients are shown in Table 1.
Removal of Serum anti-A and/or anti-B Antibodies To remove anti-A and/or anti-B antibodies,2,3 recipients received one or two sessions of double-filtration plasmapheresis (DFPP) and three or four sessions of immunoadsorption, prior to transplantation, until their anti-A immunoglobulin G (IgG)/IgM titers and/or anti-B IgG/IgM titers decreased to the level of 1:16 or below. DFPP was performed 7 days before surgery, using the following plasma separators: OP-05H (Asahi Medical Co Ltd, Tokyo, Japan) and Evaflux 2A (Kuraray Co Ltd, Osaka, Japan). Immunoadsorption was performed using a Biosynsorb A and/or B immunoadsorption column (Chemobiomed Ltd, Edmonton, Alberta, Canada). Patients showing anti-A and/or anti-B antibody titers exceeding 1:64 after surgery underwent immunoadsorption or DFPP. IgM anti-A and anti-B levels were determined using the
Table 1. Patients’ Characteristics No. of patients Age (years) Sex (M/F) Donor source Parents Siblings Spouse Incompatibility A1 3 O B3O A1B 3 A1 B 3 A1 A1 3 B A1B 3 B A1B 3 O HLA-A, -B mismatch HLA-DR mismatch
n 5 67 34.9 (8 –58) 38/29 43 10 14 23 patients 19 patients 7 patients 8 patients 4 patients 4 patients 2 patients 1.6 6 1.1 0.76 6 0.6
saline and/or Bromerin agglutination technique, as specified in the protocol, and Indirect Coomb’s test was used to measure IgG titers.
Immunosuppressive Regimen In the induction phase, methylprednisolone (MP), cyclosporine (CyA), azathioprine (AZ), antilymphocyte globulin (ALG), and deoxyspergualin (DSG) were used.2,3 MP administration was started on the day of transplantation, at a dose of 125 to 500 mg/d, and reduced to a maintenance dose of 8 mg/d by the fourth month. Oral administration of CyA, 8 to 10 mg/kg per day, was started 2 days before transplantation, and drip infusion of CyA, 3 mg/kg, was administered on the day of transplantation. CyA administration was then adjusted to maintain a CyA trough level in whole blood of between 200 and 300 ng/mL for 1 or 2 months after transplantation, and between 80 and 100 ng/mL thereafter. AZ administration, 2 mg/kg per day, was started 2 days before transplantation, and continued for 1 week, after which it was reduced to 1 mg/kg per day and adjusted according to the peripheral white blood cell count. From Department of Urology, Kidney Center, Tokyo Women’s Medical College, Tokyo; Department of Urology, Niigata University, Niigata; and Department of Surgery (III), Kidney Center, Tokyo Women’s Medical College, Tokyo, Japan. Address reprint requests to Kazunari Tanabe, MD, Department of Urology, Kidney Center, Tokyo Women’s Medical College, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162 Japan.
0041-1345/98/$19.00 PII S0041-1345(98)00965-8
© 1998 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
3130
Transplantation Proceedings, 30, 3130–3132 (1998)
COMPLICATIONS IN KIDNEY TRANSPLANT
3131 Table 3. CMV Infection
Table 2. Infectious Complications Infection
No. of Patients
CMV disease UTI Herpes zoster infection Acute hemorrhagic cystitis
10 2 2 3
ALG, 20 to 30 mg/kg per day, was begun 2 days before transplantation and continued for 14 days in general. ALG was discontinued when the platelet count decreased to 50,000/mm3 or less. DSG, 5 mg/kg per day, was administered for 5 days starting from the day of transplantation. Local irradiation of the graft was performed at a dose of 150 rad on the first, third, and fifth days after transplantation. Splenectomy was done at the time of kidney transplantation in all cases.2,3 For the treatment of acute rejection episodes, a basic dose of 500 mg MP was administered for 2 days. When rejection was not improved, muromonab CD3 (OKT3) was administered at a dose of 5 mg/d for 10 days or DSG (5 mg/kg per day) for 5 days.
Monitoring of Cytomegalovirus (CMV) Infections Antigenemia Assay of CMV Infection. The immunocytochemical detection of the pp65 antigen was performed, as previously described. Briefly, 1.5 3 105 leukocytes were centrifuged onto glass slides, fixed in acetone/methanol (1:1) for 10 minutes at 4°C, and then incubated with a mixture of the mouse monoclonal antibodies, C10 and C11 (Clonab CMV, Biotest, Germany), directed against the lower matrix protein, pp65. After reaction with alkalinephosphatase-labeled goat anti-mouse immunoglobulin antiserum, the slides were read microscopically, and pp65-positive cells were counted.
Prophylactic Administration of Trimethoprim-Sulfamethoxazole Trimethoprim-sulfamethoxazole (440 mg/80 mg) was administered, three times a day, every other day to prevent both urinary tract infection (UTI) and Pneumocystis carinii infection up to 4 months after renal transplantation.
RESULTS Patient and Graft Survival
Patient survival was 91% at 1 year and 89% at 6 years. Graft survival was 83% at 1 year and 78% at 6 years. Both patient and graft survival rates were not significantly different from those of ABO-compatible patients.3 Infectious Complications
Of 67 patients 17 recipients (25%) had 19 infectious complications after surgery (Table 2). Cytomegalovirus (CMV) infection was the most frequent infection and occurred in 10 patients (15%). No patients had a serious tissue-invasive CMV disease. Three patients had very mild tissue-invasive disease, including hepatitis, pneumonitis, and retinitis (Table 3). All CMV infections were successfully treated by ganciclovir. Nine of 10 patients with CMV disease were treated with both MP pulse and OKT3 monoclonal antibody (MAb) before onset of CMV disease.
