A case of IgA nephropathy after ABO-incompatible living kidney transplantation

A 39-yr-old Japanese man underwent living related kidney transplantation. Because the graft was ABO-incompatible, he was treated with double filtration plasmapheresis before transplantation and his immunosuppressive therapy was stronger than usual. However, immunoglobulin A nephropathy, accompanied by cellular crescents and necrotizing lesions, developed after 18 months. To our knowledge, the association of IgA nephropathy with ABO-incompatible kidney transplantation has not been reported previously.     

Long-term impact of subclinical inflammation diagnosed by protocol biopsy one year after renal transplantation

The long-term impact of subclinical acute rejection (SCAR) on renal graft function remains poorly understood. Furthermore, the interpretation of borderline lesions is difficult and their incidence is variable. The aim of this study was to analyze the characteristics of subclinical inflammation (SCI) in protocol biopsies performed 1-year after renal transplantation. SCI was defined as the presence of borderline lesions or SCAR according to the Banff 2005 classification. The patients included were a subpopulation of the CONCEPT study in which patients were randomized 3 months after transplantation to receive either sirolimus (SRL) or cyclosporine A (CsA) in combination with mycophenolate mofetil. At 1 year, we observed SCI in 37 of the 121 patients observed with an evaluable biopsy. The incidence was more frequent in the SRL group (SRL 45.2% vs. CsA 15.3%). At 30 months , SCI was associated with a significantly lower level of estimated glomerular filtration rate (mean MDRD 50.8 [±13.3] vs. 57.7 [±16.3] mL/min/1.73 m(2) , p = 0.035). In conclusion, SCI at 1-year posttransplantation is associated with worsening renal function and is more frequent in SRL-treated patients. Therefore, evaluation of SCI may be a valuable tool to allow the optimization of immunosuppressive regimens.     

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.     

IgA肾病520例临床病理分析

目的研究IgA肾病(IgAN)的临床和病理特点及其相互关系。方法对1992年11月～2003年6月温州医学院附属第一医院肾内科病理室肾活检诊断的原发性IgAN520例进行临床与病理分型关系的分析。结果520例IgAN临床表现以无症状性尿检异常最常见,占346例(66.5%),其次是慢性肾炎和肾病综合征,分别占77例(14.8%)和66例(12.7%)。病理类型以局灶节段硬化性肾小球肾炎最常见,占186例(35.8%),其次是系膜增生性肾小球肾炎、轻微病变肾小球肾炎和局灶节段增生性肾小球肾炎,分别为116例(22.3%)、104例(20%)和63例(12.1%)。结论IgAN的临床病理表现多样化并具有一定特点。临床表现最常见为无症状性尿检异常,在病理上最常见的是局灶性肾小球病变类型。     

肾移植术后IgA肾病复发

IgA肾病（IgAN）是常见的原发性肾小球肾炎之一,也是导致终末期肾病的重要危险因素。肾移植是IgAN导致的终末期肾病患者的首选治疗方式,但肾移植术后仍存在IgAN复发风险。目前有关肾移植术后IgAN复发的相关研究进展缓慢。IgAN复发的发病机制尚未明确,其病理表现不具备特异性,确诊仍依赖于肾活组织检查,且尚未见有效的复发性IgAN防治方案。本文主要从肾移植术后IgAN复发的发病机制、诊断、危险因素及治疗手段等方面介绍肾移植术后IgAN复发的最新进展,以期为临床肾移植术后IgAN复发的防治提供参考,改善肾移植受者的预后。     

A case of IgA nephropathy associated with silicosis]

A 51-year-old male who had been working as a building wrecker for 20 years, was admitted to our hospital in June 1999 for proteinuria and hematuria examination. He started this work in 1978. Twelve years later, severe coughing and bloody sputum began and he was diagnosed as having silicosis in 1995. Urinalysis on admission showed proteinuria(294 mg/day), microhematuria(20-30/hpf), RBC cast and granular cast. High serum IgA(770 mg/dl) and high serum interleukin-6(IL-6) (3,280 pg/dl) were found. A renal biopsy showed mild mesangial matrix expansion and mesangial cell proliferation with IgA deposition, which was diagnosed as IgA nephropathy. Chest X-rays showed multiple small nodular lesions on both lung fields indicating silicosis. In Nov. 1999, he resigned from his job as a building wrecker because of increasing coughing and bloody sputum associated with body weight loss. Within 3 months after stopping this work, coughing and bloody sputum disappeared and the abnormal urinalysis findings returned to normal. Serum IgA and serum IL-6 data improved to 462 mg/dl and 2.5 pg/dl, respectively. It is suggested that silicon exposure might be related to the pathogenesis of IgA nephropathy in this patient.     

