| Abstract|| |
Between September 1988 and end of 1995, 170 renal transplantations were performed at the King Fahad National Guard Hospital, Riyadh. There were 102 cadaver donor (CAD) and 68 living related donor (LRD) transplants. All patients received triple drug immunosuppression. Patients with delayed graft function received anti-thymocyte globulin instead of cyclosporin until recovery of graft function. The 1,3 and 5 year graft survival was as follows: all transplants 83.5%, 77.6%, 74.7% respectively; LRD transplants, 89.7%, 85.2%, 80.9% respectively; CAD transplants, 81.0%, 72.5%, 70.5% respectively. The commonest cause of graft loss was chronic rejection. The 1,3 and 5 year patient survival was as follows: all transplants, 97.0%, 94.7%, 93.5% respectively; LRD transplants, 98.5%, 97.0%, 95.5% respectively; CAD transplants, 96.0%, 93.0%, 92.0% respectively. The overall results in our center are comparable to those published from other centers in Saudi Arabia and abroad.
Keywords: Renal transplantation, Living donor, Cadaveric donor, King Fahad National Guard.
|How to cite this article:|
Huraib S, Al Khudair W, Saleem H, Quadri K, Romeh SA, Chaballout A, Nezamuddin N, Saeed R, Duarte R. Renal Transplant Experience at King Fahad National Guard Hospital. Saudi J Kidney Dis Transpl 1996;7:157-63
|How to cite this URL:|
Huraib S, Al Khudair W, Saleem H, Quadri K, Romeh SA, Chaballout A, Nezamuddin N, Saeed R, Duarte R. Renal Transplant Experience at King Fahad National Guard Hospital. Saudi J Kidney Dis Transpl [serial online] 1996 [cited 2020 Oct 23];7:157-63. Available from: https://www.sjkdt.org/text.asp?1996/7/2/157/39519
| Introduction|| |
Kidney transplantation in the Kingdom of Saudi Arabia began in 1979 when a living related transplantation was performed successfully at the Riyadh Armed Forces Hospital  . The approval of Islamic scholars of the concepts of brain-death and organ donation, the establishment of the National Kidney Foundation and the support of the Saudi Government had great impact on the development and advancement of renal transplantation in Saudi Arabia and currently, there are 11 active renal transplants enters in the Kingdom. Renal transplantation started at the King Fahad National Guard Hospital (KFNGH) in September, the first livingrelated donor (LRD) transplantation was performed, followed one month later by the first cadaveric donor (CAD) renal transplantation. The renal transplant patients in our program were chosen from the hemodialysis unit at KFNGH which has more than 90 patients on regular dialysis as well as about 170 patients on dialysis at 11 affiliated hospitals attached to our program. We herewith present the experience of renal transplantation at KFNGH from the beginning of the program up to the end of 1995.
| Materials and Methods|| |
From September 1988 up to the end of 1995, 170 renal transplants were performed at our center. There were 102 CAD and 68 LRD transplants including two from spouse donors. Four patients had pre-emptive transplantation. The study patients constituted a consecutive series and no patient was excluded. The demographic data of the study patients are given in [Table - 1]. Twenty patients had transplantation twice and two patients had transplantation three times. Since the beginning of the program, nine patients with positive hepatitis B surface antigen (HBsAg) have been transplanted. In addition, 18 patients with positive antihepatitis C virus (HCV) antibodies received transplantation, but only if they had normal liver biopsies or, if they had abnormal liver biopsy after treatment with interferon.
All CAD kidneys were harvested within Saudi Arabia and Euro-collins solution was used as the preservative in all cases. The mean cold-ischemia time was 17.2 hours with a range of 8-29 hours. The death of a patient with functioning graft was considered as a failed graft and all deaths occurring within six months of graft loss were considered as death due to transplantation. Primary non-function was defined as the need for dialysis in the first week posttransplantation, or failure of serum creatinine to drop by greater than 20% in the first 48 hours post-transplantation.
| Immunosuppression|| |
Two immunosuppressive protocols have been used. The first protocol was used from the beginning of the program up to August 1994, when a new protocol was introduced. The old protocol consisted of triple drug therapy in the form of cyclosporin, azathioprine and prednisone. For the CAD group, cyclosporin, in a dose of 8 mg/kg orally, was started after good renal function was achieved. In patients with delayed graft function, anti-thymocyte globulin (ATG) or anti-lymphocyte globulin (ALG) was given for a maximum of two weeks or until plasma creatinine reached approximately 300 uol/1. Prednisone was started at a dose of 100 mg/ day, tapered by 10 mg daily until reaching 20 mg per day. Azathioprine was given in a dose 1-2 mg/kg intravenously on the first post-op day, and thereafter continued orally in a dose of 1.5 mg/kg, the dose adjusted according to the white cell count. Donor specific blood transfusions were administered to the first 30 patients transplanted; this was subsequently discontinued.
