|Year : 2021 | Volume
| Issue : 3 | Page : 232-240
Posttransplant renal allograft dysfunction – A retrospective observational study
Mathew George Kunthara, Manisha Sahay, Hakim Imran Hussain, Kiranmai Ismal, P Sharmas Vali, Anuradha Kavadi, B Vikram Kumar
Department of Nephrology, Osmania Medical College and General Hospital, Hyderabad, Telangana, India
|Date of Submission||15-Oct-2020|
|Date of Decision||15-Mar-2021|
|Date of Acceptance||01-Sep-2021|
|Date of Web Publication||30-Sep-2021|
Dr. Manisha Sahay
Department of Nephrology, Osmania Medical College and General Hospital, Hyderabad, Telangana
Source of Support: None, Conflict of Interest: None
Background: In India, a large number of end-stage renal disease patients are undergoing renal replacement therapy. A successful renal transplantation relives the burden of dialysis with improved quality of life and a productive life thereafter. This also reduces the cost of health care to the government and the society. Graft dysfunction is an important cause of graft loss.The objective of this retrospective study is to evaluate the graft dysfunction and its impact on patient and graft survival. Methods: We did a retrospective record-based analysis of 83 cases (including both deceased and live-related renal transplants) from 2014 to 2019 who were on triple immunosuppression (tacrolimus, mycophenolate mofetil, and steroids) as maintenance therapy. Patients who had graft dysfunction, underwent graft biopsy and were analyzed subsequently. Results: The most common causes for graft dysfunction on biopsy were acute rejection, acute tubular injury, and calcineurin inhibitor toxicity. About 39% of the patients had infections, predominantly bacterial and viral infections. The rejections were associated with poor patient survival (statistically significant). The overall patient survival at our center after 1 year and 3 years was 88% and 84%, respectively, while the death-censored graft survival was 86% and 81%, respectively. Conclusion: In our center, following renal transplantation, patients had a fairly successful outcome. However, early detection and prompt management of the graft dysfunction can improve the graft and the patient survival.
Keywords: Allograft dysfunction, kidney transplant outcome, rejection
|How to cite this article:|
Kunthara MG, Sahay M, Hussain HI, Ismal K, Vali P S, Kavadi A, Kumar B V. Posttransplant renal allograft dysfunction – A retrospective observational study. Indian J Transplant 2021;15:232-40
|How to cite this URL:|
Kunthara MG, Sahay M, Hussain HI, Ismal K, Vali P S, Kavadi A, Kumar B V. Posttransplant renal allograft dysfunction – A retrospective observational study. Indian J Transplant [serial online] 2021 [cited 2021 Nov 29];15:232-40. Available from: https://www.ijtonline.in/text.asp?2021/15/3/232/327385
| Introduction|| |
The prevalence of end-stage renal disease requiring transplantation in India is between 151 and 232 per million population. In India, about 7500 renal transplants are being done, of which about 90% are from living donors and 10% from deceased donors. Renal transplantation is considered as best modality over dialysis and timely recognition and management of allograft dysfunction should be done. The allograft dysfunction can be due to immunological causes and nonimmunological causes. The immunological causes can be hyperacute rejection, early acute (<3 months), late acute (3–12 months), and chronic rejection (>12 months).The nonimmunological causes include acute tubular necrosis (usually < 1 month), nosocomial infections (<1 month), acute calcineurin inhibitor (CNI) toxicity (<12 months), chronic CNI toxicity (>12 months), latent infection (1–6 months), community-acquired infections (>6 months), BK nephropathy (>1 month), and recurrent/de novo glomerulonephritis (GN; any time posttransplant). Hence, renal biopsy is considered the gold standard for the essential diagnostic and prognostic information following kidney transplantation. Hence, biopsy should be obtained to assess the etiology of graft dysfunction, which may include rejection, de novo or recurrent renal diseases, infections, and drug toxicity, which will provide a guidance for the treatment. A study conducted by Williams et al. found that the biopsy changed the clinical diagnosis in 36% and the therapy in 59% of patients. The information from the biopsy has proven crucial for obtaining strategies for therapeutic intervention. Some centers do protocol biopsies which are useful in detection of unexplained pathology in functioning graft. However, with the advent of tacrolimus and mycophenolate, the incidence of subclinical rejection has been reduced to 2.6% at 3 months, as reported by Gloor et al. and Nankivell. However, the benefit of protocol biopsy is that there will be early recognition of rejection and transplant glomerulopathy. Conversely, the normal histology will inform the physician for the safe reduction of immunosuppression.
