Renal transplantation in patients with primary immunoglobulin A nephropathy.

BACKGROUND: Opinions on the clinical course and outcome of renal transplantation in patients with primary immunoglobulin A nephropathy (IgAN) have been controversial. METHODS: We conducted a retrospective single-centre study on 542 kidney transplant recipients over the period 1984-2001. Long-term outcome and factors affecting recurrence in recipients with primary IgAN were analysed. RESULTS: Seventy-five patients (13.8%) had biopsy-proven IgAN as the cause of renal failure, and their mean duration of follow-up after transplantation was 100 +/- 5.8 months. Fourteen (18.7%) of the 75 patients had biopsy-proven recurrent IgAN, diagnosed at 67.7 +/- 11 months after transplantation. The risk of recurrence was not associated with HLA DR4 or B35. Graft failure occurred in five (35.7%) of the 14 patients: three due to IgAN and two due to chronic rejection. Three (4.9%) of the 61 patients without recurrent IgAN had graft failure, all due to chronic rejection. Graft survival was similar between living-related and cadaveric/living-unrelated patients (12-year graft survival, 88 and 72%, respectively, P = 0.616). Renal allograft survival within the first 12 years was better in patients with primary IgAN compared with those with other primary diseases (80 vs 51%, P = 0.001). Thereafter, IgAN patients showed an inferior graft survival (74 vs 97% in non-IgAN patients, P = 0.001). CONCLUSIONS: Our data suggested that around one-fifth of patients with primary IgAN developed recurrence by 5 years after transplantation. Recurrent IgA nephropathy in allografts runs an indolent course with favourable outcome in the first 12 years. However, the contribution of recurrent disease to graft loss becomes more significant on long-term follow up.     

Characterization of a large Lebanese family segregating IgA nephropathy.

BACKGROUND: Familial aggregation of IgA nephropathy (IgAN) suggests that genetic factors contribute to the development of this trait. Because clinical manifestations in IgAN families are often limited to episodic haematuria, large kindreds tractable to linkage analysis have been difficult to identify. METHODS: We identified a large Lebanese-Druze kindred ascertained via an index case with biopsy-documented IgAN. We performed systematic screening of 38 family members and tested linkage to reported IgAN loci. RESULTS: Screening of this family identified 16 affected individuals, including 2 individuals with biopsy-documented IgAN and 14 with chronic renal failure or abnormal urinalyses on at least three separate occasions. This kindred spanned five generations and contained five consanguineous unions. Multigenerational inheritance suggested that autosomal dominant inheritance was most likely. Phenotypic manifestations among affected individuals varied from isolated haematuria to advanced renal failure necessitating transplantation; one instance of IgAN recurrence after transplantation was also documented. Older age was associated with greater severity of disease and higher incidence of renal failure. Parametric and non-parametric analyses with 33 microsatellite markers did not reveal any evidence of linkage to reported IgAN loci on chromosomes 6q22-23, 2q36 and 4q22-31. CONCLUSIONS: We describe one of the largest multigenerational IgAN kindreds reported to date. The high incidence of renal failure among older generations suggests a significant risk of progression to renal failure. We found no evidence of linkage to known loci, suggesting that familial IgAN encompasses multiple subtypes that will require distinction based on genetic or biomarker data.     

High incidence of urinary tract malignancy among patients with haematuria following kidney transplantation in Taiwan

Haematuria is a common complication following kidney transplantation, but few studies describing post-transplant haematuria have been published. Herein, we investigated the incidence and etiologies of persistent hematuria with kidney transplant patients in Taiwan. The medical records of 189 kidney transplant recipients with functioning grafts were retrospectively reviewed. Any episode of haematuria during routine follow-up was recorded and evaluated. The patient characteristics, possible causes of haematuria and consequent managements were reviewed. Among the 189 patients, 44 patients (23.3%) experienced 45 episodes of persistent haematuria during routine monthly follow-up at our transplant clinic. Thirty-two episodes (71%) were microscopic haematuria and 13 (29%) were gross haematuria. The most prevalent etiology explained for the persistent haematuria in our series was urologic malignancy (19 patients, 42.2%), followed by urinary tract infections (24.5%) and unexplained reasons (17.8%). Furthermore, those patients with persistent haematuria caused by urologic malignancy were also associated with significantly longer duration following transplantation and worse graft function. Haematuria is frequently seen in kidney transplant recipients and the most prevalent cause in our series is urologic malignancy. Those patients were also associated with significantly poorer graft function; however, the mechanism is still unclear.     