The new protocol being used currently, differs from the old in the use of intravenous infusion of cyclosporin at a dose of 3 mg/kg for five days starting immediately post-transplantation. The use of cyclosporin is decided, by the surgeon at the time of transplantation based on the status of the donor at organ harvesting and the cold ischemia time. The other option is to use ATG in a dose of 10 mg/kg administered in the recovery room. Prednisone is given at a dose of 1 mg/kg to be tapered by 5 mg every other day until 20 mg/day. Azathioprine (2 mg/kg) is given intra-operatively, and thereafter 1.5 mg/kg is used as a maintenance dose.
For acute rejection episodes methyl prednisolone pulse therapy (500 mg) was given intravenously for three days. If there was no positive response, a graft biopsy was performed and if this confirmed acute rejection, ATG was given for a maximum of 14 days. Acyclovir was given orally in a dose of 200 mg thrice daily for three months to all patients. The ureter is stented for a period of seven days in all patients. The Foley's catheter is removed within 24 hours of transplantation.
| Results|| |
Graft and Patient Survival
The graft survival (GS) for all transplants at 1,3 and 5 years was 83.5%, 77.6% and 74.7% respectively; for LRD grafts it was respectively 89.7%, 85.2%, 80.9% while for CAD grafts it was 81%, 72.5%, 70.5% respectively at 1,3 and 5 years [Figure - 1]. [Table - 2] shows the causes of graft loss with the commonest cause being chronic rejection. Technical causes were seen in three each of LRD and CAD transplants. The technical problems seen in LRD transplants included one case of graft artery stenosis with loss of the graft on attempting to correct it surgically and two grafts that were lost immediately after surgery due to arterial thrombosis. The technical problems seen in CAD grafts were all due to arterial thrombosis including one which was a fourmonth old en-bloc graft. Ruptured grafts were all from CAD donors including two from pediatric donors. The overall patient survival (PS) at 1,3 and 5 years was 97%, 94.7% and 93.5% respectively. The patient survival at 1,3 and 5 years for LRD transplants was 98.5%, 97%, 95.5% respectively while for CAD cases it was 96%, 93%, 92% respectively at 1,3 and 5 years [Figure - 2].
A total of 11 patients died. Three died during the transplant admission with nonfunctioning grafts while the remaining eight died with functioning graft. The causes of death included myocardial infarction (n = 2), malaria (n = 2), brain tumor and fungal infection (n = l), cytomegalovirus (CMV) infection and cardiac tamponade (n=l), cerebral infarction (n=l), cerebral hemorrhage (n=l), lymphoma (n=l), motor vehicle accident (n=l), and unknown cause.
| Acute Rejection|| |
There were a total of 59 (34.7%) episodes of acute rejection diagnosed clinically and/ or by- graft biopsy. Most of the rejection episodes occurred within the first month of transplantation and almost all of them within the first year of transplantation.
Primary Non-Functioning Grafts
Fifty-eight (34%) grafts had primary nonfunction due to acute tubular necrosis (ATN), severe rejection or graft arterial thrombosis. Forty (69%) of them recovered and 18 (31%) grafts had to be removed surgically. Majority of the primary non-functioning grafts (93%) were from cadaveric donors. One patient had a three-month period of primary non-function due to ATN. Repeated graft biopsies showed viable renal tissue with histological changes suggestive of ATN. She was maintained on small doses of cyclosporin and prednisone and was given dialysis support until she recovered after three months.
Surgical and Urological Complications
There were 36 surgical and urological complications encountered in our patients. They are listed in [Table - 3]. All the seven 50% (4.7%) episodes of urinary leak seen occurred prior to 1994, and no episodes have been seen since the practice of insertion of intra-ureteric stent was applied. Of the eight (4.7%) patients with arterial thrombosis, six lost their grafts and included three each from LRD and CAD donors. Of the five patients who had graft rupture, four were lost shortly after transplantation and one was saved surgically. Three patients had obstruction of the ureter which was corrected surgically. A lymphocele requiring surgical intervention was seen in only one case.