Patients
Duration of Tx and CMV Infection (days)
Symptoms
ALG
OKT3
MP Pulse
1 2 3 4* 5† 6 7 8‡ 9 10
30 40 50 40 50 30 40 30 20 80
Fever Fever Fever Fever Fever Fever Fever Fever Fever Fever
1 1 1 1 1 1 1 1 1 1
1 1 1 1 1 1 1 2 1 1
1 1 1 1 1 1 1 1 1 1
*CMV retinitis occurred at 6 months after transplantation. † CMV pneumonitis, which was very mild, occurred. ‡ CMV hepatitis, which was very mild, occurred.
Herpes zoster infection occurred in two patients and was successfully treated by acyclovir. Three patients had adenovirus-induced hemorrhagic cystitis. Pyelonephritis occurred in two patients. There was no fatal infection after ABOincompatible renal transplantation. DISCUSSION
There are two major barriers to successful transplantation, namely infection and rejection. Any intervention that decreases the risk of rejection and permits the use of lessintensive immunosuppressive therapy will result in a decreased risk of life-threatening infection; any intervention that decreases the risk of infection and permits the safe use of more intensive immunosuppressive therapy will decrease the risk of allograft loss from rejection.5 Although immunosuppression in ABO-incompatible renal transplantation is relatively heavier than that of ABOcompatible cases, our overall incidence of infectious complications seemed to be relatively low (25%) compared to those of other reports.5 Recent progress in the control of infectious complications have helped to reduce these complications. Viral infections are the single greatest cause of infectious disease morbidity and mortality in transplant recipients.6 The most frequent virus infection in this series was CMV infection, which occurred in 10 recipients (15%). All CMV infections were non-tissue-invasive disease or very mild tissue-invasive disease, which occurred within 90 days after surgery, and were successfully treated by ganciclovir. Nine of 10 patients with CMV disease received MP pulse therapy and OKT3 treatment. As mentioned previously,4 antilymphocyte antibody seemed to be a risk factor of CMV disease. Active CMV infection is an important cause of morbidity and mortality in renal transplant recipients and has a negative influence on graft survival. Because the intensity of immunosuppression influences the incidence and severity of CMV infection, infections usually occur during the first 4 months following transplantation and are exceedingly rare after 4 months. Therefore, intense moni-
3132
toring of infectious complications within 4 months after renal transplantation is very important to reduce morbidity and mortality. The most severe CMV infectious complication after renal transplantation is interstitial pneumonitis, which frequently has a fatal outcome. However, such a severe tissue-invasive disease does not occur suddenly without other symptoms. It is well known that fever almost always precedes a severe tissue-invasive disease, such as CMV pneumonitis. Therefore, early diagnosis of CMV infection/disease and a correct differentiation from allograft rejection remains of great importance, especially since the antiviral drug, ganciclovir, is now available. The correct diagnosis of CMV infection should be done no later than at the onset of fever, which is a very early symptom of CMV infection. Eventually, early treatment of CMV infection should significantly reduce the risk of severe CMV disease. Thus, it is reported that new and rapid diagnostic methods, such as the CMV antigenemia assay, which detects antigen in peripheral blood leukocytes, are very important for early diagnosis and successful treatment.4 Close monitoring of CMV infection greatly contributed to reducing CMV infection and eliminating fatal CMV infection even in ABO-incompatible renal transplantation. We did not encounter any serious CMV complications as early diagnosis of CMV infection can be done by CMV antigenemia assay and since ganciclovir became available.4 Two cases of herpes-zoster infection occurred in this series; however, these infections were successfully treated by acyclovir as reported by other authors.5 Adenovirusinduced hemorrhagic cystitis is known to be a self-limiting disease, and all cases in this series spontaneously subsided. Because those viral infections are very popular and usually not serious, we do not believe we need to pay special attention for them. The most common form of bacterial infection in renal transplant recipients is urinary tract infection (UTI), which is reported to occur in 35% to 80% of renal transplant recipients.5 UTI, which occurred more than 4 months’
TANABE, TAKAHASHI, TOKUMOTO ET AL
posttransplant, can be successfully managed with conventional antibiotics. However, UTI presenting in the first few months after transplantation frequently is associated with overt pyelonephritis and bacteremia. A regimen of low-dose trimethoprim-sulfamethoxazole for 16 weeks after transplantation, which we employed these 8 years, virtually eliminated urosepsis. The incidence of UTI in this series was only 3%, which was very low compared to other reports.5 Obviously a prophylactic administration of lowdose trimethoprim-sulfamethoxazole contributes to this low incidence of UTI. It is known that a low-dose trimethoprimsulfamethoxazole regimen has the added benefit of providing effective prophylaxis against Pneumocystis carinii, Nocardia asteroides, and Listeria monocytogenes as well.5 No Pneumocystis carinii pneumonitis was encountered in our institution since we employed a regimen of low-dose trimethoprim-sulfamethoxazole administration. CONCLUSIONS
A relatively higher incidence of infectious complications was noted after ABO-incompatible living kidney transplantation compared to compatible patients; however, there was no fatal infection. ABO-incompatible living kidney transplantation offers an excellent outcome without any serious infectious complications. REFERENCES 1. Alexandre GPJ, Squifflet JP, DeBruyere M, et al: Transplant Proc 17:138, 1985 2. Takahashi K, Tanabe K, Ooba S, et al: Transplant Proc 23:1078, 1991 3. Tanabe K, Takahashi K, Sonda, et al: Transplantation 65:224, 1998 4. Tanabe K, Tokumoto T, Ishikawa N, et al: Transplantation (in press) 5. Rubin RH: Kidney Int 44:221, 1993 6. Rubin RH, Wolfson JS, Cosimi AB, et al: Am J Med 70:405, 1981