Clinicopathological features of paediatric renal biopsies in Shanghai over a 31 year period

Aim: To identify the variations in paediatric renal biopsy pathology and clinicopathological features during the past 31 years. Methods: A retrospective analysis of paediatric renal biopsies performed at a single institution in Shanghai from January 1979 to December 2009 was conducted. Results: The major pathologies included minor glomerular abnormalities (MGA, 26.1%), IgA nephropathy (IgAN, 17%) and mesangial proliferative glomerulonephritis (MsPGN) without IgA deposition (11.3%). The major clinical presentations included nephrotic syndrome (NS, 39.4%), haematuria with proteinuria (24.4%) and persistent microscopic haematuria (15.1%). MGA accounted for 46.9% of the cases in NS. IgAN and HSN accounted for 24% and 28.9% of patients with concomitant haematuria and proteinuria, and thin basement membrane nephropathy accounted for 51.2% of cases with persistent microscopic haematuria. The frequency of IgAN (78.6%) was much higher than that of TBMN (29.0%) in patients with persistent microscopic haematuria with abnormal urinary albumin. Conclusion: Minor glomerular abnormalities and IgAN were the major renal diseases in our study population, and the focus of our paediatric nephrologists. The high proportion of TBMN suggested that there should be limited use of renal biopsy for patients with persistent microscopic haematuria and renal biopsy should be performed in the presence of proteinuria or abnormal levels of urinary albumin.     

Impact of recurrent disease and chronic allograft nephropathy on the long‐term allograft outcome in patients with IgA nephropathy

Although recurrent IgA nephropathy (IgAN) may lead to graft dysfunction after transplantation, donation from living related donor (LRD), with whom the risk of recurrence may be higher, is not a contraindication. Herein, we evaluated the natural history of allograft in recipients with IgAN and the risk factors influencing long‐term allograft outcome. Recurrence rate and graft survival were assessed retrospectively in 221 IgAN patients, including transplants from 139 LRDs (62.9%). Ten‐year cumulative rate for recurrent IgAN was 30.8%. The operation at younger age and donation from LRD were significant for the recurrence by multivariate analysis. Ten‐year graft survival was affected by recurrent IgAN (61.0% in recurrent IgAN group vs. 85.1% in nonrecurrent, P < 0.01). However, transplants from LRDs did not show poor graft survival when compared with those from other types of donors. In transplants from LRDs, the incidence of chronic allograft nephropathy (CAN) was lower than those in grafts from deceased donors (10.8% vs. 19.5%, P < 0.05). When CAN was considered in addition to recurrence, the variance of graft survival was affected significantly by the development of CAN than by the recurrence. These results suggest that the detection and adequate management of CAN could improve graft outcome in transplant recipients with IgAN.     

Risk factors for graft loss in patients with recurrent IGA nephropathy after renal transplantation

BACKGROUND: The recurrence rate of IgA nephropathy (IgAN) in transplanted kidneys has been reported to be >50%. Although recurrent IgAN has a benign clinical course, recent data suggest that it leads to graft loss in a substantial number of patients. METHODS: We performed a retrospective single-center analysis of 34 renal transplant recipients, with biopsy-proven IgAN as the cause of end-stage renal failure. RESULTS: Renal allograft biopsies were performed in 30 patients, of whom 24 did and 6 did not have biopsy-confirmed recurrent transplant IgAN. Recurrent transplant IgAN was more often detected in men and at later timepoints after post-transplantation. Four patients with recurrent transplant IgAN progressed to graft failure. Progression to graft failure was associated with worsened renal function, higher systolic blood pressure, and the lack of presenation of angiotensin-converting enzyme inhibitors (ACEs) at the time of allograft biopsy. Immunologic factors such as frequency of acute rejection, HLA typing, and immunosuppression did not show a relation to recurrence or graft loss. CONCLUSIONS: Recurrent transplant IgAN increased with long-term graft survival and risk factors for graft loss due to recurrent IgAN were similar to those among IgAN in native kidneys.     

