Post-transplant IgA Nephropathy Research Articles

IgA nephropathy and kidney transplantation according to the Oxford classification.

IgA nephropathy (IgAN) is the most common glomerular disease globally, and its susceptibility and the risk for the development of end-stage kidney disease are related to genetic and environmental factors. IgAN recurrence after kidney transplantation is relatively common, impacting graft function and survival. This study evaluated the risk factors and the clinical, laboratory, and histological characteristics of post-transplant IgAN recurrence based on the Oxford classification. Retrospective single-center cohort study including kidney transplant recipients with biopsy-proven pre-transplantation IgAN, with analysis of risk factors and clinical, laboratory, and histological characteristics of the IgAN recurrence cases. 53 patients fulfilled the inclusion criteria and were included in the study. The majority was male, white, eutrophic, with a mean age of 27 ± 9 years at IgAN diagnosis. Systemic arterial hypertension and proteinuria were frequent in the pretransplant period. Four recipients (7.5%) presented IgAN recurrence in a period of 6 to 122 months post-transplant. According to the Oxford classification, they had high scores of mesangial hypercellularity and segmental glomerulosclerosis in the native kidney biopsies and there was mesangial hypercellularity in all analyzed graft biopsies. None of these patients had received induction immunosuppression and all of them presented graft failure in the follow-up. In this series, there was a high prevalence of mesangial hypercellularity and segmental glomerulosclerosis on native kidney biopsies, and mesangial hypercellularity occurred in all IgAN recurrence graft biopsies. Despite the lower incidence of recurrence of IgAN post-transplant compared to previous reports, progression to graft loss was of 100%.

342.7: Audit of Posttransplant IgA Nephropathy Treatment Strategies: Single Center Study

Introduction: IgA nephropathy (IgAN) is the prevalent form of recurrent disease which has negative influence on graft survival in kidney transplant recipients. Recurrence rate varies from 13% to 50% according to the data available. Approaches to the management of such patients are controversial and there are no any certain treatment recommendations for IgAN in kidney grafts to this day. Methods: A retrospective single-center study, including 42 patients with biopsy-proven IgA nephropathy in kidney transplant, between January 2014 and August 2020, was performed. Treatment strategies were analyzed. Results: Allograft IgAN manifestation time was from 1 to 122 month, with an average of 49,59 ± 30,34 month. The main clinical signs were proteinuria more than 1.0 g per 24 hours with and without hematuria – 45,24%; proteinuria less than 1.0 g per 24 hours with and without hematuria – 42,86%; isolated hematuria – 9,52%; elevation in serum creatinine – 2,38%.18 (42,86%) patients were treated with angiotensin converting enzyme inhibitors or angiotensin II receptor blockers and 11 (61,11%) of them have lost their grafts. 2 (4,76%) patients were managed with 8 mg of methylprednisolone. 22 (52,38%) recipients received pulse therapy consisted of 3 intravenous methylprednisolone infusions at a dose of 500 to 1000 mg followed by administration of methylprednisolone orally: 16 mg - 10 cases, 20 mg - 2 cases, 24 mg – 4 cases, 32 mg – 4 cases, 48 mg – 1 case. A dose reduction period varied from 3 to 12 month, maintenance dose was 4 mg. Renal allograft failure occurred in 11 (61,11%) patients on non-steroid regimen and 6 patients treated with steroids (p=0,18). Conclusion: Lack of approved management concepts leads to various treatment regimens use in patients with posttransplant IgAN. Steroid application advisability as well as optimal dose and treatment duration remains debatable. Impact on graft survival rate is unclear. Multicenter randomized trials are required to develop kidney transplant IgA nephropathy patients care strategies.

POS-110 IGA RECURRENCAE POST RENAL TRANSPLANATION WITH HENOCH SCHONLEIN PURPURA

IgA nephropathy (IgAN) is the most common glomerular disease worldwide, and it has a slow course with up to 20-30 % of patient may develop ESRD after 20years.Patients with IgAN are good candidates for renal transplantation because they are still young with less complications and comorbidities. Lectin-independent Gd-IgA1 ELISA can detect serum Gd-IgA1 in patients with recurrent IgAN can be used as a biomarker for diagnosis and activity assessment of post-transplant recurrent IgAN