There were 58 medical complications as detailed in [Table - 4]. There were 22 episodes of severe infection. Three patients died from their infection including two, who developed malaria during a visit to their home country and one due to severe fungal infection. Five patients developed CMV infection which was diagnosed on clinical and serological grounds. Two patients had miliary tuberculosis which was treated successfully with anti-tuberculous medication. Two patients had fever and white lung but no definite diagnosis could be made even on open lung biopsy.
The different neurological complications that occurred in 10 of our patients are shown in [Table - 4]. Of the four patients with stroke, two had cerebral hemorrhage, one thrombotic stroke and one had associated brain tumor. The last patient was transferred from another dialysis center in the city for transplantation; he was known to have brain tumor prior to transplantation. Unfortunately, this information was not relayed to our center. Post-transplantation, the patient developed stroke and fungal infection and died. Two patients developed steroid-induced psychosis which improved after reduction of steroid dose. Two patients had seizures, one patient each developed tuberous sclerosis and pseudo tumor cerebri.
Two patients developed malignancy posttransplantation. One of them had a lymphoma. Cyclosporin was discontinued in this patient and he was given two courses of chemotherapy. However, he had cardiac arrest and expired just after the second course. The second malignancy was Kaposi's sarcoma which regressed after discontinuation of cyclosporin.
Seven patients had nine pregnancies after transplantation. All patients gave birth to healthy babies. One patient had an increase in the serum creatinine from 96 uol/1 prior to pregnancy to around 250-300 uol/1 postdelivery. There was no graft loss associated with pregnancy.
Fourteen patients, less than the age of 15 years, had 17 transplants. Their mean age was 11.8 + 2.9 years (range 5-14 years). They had 11 (65%) CAD and six (35%) LRD transplants. A total of 10 grafts were lost since the beginning of the program and the 1,3 and 5 years GS rates were 65%, 47%, and 47% respectively. Only two of the 14 patients died. One died nine days after transplantation with functioning graft due to massive brain infarction and the other after 45 days, yielding a patient survival rate in the first year of 86%.
| Discussion|| |
The graft and patients survival rates in our program are comparable to what has been reported from many transplant centers in the Western World as well as from other centers in Saudi Arabia. The UNOS renal transplant registry reported a one year GS in first CAD transplants to be 83.9% and patient survival to be 93.8%. For LRD transplants, the first year GS was 95.7% and PS was 97.5%  . Similarly, the Helsinki experience showed a 1,2 and 5 year GS to be 91%, 90% and 78% respectively for LRD and 88%, 82% and 73% respectively for CAD transplants  . The PS for LRD transplants at 1,2 and 5 years was reported to be 99%, 99% and 96% respectively while for CAD transplants, it was 99%, 97%. And 95% respectively at 1,3 and 5 years  .
In a report from the King Faisal Specialist Hospital, Riyadh the GS at 1 and 3 years was 83% and 69% respectively for CAD transplants and 95% and 91% respectively for LRD transplants  . The corresponding PS rates for CAD transplants were 98% and 92% and for LRD transplants were 98% and 98% respectively  .
The GS rate for pediatric patients in our program was lower than that reported in the UNOS registry  where the 3 year GS was 65% as also from the university of Minnesota  where GS at 1,2 and 5 years was reported to be 90%, 87% and 77% respectively. Majority of graft losses in our pediatric group occurred in the first three months (similar to what has been observed by the others) , . The possible reasons for this lower graft survival are: majority of our pediatric patients had CAD transplantation (65%) and there were more than usual technical problems in the initial years. Rejection (chronic or acute vascular) was the commonest cause of graft loss in all the patients. This is similar to what has been reported in large registries , . The percentage of graft loss due to death with functioning graft increased significantly with advancing recipient age.
Acute tubular necrosis is one of the major reasons for primary non-functioning graft. It is caused by ischemic insult before retrieval, during cold preservation, or during the transplant procedure. It occurs more often with CAD transplantation as was the case with our patients also. The prevalence of ATN in our study group is within the reported prevalence which varies between 25-50% , . Aggressive volume expansion along with mannitol administration may reduce the incidence of ATN  .
Although surgical and urological complications occurred in 21.2%o of the study patients, the majority of them were simple in the form of superficial wound infection which did not need surgical intervention. The occurrence of urinary leak in our patients was within the reported incidence in literature, 2.0-5.1% ,, . However, we did not have any case of urinary leak since the use of intra-ureteric stent more than two years ago. The prevalence of ruptured kidneys in our study was more than what has been reported elsewhere  . The cause of graft rupture was acute rejection, severe hypertension or renal vein thrombosis.