Recurrence of IgA nephropathy after kidney transplantation in steroid continuation versus early steroid‐withdrawal regimens: a retrospective analysis of the UNOS/OPTN database

In the past 20 years, there has been an increase in use of steroid‐withdrawal regimens in kidney transplantation. However, steroid withdrawal may be associated with an increased risk of recurrent IgA nephropathy (IgAN). Using United Network of (Organ Sharing/Organ Procurement and Transplantation Network) UNOS/OPTN data, we analyzed adult patients with end‐stage renal disease (ESRD) due to IgAN who received their first kidney transplant between 2000 and 2014. For the primary outcome, we used a competing risk analysis to compare the cumulative incidence of graft loss due to IgAN recurrence between early steroid‐withdrawal (ESW) and steroid continuation groups. The secondary outcomes were patient survival and death‐censored graft survival (DCGS). A total of 9690 recipients were included (2831 in ESW group and 6859 in steroid continuation group). In total, 1238 recipients experienced graft loss, of which 191 (15.43%) were due to IgAN recurrence. In multivariable analysis, steroid use was associated with a decreased risk of recurrence (subdistribution hazard ratio 0.666, 95% CI 0.482–0.921; P = 0.014). Patient survival and DCGS were not different between the two groups. In the USA, ESW in transplant for ESRD due to IgAN is associated with a higher risk of graft loss due to disease recurrence. Future prospective studies are warranted to further address which patients with IgAN would benefit from steroid continuation.     

Polyomavirus nephropathy after renal transplantation: a single centre experience

BACKGROUND: Polyomavirus associated nephropathy (PVN) in renal transplant recipients has been observed with increasing frequency recently and has emerged as a cause of allograft failure linked to highly potent new immunosuppressive regimens containing tacrolimus or mycophenolate mofetil (MMF). METHODS: Polyomavirus associated nephropathy was identified in nine out of 182 patients who received renal transplantation between October 1998 and July 2003. PVN was confirmed by allograft biopsy. The clinical records of these nine patients were reviewed, as were all of the allograft biopsies. Electron microscopy was performed in all nine cases. After the diagnosis of PVN, maintenance immunosuppression was reduced. The clinical course and outcome of the PVN patients were reviewed in relation to manipulation of immunosuppressive agents. RESULTS: There were nine cases of PVN in renal transplant recipients and the incidence of PVN was 4.9%. All patients with PVN were under triple immunosuppression comprising tacrolimus and MMF. The mean time to a diagnosis of PVN was 7.8 months after transplantation. Three of the nine patients received antirejection therapy prior to PVN. Seven out of nine PVN patients presenting acute allograft dysfunction were initially treated with high-dose intravenous steroid pulse or OKT3 before reduction of the immunosuppression. After reduction of the immunosuppression, seven patients stabilized their renal function. Two (22%) lost their grafts due to persistent PVN and chronic rejection. Two (22%) patients later developed acute rejection after reduction of the immunosuppression. CONCLUSION: PVN can cause allograft dysfunction and graft loss. Renal allograft recipients who are at risk of PVN should be routinely screened with urine cytology and quantitative measurements of viral load in the blood, particularly patients who had graft dysfunction. Early diagnosis and judicious alteration of immunosuppressive agents might permit a superior prognosis and reduce the graft loss from PVN in renal transplant recipients.     