Aims and objectives
The aim of the study was to investigate the etiology of the graft dysfunction, and to assess outcomes in terms of graft loss or death. The patient survival was defined as time of transplant to death and death-censored graft survival as time from transplant to the requirement of dialysis excluding the graft loss due to death. The factors contributed to the death-censored graft survival and patient survival were assessed accordingly.
| Methods|| |
A retrospective record-based analysis of 83 transplant recipients between January 2014 and December 2019 was performed. Patients with incomplete records were excluded, 48 transplant recipients underwent an indication biopsy following the graft dysfunction. The selection of patients is shown in [Figure 1]. Routine blood and urine examinations, renal function tests, and therapeutic drug monitoring, were conducted. Biopsy was done as indicated. No protocol biopsies were done. Pyelonephritis and other potential sources of obstruction in the urinary tract were excluded prior to the renal biopsy. CNI toxicity was defined by including at least one of the following: isometric vacuoles in proximal tubular cells, arteriolar hyalinosis with nodule formation in at least one arteriole and presence of interstitial inflammation and tubular atrophy in a stripped manner along with or without global glomerulosclerosis, vacuolization of smooth muscle cells of arterioles, tubular microcalcinosis, ischemic shrinkage of glomeruli, and hyperplasia of juxtaglomerular apparatus (graded from 0 to 3), as detailed in [Table 1].
|Table 1: Histological classification and grading for calcineurin inhibitor toxicity|
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Standards of care immunosuppression and posttransplant monitoring
Induction was given consisting of Fresenius-antithymocyte globulin (F-ATG) (40% [n = 33]) or basiliximab (4% [n = 3]). The protocol for deceased donor transplant was to give F-ATG 4–5 mg/kg as divided doses and for live transplant (especially for high risk) along with intravenous (IV) methylprednisolone 500 mg on day 0, followed by 250 mg on day 1 and day 2. Basiliximab was used at a dose of 20 mg on day 0 and on day 4. Following which, patients were treated with standard triple immunosuppression with tacrolimus (measured by fluorescence polarization immunoassay technology; maintaining trough level 7–10 ng/ml in the 1st month and 3–7 ng/ml subsequently; if patient did not receive induction, 8–10 for the 1st month and 3–7 ng/ml subsequently), mycophenolate mofetil (1 g BD) and prednisolone (initiated at 40 mg/day, tapered to 10 mg over a period of 2 months), along with valganciclovir for 100 days and septran DS for 1 year. Patients who developed tacrolimus toxicity were further converted to sirolimus. The above immunosuppressive drugs were given free of cost under the government scheme. The patients were followed up by routine laboratory investigations weekly for the first 3 months, fortnightly for the next 3 months, and monthly thereafter. The investigations were complete urine examination, hemogram, renal function tests, and ultrasound. The trough (C0) level of tacrolimus was measured monthly for the first 6 months, followed by 3 monthly intervals thereafter. Blood cultures, urine cultures, and appropriate investigations were done during infections.
All the patients were followed up till graft loss and/or death. The results were analyzed in terms of age of donor and recipient, serum creatinine, graft ischemia time, graft function, posttransplant complications, and graft and patient survival.
Indication and procedures in biopsy
The indications for percutaneous biopsy included: (1) increase in the serum creatinine level to >25% above baseline; (2) graft dysfunctions (delayed or slow graft dysfunction), with oliguria or anuria; (3) chronic renal graft dysfunction, i.e., rise of creatinine over a period of months; (4) abnormal urinalysis with either persistent glomerular hematuria and/or proteinuria.