POS-762 IgA NEPHROPATHY IN KIDNEY TRANSPLANT RECIPIENTS: ONE CENTER EXPERIENCE

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis leading to end-stage kidney disease. Every year more and more patients with IgAN undergo kidney transplantation and each of these patients has the risk of recurrence in their renal transplant. As overall kidney graft survival rate has been improved the prevalence of recurrent glomerulonephritis, in particular IgA nephropathy, is expected to increase. Data from 612 kidney transplant biopsies performed in Minsk, Belarus from 2015 to 2020 were retrospectively evaluated. Cases of pre- and/or posttransplant IgA nephropathy were analyzed. 42 cases (6,86%) of posttransplant IgA nephropathy were identified. Only 8 of them (19%) had biopsy-proven IgA disease in native kidneys, so could be regarded as recurrent IgAN patients. Male to female ratio was 2:1. Mean age was 41,71 ± 11,78 years. Clinical indications for renal graft biopsy were: proteinuria more than 1.0 g per 24 hours with and without hematuria – 45,24%; proteinuria less than 1.0 g per 24 hours with and without hematuria – 42,86%; isolated hematuria – 9,52%; elevation in serum creatinine – 2,38%. The term from transplantation to IgAN revealing was from 1 to 122 month, with an average of 49,59 ± 30,34 month. 13 patients (30,95%) have lost their graft function and 11 of them (84,6%) had proteinuria greater than 1.0 g per day. The prevalence of IgA nephropathy in kidney transplant recipients was 6,68% and only 19% of posttransplant IgAN cases were considered as recurrent. The main clinical manifestation of IgAN in renal graft was proteinuria associated with hematuria. Graft survival rate was 69,05%. Such well-known risk factor of IgAN poor outcome in native kidneys as proteinuria more than 1.0 g per day potentially hold true to recurrent disease, as 84,6% of posttransplant IgAN patients with non-functional transplant had severe proteinuria. Histological verification of native kidney primary disease is definitely required for risk stratification and early recurrence predicting.

Glomerular C4d in Post-Transplant IgA Nephropathy is associated with decreased allograft survival

BackgroundGlomerulonephritis (GN), including post-transplant IgAN (post-Tx IgAN) is an important contributor to decreased long-term allograft survival. The immunopathological detection of the complement degradation product C4d in glomeruli (C4dG) has been recently described as a risk factor in native kidney IgAN, however little is known about C4dG deposition in post-Tx IgAN. We hypothesized that glomerular C4d may indicate a more aggressive disease course and worse allograft survival in patients with post-Tx IgAN.MethodsIn this retrospective study we assessed the presence and clinical relevance of C4dG in patients with post-transplant IgAN. We analyzed 885 renal allograft recipients, including 84 patients with post-transplant GN. All patients were transplanted between January 1999 and April 2006 and underwent at least one biopsy for differnt causes. The primary endpoint was death-censored graft survival, with a median follow-up of 9.6 (IQR 3.8–13.2) years.ResultsThe prevalence of post-Tx GN was 9.5%. Twenty-seven patients with post-Tx IgAN were included. C4dG positive patients (N = 18, 66.7%) had significantly worse allograft survival compared to C4dG negative post-Tx IgAN patients and patients without post-Tx IgAN [C4dG positive: 27.8% vs. 55.6% and 66.0%; log-rank: p = 0.01]. C4dG remained a significant risk factor (HR 2.22, 95% CI 1.27–3.87) for allograft loss even after adjustment for T cell mediated rejection (TCMR) and antibody mediated rejection.ConclusionGlomerular C4d deposition is an independent risk factor for worse graft-survival in patients with post-Tx IgAN, even after adjusting for other risk factors such as antibody mediated rejection. Assessment of glomerular C4d deposition may provide a valuable prognostic risk assessment tool to identify high risk patients in post-Tx IgAN.Graphic abstract

Concurrent Antibody-Mediated Rejection in Post-Transplant IgA Nephropathy – Diagnosis Using a Stepwise Approach of Graft Morphology