Live donor renal allograft in end-stage renal failure patients from immunoglobulin A nephropathy

BACKGROUND: The purpose of this study was to attempt to resolve two important issues, i.e. to determine (1) whether the course of recurrent immunoglobulin A nephropathy (IgAN) is benign, and (2) whether it is advisable to use a related donor. METHODS: We evaluated the long-term outcome, in terms of recurrence and graft survival, after live related or unrelated donor renal transplantation, and assessed the validity of the use of related donors in 90 grafts in 89 IgAN patients. RESULTS: Ten-year graft survival for IgAN patients was 66%, compared with 84% for 107 reference recipients who had other kinds of glomerulonephritis (GN), and with 69% in 90 other recipients who had non-GN renal failure (P=0.27). In 43 grafts, 54 event graft biopsies were performed, documenting the presence of mesangial IgA deposits in 19 of those grafts. In eight grafts, lesions were accompanied by chronic rejection (CR). Ten-year cumulative recurrence was 44%. Ten grafts were lost: by CR (n=3) or acute rejection (n=1) in 24 recurrence-free recipients, by CR (n=2) or recurrence (n=2) in 19 recurrent patients, and by patient death (n=2) in 46 patients devoid of graft biopsy. We found no difference in 10-year graft survival between the recurrent and recurrence-free patients (63% vs. 74%, P=0.98), or the proportion of related donors (68% vs. 83%, P=0.25). The presence or matching of HLA B12, B35, or DR4 did not affect the recurrence. CONCLUSIONS: Recurrence increased to 44% with longer follow-up, but this did not limit the graft outcome. Recurrence was not affected by the kind of live donor. We conclude that live related or unrelated kidneys should be offered to IgAN patients.     

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

BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.     

Does angiotensin blockade influence graft outcome in renal transplant recipients with IgA nephropathy?

BACKGROUND: IgA nephropathy (IgAN) is a frequent cause of end-stage renal disease (ESRD) and recurrent disease causes deterioration and graft loss in transplant recipients. No definitive management is known to reduce the risk or severity of recurrent IgAN, and the evidence to support the use of renin-angiotensin system blockade in such patients is limited. METHODS: All 1137 renal transplants performed at the Belfast City Hospital over a 27-year period were reviewed. A total of 75 patients with ESRD due to biopsy-proven IgAN were identified; 39 of them had been prescribed an angiotensin-converting enzyme inhibitor (ACEi) or angiotensin-II type I receptor blocker (ARB). RESULTS: The two groups were well-matched in terms of demographic details, immunosuppressive regimens and duration of follow-up (median 65 months, range 18-261 months). The 5- and 10-year graft survivals were higher in those prescribed ACEi/ARB therapy compared with those who were not, although these differences did not reach statistical significance (92.9 vs 86.5%; P = 0.34 and 81.6 vs 72.7%; P = 0.32, respectively). These results were similar when censored for death with a functioning graft. In the group where an ACEi/ARB was not prescribed, all four with biopsy-proven recurrent IgAN progressed to ESRD, compared with three out of nine in the group treated with an ACEi/ARB. CONCLUSIONS: In transplant recipients with ESRD due to biopsy-proven IgAN, a trend towards improved 5-year and 10-year graft survival was seen in those prescribed ACEi/ARBs. All with recurrent IgAN in their grafts who were not treated with ACEi/ARB therapy progressed again to ESRD.     

Recurrence of IgA nephropathy among renal allograft recipients from living donors is greater among those with zero HLA mismatches