The low CMV infection in our series could be because of the prophylactic use of acyclovir and/or the cautious immunosuppressive regimen  . There were no deaths encountered from CMV infection. The rate of malignancy also was low (1.2%) in comparison to other centers. Skin cancer was the highest malignancy reported in the Helsinki series  . In Saudi Arabia, Kaposi's sarcoma has been reported to be common , ; however, it was seen in only one of our patients. The rate of development of diabetes mellitus posttransplantation is lower in our series than what has been reported by others from Saudi Arabia, 9.2 - 14.9% , as well as from outside the Kingdom, 9.1-18.6%  .
In conclusion, the overall success of renal transplantation in our hospital is due to the collaborative teamwork, better under standing and a high awareness of our community coupled with the support of the hospital administration, Saudi Center for Organ Transplantation, religion scholars and all government agencies.
| References|| |
|1.||Al Khader AA, Sulaiman MH, Dhar JM. Renal transplantation in the Kingdom of Saudi Arabia, a look back at the first decade. Saudi Kidney Dis Transplant Bull 1990;l:63-8. |
|2.||Cecka JM, Terasaki PI. The UNOS scientific renal transplant registry, in Terasaki JM Cecka PI (eds): Clinical Transplants 1994; 1-18. |
|3.||Salmela K, Kyllnonen L, Eklund B, et al. Thirty years of renal transplantation in Helsinki, n Terasaki JM, Cecka PI (eds): Clinical Transplants 1994;219-28. |
|4.||Lundgren G, Alfurayh O, Collste C, et al. The kidney transplantation program at King Faisal Specialist Hospital and Research Center, Riyadh. Transplant Proc 1992;24:336-8. |
|5.||Chavers BM, Matas A, Gillingham KJ, Schmidt WJ, Najarim JS. Clinical transplants. Terasaki and Cecks, eds 1994;203-12. |
|6.||Belli LS, De Carlis L, Del Favero E, et al. The role of donor and recipient factors in initial renal graft non-function. Transplant Proc 1988;20:861-4. |
|7.||Brophy D, Najarian JS, Kjellstrand CM. Acute tubular necrosis after renal transplantation. Transplantation 1980;29:245-8. |
|8.||Landsberg D, Rae A, Chiu A, et al. The original St. Paul's experience: renal transplantation without acute tubular necrosis. Transplant Proc 1988;20:1233:4. |
|9.||Rigg KM, Proud G, Taylor RM. Urological complications following renal transplantation. A study of 1016 consecutive transplants from a single center. Transpl Int 1994;7(2): 120-6. |
|10.||Mundy AR, Podesta ML, Bewick M, Rudge CJ, Ellis FG. The urological complications of 1000 renal transplants. Br J Urol 1981; 13:391-402. |
|11.||Hakim H, Iskandarani S, Basri N, et al. Review of surgical complications of renal transplantation in the Jeddah Transplant Program. Transplant Proc 1992;24:1834-5. |
|12.||Said R, Duarte R, Chaballout A, El Boghdadly S, Nezamuddin N, Mattoo T. Spontaneous rupture of renal allograft. Urology 1994;43:554-8. |
|13.||Rostaing L, Crespin A, Icart J, et al. Cytomegalovirus (CMV) prophylaxis by acyclovir in pre- transplant CMV-positive renal transplant recipients. Transpl Int 1994;7:5331-35. |
|14.||Kyllonen L, Pukkala E, Eklund B. Cancer incidence in a kidney transplanted population. Transpl Int 1994;7:5350-52. |
|15.||Qunibi W, Akhtar M, Sheth K, et al. Kaposi's sarcoma: the most common tumorafter renal transplantation in Saudi Arabia. Am J Med 1988;84(2):225-32. |
|16.||Al Suleiman M, Haleem A, Al Khader A. Kaposi's sarcoma after renal transplantation. Transplant Proc 1987;19:2243-4. |
|17.||Basri N, Aman H, Adiku W, Baraqdar A,Bonatiro I, Nezamuddin N. Diabetes mellitusafter renal transplantation. Transpl Proc1992;24(5):1780-l. |
|18.||Roth D, Milgron M, Esquenazi V, Fuller L, BurkeG, Mitter J. Post-transplant hyperglycemia. Increased incidence in cyclosporine-treated renal allograft recipients. Transplantation 1989;47:278-81 |
Department of Medicine, King Fahad National Guard Hospital, P.O Box 22490, Riyadh 11426
[Figure - 1], [Figure - 2]
[Table - 1], [Table - 2], [Table - 3], [Table - 4]