Objectives: To show the effects of different factors on development and outcome of early kidney allograft dysfunction.
Materials and Methods: Two hundred thirty-one kidney transplant recipients were divided into 2 groups: group 1 (125 patients transplanted from 1999-2004) and group 2 (106 patients transplanted from 2008-2013). Age range was 12 to 62 years (group 1) and 7 to 71 years (group 2). Deceased-donor transplant was more frequent in group 1 (76.8%), and living-donor transplant in group 2 (68.8%). In group 1, transplant was performed for glomerulonephritis or pyelonephritis; in group 2, additional risk factors (18 patients) included diabetes (11 patients), systemic lupus erythematosus (5 patients), amyloidosis (1 patient), and aortic and mitral valve replacement because of bacterial endocarditis (1 patient). In groups 1 and 2, immunosuppression after transplant included cyclosporine, mycophenolate mofetil, and steroids; patients in group 2 also had induction with anti-CD25 monoclonal antibodies.
Results: Primary graft function occurred in 89 patients in group 1 (71.2%) and 83 patients in group 2 (78.3%). Immediately after transplant, delayed graft function included anuria, oliguria, adequate amount of urine, and secondary delayed function (several days of polyuria followed by decreased urine output). Ischemia was a leading cause of delayed renal graft function. Anuria after living-donor transplant was a sign of vascular thrombosis. Rejection was the main cause of secondary delayed graft function, which occurred in only group 1. Survival at 1 year in patients with delayed graft function was 80% in group 1 and 100% in group 2 because of the absence of septic complications.
Conclusions: Despite extension of indications, primary functioning of kidney transplants and patient survival increased. Improved care enables long-term rehabilitation of recipients and expanding criteria for kidney transplant.
Key words : Delayed graft function, End-stage renal disease, Kidney transplant
Introduction
Kidney transplant is a major challenge in children, older adults, and patients who have risk factors such as diabetes mellitus, systemic lupus erythematosus, and long-term maintenance dialysis.1-12 In recent years, more patients who previously were not considered transplant candidates have been referred for kidney transplant. We reviewed the effects of different factors on development and outcome of early kidney allograft dysfunction.
Materials and Methods
Two hundred thirty-one kidney transplant recipients were divided into 2 groups: group 1 (125 patients transplanted from 1999-2004) and group 2 (106 patients transplanted from 2008-2013). Age range was 12 to 62 years (group 1) and 7 to 71 years (group 2). Deceased-donor transplant was more frequent in group 1 (76.8%), and living-donor transplant was more frequent in group 2 (68.8%). Maximum duration of dialysis treatment in patients with anuria was 3 years in group 1 and 13 years in group 2. In group 1, transplant was performed for glomerulonephritis or pyelonephritis; in group 2, additional risk factors (18 patients) included diabetes (11 patients), systemic lupus erythematosus (5 patients), amyloidosis (1 patient), and aortic and mitral valve replacement because of bacterial endocarditis (1 patient). Twelve kidney transplants were performed simultaneously with ipsilateral nephrectomy in group 2. In groups 1 and 2, immunosuppression after transplant included cyclosporine, mycophenolate mofetil, and steroids; patients in group 2 also had induction with anti-CD25 monoclonal antibodies.
Results
Primary graft function occurred in 89 patients (71.2%) in group 1 and 83 patients (78.3%) in group 2 (Table 1). With initial renal function, diuresis for the first day after transplant ranged from 2 to 51 liters, and all patients had urine with low specific gravity; patients with delayed renal graft function were more difficult to interpret and treat. Delayed graft function was defined as the need for dialysis during the first week after kidney transplant.1 Immediately after kidney transplant, 4 different types of clinical course of delayed renal graft function were defined: anuria, oliguria, adequate amount of urine, and secondary delayed function (several days of polyuria followed by decreased urine output including anuria). Ischemia was a leading cause of early delayed renal graft function (Tables 2 and 3). Anuria after living-donor transplant was a sign of vascular thrombosis. Rejection was the main cause of secondary delayed graft function, and this occurred only in group 1. Survival at 1 year in patients with delayed graft function was 80% in group 1 and 100% in group 2, primarily because of the absence of septic complications (Tables 2 and 3).
Discussion
The comparison of the importance of graft ischemia, rejection, thrombosis, infection, and drug-induced complications enables the consideration of ischemia as the main reason for renal graft dysfunction. So that severe renal dysfunction in group 1 with most deceased nonheart beating donor transplants occurred more frequently (28.8%) then it did in group 2 (17.1%) with most living-donor transplants. This is the reason that the absence of kidney function in grafts taken from living donors is a potential sign of vascular thrombosis of the graft or transplant rejection. Insufficient renal graft function in some cases was caused by multiple causes, such as acute rejection in a kidney with underlying tubular damage or infection. In analyzing all cases of delayed graft function, we could not identify cyclosporine nephrotoxicity (with monitoring of cyclosporine concentration in the blood) as a separate cause of renal dysfunction.
In delayed graft function with anuria, it was necessary to consider the differential diagnosis with primary nonfunctioning graft. With primary nonfunctioning graft, the continuation of immunosuppression created the additional risk for the development of sepsis and other severe complications. Doppler ultrasonography was the most available and informative study in patients with equivocal diagnosis. If the cause of oliguria remained unclear, initial course of steroids, antithymocyte globulin, antimicrobial and diuretic treatment, were not effective, and the progression of intoxication was evident, the graft was removed. At histologic examination of such grafts, acute rejection was observed in all cases.
Another difficult task in patients with delayed graft function, but with adequate diuresis, was the determination of the necessity of hemodialysis. In patients with unstable hemodynamics and an early postoperative wound, the optimal choice to avoid life-threatening uremia and complications of hemodialysis depended on diuresis dynamics, changes of urea and creatinine concentration in blood and urine tests, and the general state of the patient. Patients with delayed graft dysfunction had an average 5.8 ± 0.7 hemodialysis sessions. With anuria after renal transplant, the most effective treatment was early, brief hemodialysis sessions without ultrafiltration and heparinization, when possible. If anuria continued > 1 month, graft recovery usually was not observed. Only in 1 patient, diuresis resumed and the patient recovered, with creatinine level normalizing on day 45 of anuria after kidney transplant. In 1 patient, despite anuria, normal concentration of blood hemoglobin (without erythropoietin prescription) was observed, and this was the reason to not perform transplant nephrectomy in the subsequent year.
Determination of the cause of early kidney graft dysfunction and predicting the clinical course, including retrospective interpretation of similar clinical situations, has enabled us to plan treatment programs more accurately and improve the efficiency of renal transplant.
In conclusion, despite the extension of indications, our data shows that the frequency of primary functioning kidney transplant and patient survival increased. Improved care enables long-term rehabilitation of recipients and expanding criteria for kidney transplant.
References:
Volume : 13
Issue : 1
Pages : 228 - 230
DOI : 10.6002/ect.mesot2014.P21
From the Transplant Center, Regional Clinical Hospital, Donetsk, Ukraine
Acknowledgements: The authors have no conflicts of interest to declare,
and they received no financial support for the study.
Corresponding author: Viktor K. Denisov, Transplant Center of Regional
Clinical Hospital, Prospekt Illycha 14, Donetsk 83000, Ukraine
Phone: +38 067 296 75 24
Fax: +38 062 332 24 81
E-mail: dontransplant@mail.ru
Table 1. Kidney Graft Function in the Different Clinical Groups
Table 2. Causes and Outcomes of Delayed Graft Function in Group 1
Table 3. Causes and Outcomes of Delayed Graft Function in Group 2