BACKGROUND: Risk factors contributing to recurrence of IgA nephropathy (IgAN) after transplantation are unclear. Some (but not all) series have suggested greater degrees of human leukocyte antigen (HLA) matching play a role. METHODS: Using registry data including all kidney transplants performed in Australia and New Zealand between 1987 and 2004 we examined IgAN recurrence among living donors with zero HLA-mismatches. RESULTS: Of 1354 grafts performed in recipients with IgAN, live donors (LDs) accounted for 488 including 108 with zero HLA-mismatches. Biopsy-proven IgAN recurrence was reported for 110 (7%) of grafts overall, but 17% of those who received zero HLA-mismatched LD grafts (HR for recurrence free graft survival 2.7 [95% CI 1.5-5.1], P=0.001). There was no significant difference in recurrence rates between zero and >or=1 HLA-mismatched grafts from cadaveric donors (CDs). Recurrence of IgAN was associated with worse graft survival, more so among LD recipients (HR 8.5 [4.8-15.2], P<0.001) than CD recipients (HR 4.5 [2.6-7.5], P<0.001). However, there was no difference in graft survival between zero and >or=1 HLA mismatched LD recipients whose native disease was IgAN. In contrast, zero HLA mismatched recipients of kidneys with other primary renal disease enjoyed a graft survival advantage. No difference in recurrence rates was seen among those with HLA B12, B35 or DR4. CONCLUSIONS: The increased rates of IgAN-related graft loss among zero HLA-mismatched LD recipients counterbalance the advantage normally seen among zero HLA-mismatched recipients. However, since graft survivals are similar, there is no reason to avoid donor-recipient pairs with zero HLA-mismatches in this setting.     

Steroids and Recurrent IgA Nephropathy After Kidney Transplantation

We studied the impact of steroid use on kidney graft loss due to recurrent IgA nephropathy (IgAN). We used data from the Australia and New Zealand Dialysis and Transplant Registry (ANZDATA) to conduct a survival analysis of adult recipients of a first kidney transplant for IgAN who received a graft between 1988 and 2007. Predictors of graft loss due to recurrent IgAN were analyzed in a competing risk survival analysis with steroid use modeled as a time‐varying covariate. Fifteen hundred twenty‐one recipients with kidney failure due to biopsy‐proven IgAN received a first kidney transplant during the study period. Four hundred and twenty‐eight recipients experienced graft loss, of which 54 losses (12.6%) were attributed to recurrent IgAN. The overall 10‐year cumulative incidence of graft loss from recurrent IgAN was 4.3% (95% CI 3.1–5.8). Prevalence of steroid use was 92% at baseline, 84% at 1 year and 64% at 5 years. After adjusting for age, sex, HLA mismatch, dialysis duration and transplant era, steroid use was strongly associated with a reduced risk of recurrence (subhazard ratio 0.50, 95% CI 0.30–0.84). These results suggest that the risk of graft loss from recurrent disease should be considered when tailoring immunosuppression for patients with IgAN.     

Is microscopic haematuria a urological emergency?

OBJECTIVE: To determine the prevalence of urological pathology in a retrospective and prospective study of patients with microscopic haematuria attending a haematuria clinic. PATIENTS AND METHODS: Between January 1998 and May 2001, 781 patients attended the haematuria clinic; of these, 368 (47%; median age 60 years, range 18-90) had a history of microscopic haematuria, as detected by urine dipstick testing. These patients were investigated by urine culture and cytology, renal ultrasonography, intravenous urography (IVU), flexible cystoscopy, urea and electrolyte analysis, and assay of prostate specific antigen (PSA) where appropriate. RESULTS: Urine cytology showed no malignant cells in any patient with a history of microscopic haematuria. In 143 patients (39%), urine cytology showed no red blood cells and all other investigations were normal. Of the remaining 225 patients, IVU showed a tumour in one (bladder), renal stones in 15 and an enlarged prostate in two. Renal ultrasonography detected no additional pathology. Urine analysis showed one urinary tract infection. Flexible cystoscopy detected five patients with a bladder tumour (all G1pTa), two urethral strictures, five bladder stones and enlarged prostates, six enlarged prostates only, and nine red patches in the bladder, showing one patient with carcinoma in situ. No PSA levels were suggestive of prostate cancer. CONCLUSION: Patients with dipstick-positive haematuria should be re-assessed by urine microscopy before referral. As only 1.4% of patients had a malignant pathology (all noninvasive), microscopic haematuria should be regarded as a separate entity from macroscopic haematuria, and such patients do not need to be referred urgently.     