Background Diagnosis of concurrent antibody-mediated rejection (AMR) is difficult in cases of post-transplant IgA nephropathy (TxIgAN) with glomerular inflammation. Glomerular inflammatory cell infiltration may be seen either in the contexts of AMR or immune complex-mediated injury and described as ‘glomerulitis’ (‘G’) or ‘endocapillary hypercellularity’ (‘E’), respectively. Methods We analyzed 40 renal allograft biopsy samples of 37 TxIgAN patients having glomerular inflammatory cells (‘E’ and/or ‘G’) between January 1992 and December 2016, in search for ancillary morphologic features in the diagnosis of concurrent AMR. Results Glomerular inflammation was described as ‘G’, ‘E’, or both in 11, 14, and 15 biopsies, respectively. Morphologic features supportive of acute and chronic AMR (AAMR and CAMR, respectively), comprising peritubular capillaritis, glomerular basement membrane doubling, peritubular capillary basement membrane multilayering, and peritubular capillary C4d staining, were sequentially examined, which revealed nine AAMR and 14 CAMR. C4d was positive in 77.8% of AAMR and 42.9% of CAMR. Of the remaining 17 biopsy samples without AMR, mesangial hypercellularity and/or crescents were present in 14 samples. In four samples, acute T cell-mediated rejection coexisted. Conclusions Diagnosis of concurrent AMR can be aided by using a stepwise approach of morphologic features of AMR in cases of TxIgAN with glomerular inflammation.

Early post-transplant serum IgA level is associated with IgA nephropathy recurrence after kidney transplantation.

IgA nephropathy (IgAN), the most frequent primary glomerulonephritis, affects young patients and is associated with a high risk of progression to end-stage renal disease. Consequently, patients with IgAN constitute an important proportion of candidates for kidney transplantation. Several studies showed a significant risk of IgAN recurrence on kidney graft, but the risks factors for recurrence remain to be accurately evaluated. Indeed, early identification of at risk patients may allow the optimization of treatment and the reduction of recurrence rate on the graft. In the present work, we studied the relationship between post-transplant serum IgA (sIgA) levels and the risk of IgAN recurrence after kidney transplantation. Recipients with IgAN had higher levels of sIgA as compared to patients with other nephropathies (p<0.05). The prevalence of IgAN recurrence was 20.8% during the period of analysis (mean follow-up of 6 ± 3.2 years). Serum IgA levels at M6, M12 and M24 post-transplant were significantly higher in patients with IgAN recurrence as compared to those without (p = 0.009, p = 0.035 and p = 0.029, respectively). Using receiver operating curve (ROC), sIgA at M6 and M12 post-transplant were significantly associated with IgAN recurrence (AUC = 0.771, p = 0.004 and AUC = 0.767, p = 0.016, respectively), while serum creatinine and proteinuria were not. Serum IgA level at month 6 was significantly associated with the occurrence of post-transplant IgA recurrence, whether it was analyzed as a continuous or a categorical variable. After successive adjustment on age, gender and proteinuria, sIgA remained a significant risk factor of post-transplant IgAN recurrence. Finally, survival free of IgAN recurrence was significantly better in patients with sIgA<222 mg/dL at month 6 as compare to IgAN patients with sIgA≥222 mg/dL (p = 0.03). Thus, the present work supports a link between post-transplant sIgA levels and IgAN recurrence and suggests that sIgA may be a valuable predictive biomarker of IgAN recurrence in kidney transplant recipients.

Clinical Features, Treatment and Prognostic Factors of Post-Transplant Immunoglobulin A Nephropathy

BackgroundInitially described as a relatively benign condition, recent studies report graft loss in up to 50% of the patients with post-transplant IgA nephropathy. There is no evidence for the best therapeutic approach, and prognostic factors remain to be elucidated.Material/MethodsSingle center retrospective analysis of patients >12 years old, with clinically relevant post-transplant IgA nephropathy (proteinuria ≥1.0 g/g and/or graft dysfunction) and ≥6 months follow-up after diagnosis (n=47).ResultsLiving donor transplants represented 85% of cases. Dysmorphic hematuria (100%), blood pressure elevation (95.7%), renal dysfunction (70.2%) and subnephrotic proteinuria (60.6%) predominated at presentation. Using the Oxford Classification, mesangial proliferation was the main histological lesion (91%). Treatment consisted mostly of blockade of the renin angiotensin system (89.4%) and modification of immunosuppression (85.1%), mainly by increasing oral steroids dose (83%), with venous pulse therapy in 63.8% of cases. Partial and complete remission occurred in 48.9% and 17% of cases, respectively. One patient died (sepsis) and 15 patients (31.9%) lost their grafts due to nephropathy. The percentage of decrease in glomerular filtration rate at diagnosis was independently associated with partial remission (HR 0.97, 95% CI 0.94–0.99, p=0.01) and graft loss (HR 1.13, 95% CI 1.06–1.20, p<0.001). Deceased donor (HR 28.04, 95% CI 4.41–178.39, p<0.001) and donor age (HR 1.1, 95% CI 1.04–1.16, p=0.001) were also risk factors for graft loss.ConclusionsDespite treatment, most patients with post-transplant IgA nephropathy in this cohort study presented unfavorable outcomes, and graft dysfunction at diagnosis appeared to be the main prognostic marker.