Renal biopsy was done using ultrasonography-guided method with a 16-gauge needle (Bard). Each sample was tested for adequacy and subjected to light microscopy, electron microscopy, and immunofluorescence analyses (for immunoglobulin A [IgA], IgG, IgM, C1q, C3, and C4d). These were examined by two pathologists in an independent, blinded fashion. The final biopsy results were obtained based on modified BANFF classification (rejection, transplant glomerulopathy, etc.) and patients were treated accordingly. There were no major complications following the procedure except for the hematuria. About 6% of the biopsied patients had gross hematuria which resolved spontaneously after 6–8 h.
Data entry was done in Microsoft Excel and was analyzed with Stata 12 software. Demographic characteristics were summarized with descriptive statistics (mean and standard deviation for continuous variables and frequency and percentages for categorical variables). P < 0.05 was considered statistically significant. For time to event data, survival analysis using Kaplan–Meier approach and log-rank test was carried out. To account for the confounding effects of various covariates, multivariable hazards ratios (with their 95% confidence intervals) were also calculated for time to outcomes of death and graft loss using Cox proportional hazard model. Assumption of proportionality of hazard over time was tested before undertaking Cox proportional hazard model.
The patient consent has been taken for participation in the study and for publication of clinical details and images. Patients understand that the names and initials would not be published, and all standard protocols will be followed to conceal their identity.
As the study is a retrospective analysis of patient records, ethics committee approval is not deemed not necessary. The study was done in accordance with Declaration of Helsinki.
| Results|| |
Out of the 83 patients, 80% (n = 66) were male and 20% (n = 17) were female, with a mean age of the patients being 32.70 (standard deviation ± 9.36) years. About 55% (n = 45) underwent live-related transplant, of which (n = 5 were spousal) and 45% (n = 38) underwent deceased donor transplantation. The recipient characteristics are detailed in [Table 2]. All the live-related transplants had a median haplomatch of 3/6 while spousal had zero matches. None of the patients received dual kidneys. The distribution of native kidney diseases is shown in [Figure 2]. The mean serum creatinine levels were at the 1st month posttransplant 1.21 ± 0.57 mg/dl. A total of 12% (n = 10) had developed delayed graft function (DGF). About 19% (n = 16) had developed new-onset diabetes mellitus in after the transplant.
The mean age of the donors was 39.9 ± 13.05 (range: 13–67) years. Overall about 44.5% (n = 37) were female and 55.5% (n = 46) were male. Relationship in live donors was mother as donor (n = 23), father (n = 12), sister (n = 3), brother (n = 2), and wife (n = 5), respectively. In deceased donors, 74% (n = 31) were male, while in live-related donors, 64% (n = 26) were female. The most common cause of brain stem death was trauma (intracranial bleed) followed by aneurysmal bleed. There were no donations after cardiac death. The mean cold ischemic times were 4.48 ± 3.6 h. The Kidney Donor Profile Index (KDPI) scores for the deceased donors and the Living Donor KDPI (LKDPI) are depicted in [Figure 3].
About 57% (n = 48) underwent renal biopsy. Some patients s(n = 8) underwent repeat renal biopsy. The biopsy results are shown in [Figure 4]. The timeline of graft dysfunction and their etiologies are detailed in [Table 3].
Among 56 biopsies (48 first time and 8 repeat) , 39.2% (n = 22) had graft dysfunction due to rejection. About 45.5% had cadaver donation. Overall, about 21.4% (n = 12) of the cases had acute T cell rejection (TCR) while 17.80% (n = 10) had Antibody mediated rejection (ABMR) [Figure 5]. Three cases were of active ABMR and five cases of chronic active ABMR. None had C4d-negative ABMR. Three out of nine cases of ABMR had DSA positivity. Patients with Banff 1a were treated with IV methylprednisolone (3–5 mg/kg for 3 days and increased maintenance prednisolone dose). Patients with Banff 1b onward were additionally treated with ATG along with escalated doses of steroids. The patients who developed acute TCR during the immediate not early transplant period (<7 days) comprised 42% (n = 5) while 48% (n = 7) had TCR in the later period. Two patients who developed active ABMR in the immediate posttransplant period were categorized under high-risk group (1st case – 2nd transplant and 2nd – recent pregnancy + multiple blood transfusions) even after induction and both expired despite treatment. Patients with chronic active ABMR (n = 5) were managed with IV methylprednisolone, along with IV immunoglobulin (IVIg) and rituximab. One among them died due to sepsis. Two cases who had initially acute TCR on biopsy (after 1 year posttransplant), had chronic active AMR on subsequent biopsy with associated microvascular injury (after 3 months and 6 months of the first biopsy, respectively) which were treated with IVIg and rituximab.