Hepatic dysfunction in kidney transplant recipients: prevalence and impact on graft and patient survival

Background Liver disease has emerged as an important cause of morbidity and mortality in renal transplant recipients. Liver insufficiency is the cause of death in up to 28% of long-term survivors after renal transplantation. The aim of this work was to evaluate the prevalence and causes of hepatic dysfunction in renal transplant recipients in Egypt, and its impact on both renal graft function and patient survival. Methods This study comprised 447 kidney transplant recipients who received their grafts between January 1999 and December 2003 at Mansoura Urology and Nephrology Center. Among these recipients, 104 patients showed persistent hepatic dysfunction, while the remaining 343 had normal liver function or transient hepatic dysfunction of less than 6 months’ duration. Results We found that the prevalence of persistent hepatic dysfunction in our recipients was 23.3%. Infections such as hepatitis C virus (HCV;, with longer dialysis duration and blood transfusion as risk factors), HBV, and cytomegalovirus (CMV), were the main causes of persistent hepatic dysfunction. Drugs (e.g., the sirolimus and tacrolimus; cyclosporine; and azathioprine) were also associated with hepatic dysfunction. We did not find a significant impact of hepatic dysfunction on either patient or graft survival. Conclusions Viral infections–especially HCV and CMV–were more prevalent in the group of patients with persistent hepatic dysfunction, with duration of dialysis as an important risk factor for HCV infection. Dose-dependent cyclosporine-induced hepatic dysfunction was observed early post-transplant. Neither tacrolimus- nor sirolimus-associated hepatic dysfunction was dose-dependent. Hepatic dysfunction had no significant impact on either patient or graft survival; however, this finding may be due to the relatively short duration of follow up.     

Polyomavirus BK and JC infections in well matched Finnish kidney transplant recipients

Since 2003, only one case of polyomavirus-associated nephropathy (PVAN) has occurred in our clinic despite screening protocols. In contrast to BK virus, the role of JC virus in PVAN is unclear. We studied the incidence and impact of polyomavirus BK and JC viruria and PVAN in well-matched Finnish kidney transplant recipients. All Helsinki University Hospital kidney transplant recipients between 2004 and 2006 were prospectively followed ( n  = 163). Patients with a 12-month protocol-biopsy taken and polyomavirus urinary secretion screened by PCR were studied ( n  = 68). Cyclosporine-based triple-drug immunosuppression was usually used. BK or JC viruria was detected in 18 (27%) and 14 (21%) patients after transplantation respectively. Persistent BK or JC viruria was found in 5 (7%) and 9 (13%) patients. No cases of PVAN were diagnosed from protocol biopsies or from biopsies taken for clinical indications. A positive BK or JC viruria or persistent viruria was not associated with reduced renal function at follow-up, histopathologic changes in 12-month protocol biopsies, or acute rejections. The incidence of BK and JC viruria was similar to what has been previously reported, but no cases of polyomavirus-associated nephropathy were seen in our well-matched kidney transplant population.     

Recurrent IgA nephropathy after renal transplantation

Recurrence of the original disease is now the third most frequent cause of allograft loss at 10 years after transplantation in patients with underlying glomerulonephritis. IgA nephropathy (IgAN), the most common type of glomerulonephritis, histologically recurs in up to 60% of the patients. Initially considered to be a relatively benign phenomenon, several studies, which included a total of almost 1200 patients with underlying IgAN, have now established that after a mean follow up of 5 years, approximately 13% of the patients will exhibit some recurrence-related renal graft dysfunction and approximately 5% will have lost their graft as a result of recurrent IgAN. The only established predictor of graft loss is the time elapsed since renal transplantation. The risk of recurrence-associated graft loss increases to approximately 25% if a prior graft has already been lost as a result of recurrent IgAN. Whether living, related donor kidneys are at higher risk for recurrence is controversial. Despite all these issues, graft survival in patients with underlying IgAN compared with patients with other renal diseases is excellent. In patients with recurrent IgAN, no specific therapy other than optimal supportive care has been established.     