A Novel Biomarker for Post-Transplant Recurrent IgA Nephropathy

BackgroundThe serum levels of galactose-deficient immunoglobulin (Ig)A1 (Gd-IgA1) represent the most promising candidate biomarker for IgA nephropathy (IgAN). The aim of this study was to evaluate the serum levels of Gd-IgA1 as a novel noninvasive biomarker for post-transplant IgAN recurrence. MethodsSerum Gd-IgA1 levels of 18 patients with recurrent IgAN were compared with control renal transplant recipients (n = 23) with non-recurrent IgAN and control non-transplant IgAN patients (n = 44) and healthy relatives (n = 11). Serum Gd-IgA1 levels of patients were measured with the use of KM55 enzyme-linked immunosorbent assay (ELISA). The effects of serum Gd-IgA1 concentrations on IgAN recurrence, post-transplant events, and graft survival were evaluated. ResultsAll recurrent IgAN patients presented with renal dysfunction (mean serum creatinine, 1.62 ± 0.39 mg/dL) and detectable proteinuria at the time of diagnosis. Serum Gd-IgA1 levels of recurrent IgAN patients (8735 ± 10854 ng/mL [log10: 3.71 ± 0.45]) were significantly higher than those of non-recurrent IgAN patients (4790 ± 6089 ng/μL [log10: 3.31 ± 0.64]) (P = .027). Serum Gd-IgA1 levels of non-transplant IgAN patients were significantly higher (8791 ± 8700 ng/μL [log10: 3.79 ± 0.36]) than those of non-recurrent IgAN patients (4790 ± 6089 ng/μL [log10: 3.31 ± 0.64]) and healthy relatives (2615 ± 1611 ng/μL [log10: 3.34 ± 0.27]) (P < .001 and P = .021, respectively). Receiver-operating characteristic curve analysis revealed that the area under the curve for recurrence of IgAN was 0.69 (0.53–0.85) for serum Gd-IgA1 (P = .038). Biopsy-confirmed allograft rejection rates were similar in the recurrent IgAN group [3 (17%)] compared with the non-recurrent IgAN [6 (26%)] group (P = .47). Graft failure rate was not also significantly different in the recurrent IgAN group [4 (22.2%)] compared with the non-recurrent IgAN group [2 (8.7%)] (P = .224). ConclusionsThis novel lectin-independent Gd-IgA1 ELISA that can detect serum Gd-IgA1 in patients with recurrent IgAN can be used as a biomarker for diagnosis and activity assessment of post-transplant recurrent IgAN.

IgA NEPHROPATHY IN PATIENTS RECEIVING A RENAL TRANSPLANT.

IgA nephropathy (IgAN) is the third most frequent cause of renal graft loss among patients with primary glomerulonephritis. To assess clinical and laboratorial profile of patients with pre and/or post transplant IgAN, in addition to patient and graft survival in both groups. Data from 146 patients who had received a renal transplant were retrospectively collected and were divided in two groups: group 1-patients with biopsy-documented IgAN as the underlying native kidney disease (n = 128); group 2-patients who developed post-transplant IgAN independent of the underlying disease (n = 18). Patients submitted to renal transplantation (1998-2010) with pre and/or post transplant IgAN. Clinical and laboratorial evaluation of renal function of 146 post transplant IgAN patients. Recipients and deceased donors exhibited a higher degree of HLA compatibility (1.0 vs. 2.5 mismatches for groups 1 and 2, respectively). The main post-transplant IgAN presentation was haematuria associated with non-nephrotic proteinuria (44.4%). A histological pattern of focal segmental glomerulosclerosis was observed in 59.2% of biopsy samples. The 10-year patient survival was 93.5% in group 1 and 100% in group 2, and the graft survival rates were 58.5 and 87.2%, respectively. The rate of post-transplant IgA diagnosis in our case series was 11%, and IgAN was diagnosed late in the course of transplantation. In most cases, IgAN manifested as haematuria and non-nephrotic proteinuria, without renal graft dysfunction, and this picture might explain late indication of graft biopsies. The 10-year patient survival rates were excellent.