8.9% (n = 5) of the cases had biopsy-proven acute tubular necrosis, of which one patient had transient hypotension and two others had renal arterial thrombosis and one patient had cytokine release syndrome following F-ATG administration, leading to DGF. One patient had complete renal arterial thrombosis leading to graft necrosis, for which graft nephrectomy was done and the patient was continued on maintenance hemodialysis.
About 21.4% (n = 12) had biopsy-proven acute tubular injury, of which 25% occurred in the immediate posttransplant period. These were due to bacterial pneumonia and urinary tract infection (UTI) ( Escherichia More Details coli and Klebsiella), recovered with broad-spectrum antibiotics.
Overall, 10.7% had CNI toxicity, of which chronic CNI toxicity was seen in (n = 5) and the histological changes are shown in [Table 4]. All those who developed CNI toxicity had their trough levels (C0) within their respective therapeutic target level. In our cases, arteriolar hyalinosis was the most common histological feature seen, particularly affecting the media or periphery of the arteriolar wall, along with vacuoles in smooth muscle cell arterioles. Only one patient had acute toxicity with significant vacuolization in PTC (Grade 3), along with thrombotic microangiopathy changes.
8.9% (n = 5) had recurrence following the posttransplant period; in immediate posttransplant period, two cases had atypical hemolytic-uremic syndrome (aHUS; anti-factor H ab+) with TMA on biopsy and one had FSGS recurrence. The other two cases were IgA nephropathy (IgAN; after 2 years of transplant) and membranoproliferative GN (after 4 years). In those with aHUS recurrence, plasmapheresis was done. Eculizumab could not be used due to high cost and nonavailability. One patient underwent graft nephrectomy. The patient with FSGS was treated with rituximab and plasmapheresis but succumbed due to sepsis.
The posttransplant infections were common among these patients, with 39% (n = 34) developing infections. As shown in [Figure 6], 24%, 36%, and 40% developed during the first 3 months, 3–12 months, and > 12 months, respectively. The bacterial infections were seen in 39% (n = 13), which were almost equal to viral infections, in our study. Common infections were UTIs (21%), pneumonia (12%), and septic focus like gastrointestinal infection and arthritis (6%). UTI was common during the early posttransplant period. Causative organisms were E. coli (44%), Klebsiella (22%), Candida albicans (12%), Acinetobacter (11%), and Pseudomonas (11%). Recurrent UTI was seen in 12% (n = 4) and was managed with antibiotic prophylaxis. 18% (n = 6) had Koch's disease (pulmonary [n = 5] and miliary tuberculosis [TB] [n = 1]), of which two of the patients with Koch's disease had associated aspergillosis and cytomegalovirus (CMV) colitis. Viral infections were seen in 39% (n = 13). CMV infections were seen in 18% (n = 6) and were tissue invasive (CMV colitis) in 3 and one patient had invasive disease in kidney. A case of BK nephropathy along with herpes labialis after 1 year posttransplant, was managed by decreasing the immunosuppression. Two patients had dengue acute kidney injury (AKI) and recovered. One patient had parvovirus-related anemia and was treated with IVIg. Overall, 22% (n = 7) had fungal infection; (n = 3) had invasive pulmonary aspergillosis while 4 had candidiasis. One patient had HCV-related crescentic membranoproliferative GN after 24 months of transplant and was associated with cryoglobulinemia. It was managed with sofosbuvir with velpatasvir (genotype 3) along with steroids.