Efficacy of tonsillectomy for patients with recurrence of IgA nephropathy after kidney transplantation

Abstract:  From January 2007, we started to perform the tonsillectomy for every patient with recurrent IgA nephropathy (IgAN) after kidney transplantation. Up to September 2008, four recipients with primary IgAN had biopsy-proven recurrent IgAN. They had also progressive hematuria or proteinuria from on the average 14.3 months after transplantation. Then their specimens diagnosed as recurrent IgAN were collected and they underwent tonsillectomies on the average 52.3 months after transplantation. Abnormal urinary findings of all patients favorably improved after tonsillectomy. All cases but one had mild renal injury, where the severity of glomerular lesions, glomerular hypercellularity, segmental lesions, and sclerosis was mild, and no deteriorated serum creatinine (SCr) before their tonsillectomies. Even the case with exacerbated SCr and severe renal injury, where the severity of glomerular lesions was severe, had her urinary findings ameliorated promptly after tonsillectomy likely as others. At present, they have almost no symptoms after tonsillectomy and no remarkable change of SCr level compared with before and after tonsillectomy and maintain ameliorated urinary findings continuously. Tonsillectomy had possibility to be a favorable treatment of hematuria or proteinuria in recurrent IgAN recipients.     

IgA Nephropathy in Renal Allografts: Increased Frequency in Native American Patients

We investigated the frequency of IgA nephropathy in transplanted kidneys in 2 ethnic groups in New Mexico (USA). A total of 80 renal graft biopsies were obtained from 66 patients when clinically indicated for the differential diagnosis of graft dysfunction. Glomerulonephritis was present in 16 patients, in biopsies obtained after the first posttransplantation month. The frequency of IgAN in allografts was not the same in Native Americans and in Caucasians: Nondonor IgAN was observed in 4/18 biopsies from Native American patients (22.2%) but only in 4/48 biopsies from Caucasians (8.3%) (p < 0.01). This study demonstrates that in New Mexico the frequency of IgAN in transplanted kidneys in Native American patients is 2.7 times higher than in Caucasian graft recipients.     

Clinical effectiveness of steroid pulse therapy combined with tonsillectomy in patients with immunoglobulin A nephropathy presenting glomerular haematuria and minimal proteinuria

Aim: The effectiveness of steroid pulse therapy combined with tonsillectomy (ST) has been shown in immunoglobulin A nephropathy (IgAN) patients with moderate or severe urinary abnormalities. The present study aimed to clarify whether the effectiveness may be extrapolated to IgAN with minor urinary abnormalities, and whether the effectiveness may depend on the histological severity with minor urinary abnormalities. Methods: Data on 388 IgAN patients diagnosed by renal biopsies between 1987 and 2000 in Sendai Shakaihoken Hospital, who presented glomerular haematuria and minimal proteinuria (≤0.5 g/day) at baseline, were analyzed. Cox regression was used to examine associations between baseline use of ST and subsequent clinical remission (CR), defined as negative proteinuria by dipstick and urinary erythrocytes of less than 1/high‐power field. The instrumental variable method was also used to overcome confounding by treatment indication. Results: During a median follow up of 24 months, we observed 170 CR cases. Patients receiving ST were younger and showed a better case‐mix profile. Patients with ST had a significantly higher rate of CR than patients without tonsillectomy or steroid pulse in an unadjusted (hazard ratio (HR) = 5.51, 95% confidence interval (CI) = 3.33–9.12, P < 0.001) or adjusted Cox model (HR = 4.65, 95% CI = 2.43–8.88, P < 0.001). Less severe histological findings were substantially associated with higher CR rate in ST group. Adjusting for confounding by treatment indication showed an attenuated but still significant effect of ST (HR = 3.10, 95% CI = 2.02–4.77, P < 0.001). Conclusion: ST significantly increased the probability of CR in IgAN patients with glomerular haematuria and minimal proteinuria, and it was more effective in those with less severe histological findings.