Peritubular capillary C4d deposition and renal outcome in post‐transplant IgA nephropathy

Immunological staining of the transplanted kidney for C4d in peritubular capillaries (C4d(PTC)) has emerged as a useful method to detect antibody-mediated rejection in situ. In this retrospective study, we evaluated the prevalence of C4d(PTC) deposition in allograft renal biopsies diagnosed of IgA nephropathy (IgAN) and analysed its clinical significance. Sixty-six biopsy specimens of post-transplant IgAN, which were obtained to evaluate azotemia and/or heavy proteinuria, were examined by immunohistochemical staining of the paraffin sections with polyclonal antibody for C4d. C4d was stained positively in peritubular capillaries in 16 (24%) of the 66 cases. The C4d(PTC)-negative (n=50) and C4d(PTC)-positive groups (n=16) were not different in recipient gender, age, donor age, type of donor (living vs. cadaveric), interval from transplantation to graft biopsy (41.6+/- 21.8 vs. 48.3+/-26.1 months) and post-biopsy follow-up period (60.3+/-23.3 vs. 56.9+/-25.4 months). During the follow-up period, 12 of 50 (24%) although the incidence of graft failure was not different by the C4d deposition in peritubular capillaries, intervals from renal biopsy to graft failure tended to be shorter in C4d(PTC)-positive cases than C4d(PTC)-negative cases. In Kaplan-Meier analysis, the renal allograft function of the C4d(PTC)-positive group deteriorated more rapidly than that of the C4d(PTC)-negative group (p<0.05). Histologically, the C4d(PTC)-positive group had findings suggestive of acute cellular rejection more commonly than the C4d(PTC)-negative group (p<0.01). Evidence of humoral rejection, as demonstrated by C4d(PTC) deposition, was concurrently present in significant portions of post-transplant IgAN biopsy specimens and was associated with more rapid deterioration of renal function. These results suggest that C4d(PTC) positivity needs to be determined at the time of biopsy even in cases of post-transplant glomerulonephritis and immunosuppression may need to be modified accordingly.

Peritubular capillary C4d deposition and renal outcome in post-transplant IgA nephropathy

Peritubular capillary C4d deposition and renal outcome in post-transplant IgA nephropathy

IgA Nephropathy in Kidney Allograft Recipients—Therapeutic Perspective

Introduction A growing number of patients are losing their kidney allografts due to glomerulonephritis. Although posttransplant IgA nephropathy (IgAN) is regarded as benign, it may lead to late allograft loss in a substantial number of patients. The aim of this study was to evaluate the influence of posttransplant IgAN on long-term transplantation outcomes, risk factors for progression of graft dysfunction, and effectiveness of therapeutic interventions. Patients and methods We evaluated, potential risk factors for accelerated graft loss among 27 kidney allograft recipients with posttransplant IgAN, comparing graft survival in a control group matched for population and transplantation-related parameters. We evaluated the effectiveness of therapeutic interventions regarding immunosuppressive regimen, and hypertension control including angiotensin converting enzyme inhibitor (ACEI) usage with Kaplan-Meier, Cox proportional hazard plots, and log-rank tests in statistical analyses. Results Compared with the control group, patients with IgAN experienced a 6.57 higher risk for dialysis dependence ( P < .01, 95% CI 1.4 to 30.83). The risk for accelerated graft loss in the course of IgAN was associated with graft dysfunction (RR = 2.16 for additional 1 mg/dL of serum creatinine at glomerulonephritis presentation; P < .03, 95% CI 1.2 to 4.36) and intense proteinuria as evidenced by a RR = 4.67 for the presence of the nephrotic syndrome ( P < .05, 95% CI 0.95 to 22.8). Immunosuppression enhancement resulted in a significantly decreased risk of dialysis dependence, namely, RR = 4.76 (95% CI 1.12 to 20, P < .04). With ACEI treatment there was a tendency for a 2.8-fold decreased risk of dialysis dependence, without reaching statistical significance ( P = .14). Conclusions Patients with posttransplant IgAN may benefit from intensifying maintenance immunosuppression, which slows progression to end-stage graft dysfunction.