|Figure 6: Timeline and trends of infection in renal transplant recipients|
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The patient survival rates are shown in Kaplan–Meier curves, as in [Figure 7]. The Kaplan–Meier curve for the graft survival in live-related donation and cadaver donation is shown in [Figure 8], which were almost equal at 3 years posttransplant. The graft survival with respect to KDPI and LKDPI is shown in [Figure 9]. As the scores of KDPI and LKDPI increased, the patient survival decreased, which was statistically significant (P = 0.03; P = 0.04).
|Figure 8: KM plot comparing graft survival of live donation and cadaver donation|
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|Figure 9: KM plot graft survival with respect to Kidney Donor Profile Index and Living donor Kidney Donor Profile Index|
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The serum creatinine after 1 year was 1.27 ± 0.52 mg/dl (77 patients) and after 3 years 1.5 ± 0.56 mg/dl (54 patients). The overall patient survival at our center after 1 year and 3 years was 88% and 84%, respectively, while the graft survival was 86% and 81%, respectively.
9 patients died due to sepsis. About 40% of the patients died with a functioning graft. Two patients had home deaths and the causes of death were unknown. However, rejections were statistically significantly associated with poor patient survival (P < 0.029), as shown in [Table 5]. Factors affecting the patient survival were age (younger age), hazard ratio [HR]: 1.02 (95% confidence interval [CI]: 0.97–1.08); female sex, HR: 2.1 (95% CI: 0.7–6.4); infections, HR: 1.5 (95% CI: 0.58–4.1); deceased donor, HR: 1.7 (95% CI: 0.5–5.8); and induction, HR: 1.7 (95% CI:0.5-2.8). Other contributing factors for poor graft and patient survival were poor compliance (3.6%), delayed presentation with late diagnosis, and high KDPI/LKDPI scores.
| Discussion|| |
AR (acute rejection) remains the main cause of graft dysfunction following transplant. Sellares et al. showed 35% had AR including TCR, ABMR, and borderline rejection. In our study, 30% (n = 17) who underwent the graft biopsy, had acute rejection. With the introduction of the induction and triple immunosuppression, the incidence of rejection has been drastically decreased. The immunological matching between the donor and recipient has also contributed to the decrease in rejections. Nankivell et al. found that the risk of acute rejection in the 1st year posttransplantation was < 15%. In our study, about 13% had developed AR during the 1st year of posttransplant, of which 81% (n = 9) were acute TCR. The acute rejection was seen in bimodal pattern, being common in immediate (<7 weeks) posttransplant period (22% [n = 5] among TCR and 9% [n = 2] among ABMR, respectively) and following 1 year posttransplant 45% (n = 10). 80% (n = 4/5) who developed a/c TCR in the immediate posttransplant were live-related transplants and did not receive induction. In our study, the predominant types of acute TCR were Type 1a (42%; n = 5), followed by Type 1b (33%; n = 4), Type 2a (17%; n = 2), and Type 2b (8%; n = 1), respectively. None of them had Type 3 rejections. Late AR is defined as acute rejection occurring after 3 months of transplant. This can occur in a setting of decreased immunosuppression in the context of infections, drug toxicity, or malignancy. A study by Jin et al. showed that patients who had AR in the 1st year posttransplant had 96% recovery, when compared to 85% recovery in AR after 1 year posttransplant, and concluded that late AR is associated with graft loss and poor outcome. This was in contrast to our study which showed that there was no difference in graft loss and outcome, comparing the AR within early and late periods, even though the degree of histopathological injury was higher in late AR than early AR.
CNI nephrotoxicity is manifested either as AKI or TMA or as chronic progressive renal disease. Other renal effects of the CNIs include tubular dysfunction. In acute toxicity, biopsy typically reveals an acute arteriolopathy, ATN, or rarely HUS. Chronic toxicity is characterized by arteriolar hyalinosis, vacuolization, and striped fibrosis. A study conducted by Sharma et al. found that 88% of the patients had arteriolar hyalinosis and 71% had vacuoles in SMC arterioles in patients with CNI toxicity. In a study by Taheri et al., 8.6% had CNI toxicity. In another study by Zhang et al., 10.6% had CNI toxicity which was almost similar to our study, comprising 10.7% of graft dysfunction with CNI toxicity.