Segmental glomerulosclerosis in IgA nephropathy after renal transplantation: relationship with proteinuria and therapeutic response to enalapril.

Although graft dysfunction has been increasingly reported in post-transplant IgA nephropathy (Tx-IgAN), intragraft morphological changes have been largely overlooked. We evaluated glomerular changes in Tx-IgAN to identify the histological features pertaining to significant proteinuria and therapeutic response to enalapril. Fifty-four renal allograft biopsies, diagnosed as Tx-IgAN at a median of 46 months after transplantation, were the subject of the study. In 10 patients, glomerular morphometry was performed. In 14 patients who have been treated with enalapril for more than 12 months, we correlated the therapeutic response to enalapril with allograft histology. No uniform pattern was found in the glomeruli of Tx-IgAN. The glomerular mesangium was mostly indistinct. Interstitial fibrosis was negative or mild in 88.9%. By morphometry, the glomerular tuft areas and mesangial areas were significantly larger in Tx-IgAN than those of the normal native kidney (p < 0.05), but were not different from transplant cases without glomerulonephritis. Proteinuria of >/=1 g/24 h was correlated with glomerulosclerosis, interstitial fibrosis and interstitial inflammation at time of biopsy (p < 0.005). The presence of segmental sclerosis (SS) correlated well with the amount of 24-h proteinuria (p < 0.001). After treatment with enalapril, the amount of proteinuria reduced in 64.3%. Therapeutic response to enalapril tended to be less effective in patients having SS (28.6 versus 71.4%), but this finding did not reach a statistical significance. Significant proteinuria was associated with advanced chronic injury, especially with the presence of SS in Tx-IgAN, but anti-proteinuric effect of enalapril was not affected by graft histology. It remains to be clarified whether glomerular mesangial expansion plays a role in graft dysfunction in a subset of Tx-IgAN showing prominent mesangial changes.

Nuclear factor kappa B activation in glomeruli of posttransplant IgA nephropathy using southwestern histochemistry

Nuclear factor kappa B activation in glomeruli of posttransplant IgA nephropathy using southwestern histochemistry

A clinicopathological study of IgA nephropathy in renal transplant recipients: beneficial effect of angiotensin-converting enzyme inhibitor.

Prolonging the survival of transplant kidneys is a major task of modern nephrology. It has recently been shown that deteriorating renal function and substantial graft loss were observed in 55% of renal allograft recipients with recurrent IgA nephropathy (IgAN) at long-term follow-up. To gain a useful insight into the therapeutic approach towards protecting allograft kidneys from deteriorating graft function, we compared the histological characteristics of post-transplant IgAN to primary IgAN and investigated the effects of an ACE inhibitor. Twenty-one patients with post-transplant IgAN and 63 patients with primary IgAN were included in the histopathological study. The effectiveness of angiotensin-converting enzyme (ACE) inhibitor treatment in post-transplant IgAN was also studied in 10 patients. The prevalence of glomeruli with adhesions and/or cellular crescents in primary IgAN was significantly greater than in post-transplant IgAN (P<0.05), but the proportion of glomeruli with segmental sclerosis was similar in both groups. The rate of global obsolescence, and the degree of interstitial fibrosis in post-transplant IgAN were significantly greater than in primary IgAN (P<0.05). The degree of glomerular obsolescence and the severity of interstitial fibrosis correlated with the severity of glomerular lesion in primary IgAN, but not in post-transplant IgAN. In primary IgAN, glomerular diameter significantly correlated with the proportions of glomerular obsolescence, but not in post-transplant IgAN, suggesting that allograft kidneys may be in a hyperfiltration state. Both the blood pressure and the urinary protein excretion significantly improved after ACE-inhibitor treatment (P<0.001). In post-transplant IgAN, histopathological lesions indicative of acute inflammatory insults were suppressed, and glomerular hypertrophy, which may relate to haemodynamic burden such as hyperfiltration, was prominent. Preliminary study of ACE-inhibitor treatment in 10 patients showed favourable effects. A future long-term follow-up study is required to establish the effectiveness of ACE inhibitors in treatment of post-transplant IgAN.

Posttransplant IgA nephropathy: A clinicopathological study in comparison with IgA nephropathy in native kidney

Posttransplant IgA nephropathy: A clinicopathological study in comparison with IgA nephropathy in native kidney