A study by Jiang et al. found that GN recurrence occurred in 10.5% of transplants and was most common in mesangiocapillary GN (MCGN). The median time for recurrence was shorter for FSGS compared to IgAN. GN recurrence was less common in patients over 50 years of age and after unrelated kidney donation. The authors also identified that there is a significantly higher risk of recurrence in secondary grafts following recurrence in a primary allograft for FSGS but not IgAN, MCGN, or membranous nephropathy (MN). At 10 years, recurrence occurred in 8.7%, 10.8%, 13.1%, and 13.4% of allografts for FSGS, IGAN, MCGN, and MN, respectively. Uffing et al. found that about 32% of the patients developed recurrent FSGS following transplant. Only 57% had attained complete to partial response while 43% had no response to rituximab and plasmapheresis. In our study, one patient who developed FSGS was treated with rituximab and plasmapheresis but had immediate mortality due to sepsis. Salvadori et al. stated that recurrence is more after 2 years of transplant with an incidence rate of 20%–30%.
The etiology of graft dysfunction in various other studies is shown in [Table 6].
Bacterial infections are approximately twice as frequent as viral infections in RTR. Vascular access and UTIs were the most frequent bacterial infections, whereas CMV was the most common viral infection. In our study, UTI was seen in 21%. About 18% and 3% of infections were due to CMV and BKV, respectively. Fungal infections were seen in 22%. This was in similar to a study conducted by Kumar et al. A study conducted by Basiri et al. found that the prevalence of posttransplant TB was between 2% and 15% in Asian countries. Kumar et al. found that posttransplant TB prevalence was 17%. Our study also showed among infections 18% were due to TB.
Mukhopadhyay et al. in a retrospective analysis in live-related renal transplants, showed that the rates of death-censored renal allograft survival at 1, 3, and 5 years after transplant were 94%, 90%, and 79%, respectively, while the patient survival at 1, 3, and 5 years was 92%, 87%, and 83%, respectively. A study conducted by Patel et al. found that with a mean follow-up of 2.18 ± 1.75 years, the patient and graft survival rates were 74.57% and 86.8%, respectively, in deceased donor transplant. Sujit et al. analyzed for 105 cadaver transplant cases and concluded that the 1-year recipient survival and graft survival rates are 75.8% and 89.5%, respectively. A retrospective analysis of 68 deceased donor kidney transplant patients by Prabahar and Soundararajan showed that the 5-year patient and graft survival rates were 61.7% and 58.8%, respectively. The overall patient survival at our center after 1 year and 3 years was 88% and 84%, respectively, while the graft survival was 86% and 81%, respectively. This may be due to the fact that in deceased donors, the induction therapy has led to increased risk of infections, while in living donations, avoidance of induction therapy has led to increased risks for the rejection.
In a study by Ozkul et al. from Pakistan, including both live-related and deceased transplants, had a 1-year and 5-year graft survival of 96% and 90%, respectively. Yet, another study by Galabeda et al. from Sri Lanka had a graft survival of 97.8%, 94.4%, and 93.5% at 1, 3, and 5 years, respectively, and a patient survival of 87%, 83%, and 82.2% at 1, 3, and 5 years, respectively. In our study also, there was no statistically significant difference between the patient and survival between deceased donor and live-related transplants at 3 years. The reasons for the graft failure in our center can be due to multiple factors such as incompliance to drugs, rejections, repeated infections, late presentations of the patients, high KDPI (especially in deceased donors), and very poor socioeconomic background patients.
It was a single centre study.
| Conclusion|| |
Rejections, acute tubular injury and drug toxicity were important causes of graft dysfunction in our study. The overall patient survival at our center after 1 year and 3 years was 88% and 84%, respectively, while the graft survival was 86% and 81%, respectively. There was no significant difference between outcomes in live and deceased donor transplantation.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]