IgA serology in recurrent and non-recurrent IgA nephropathy after renal transplantation

BACKGROUND: This study investigated whether abnormal circulation of macromolecularIgA and IgA with altered glycosylation or electrical chargeplays a role in the recurrence of IgA nephropathy (IgAN) aftertransplantation. STUDY DESIGN: A total of 92 renal transplant patients were enrolled; 52 IgANpatients and 40 with other non-IgAN. The IgAN group included10 patients showing IgA mesangial deposits in the grafted kidneys(recurrent group) and 10 who did not (immunohistochemicallyproven non-recurrent group). In addition another 22 IgAN transplantpatients were clinically free of recurrent disease. METHODS: The analyses included macromolecular IgA (IgAIC) detected bythe conglutinin assay (K), heavy IgA precipitated in 2.5% polyethyleneglycol (PEG), IgA-fibronectin aggregates (IgA/F Aggr), mixedIgA/IgGIC, IgA binding to mesangial matrix components (fibronectin,laminin, type IV collagen) or polycations (poly-L-lysine) andIgA with altered glycosylation (Jacalin-binding assay). RESULTS: After transplantation, IgAN patients displayed significantlyhigher mean levels for each variable measured than non-IgAN(ANOVA, P <0.05). By stepwise regression analysis, the bindingof IgA to fibronectin had the highest coefficient. By comparingdata in recurrent and clinically non-recurrent IgAN, we observedthat two groups could be distinguished by the results of thetwo assays for macromolecular IgA (conglutinin IgAIC and IgA-fibronectinaggregates) and IgA with increased affinity for type IV collagen(P <0.05). When the selected group of immunohistochemicallyproven non-recurrent IgAN was compared to the recurrent one,a statistically significant difference was found only for thebinding of IgA to type IV collagen (P<0.05). Data from thistest were significantly related with proteinuria (P<0.05)and microscopic haematuria (P <0.04). CONCLUSION: Even though the IgA serology of renal transplant IgAN patientsshows peculiar features and recurrent and non-recurrent IgANdiffer in many aspects, the prevalence of positive data in thetwo groups had no predictive value. This suggests that the recurrenceof IgAN is modulated by factors affecting the interaction betweencirculating abnormal IgA and mesangial cells and/or matrix.     

Recurrent IgA nephropathy after renal transplantation and steroid withdrawal

Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis; the reported recurrence rate of IgAN after renal transplantation is as high as 13%‐50%. The impact of immunosuppressive therapy and steroid withdrawal on the risk of recurrence of IgAN is still under debate. We performed a retrospective single‐center study, selecting 123 kidney transplants (rtx) in 120 patients, between January 1995 and December 2012, with IgAN on the native kidney. In 51 of 123 transplants, at least one post‐transplantation biopsy for clinical indication was performed; in 28 of 51 transplants, IgAN recurrence (IgANr) was demonstrated. This group (G1; N = 28) was compared with a group without IgANr (G2; N = 23). In our study, clinically evident IgANr rate was 54.9% (28/51) on biopsied patients. At discharge, the use of the immunosuppressant drugs (tacrolimus, cyclosporine A, mycophenolate mofetil, azathioprine, mTor inhibitors) was not associated with an increased risk of IgANr (P = NS). At discharge, all patients were steroid treated. Neither the use of tacrolimus, mycophenolate mofetil, nor mTor inhibitors (mTori) at biopsy time were associated with IgANr. However, IgANr was significantly higher in patients who experienced steroid withdrawal at any post‐transplantation time (OR 7.7 P = .03). The median time to recurrence after steroid withdrawal was 59 months (min 4.18, max 113.2).     

A case of IgA nephropathy and renal hemosiderosis associated with primary hemochromatosis

IgA nephropathy associated with liver cirrhosis is a common disease, unlike hemochromatosis-associated renal involvement, which is uncommon. A 55-year-old man was admitted to our hospital for the acute deterioration of renal function. Laboratory tests showed extremely high transferrin saturation and serum ferritin level. Furthermore, magnetic resonance imaging revealed low-intensity signals in both T1- and T2-weighted images within the liver, diagnosed as primary hemochromatosis. Renal biopsy showed mesangial IgA deposition with cellular crescent and hemosiderin in both glomerular and tubular epithelial cells. Renal function worsened progressively after admission, and thus steroid pulse therapy was started. Renal dysfunction improved, but the patient died of cerebral hemorrhage. The present case was considered IgA nephropathy and renal hemosiderosis secondary to primary hemochromatosis. To our knowledge, this is the first report that describes the above complications in association with primary hemochromatosis.     

肾移植术后IgA肾病复发危险因素分析

目的 探讨肾移植术后IgA肾病复发的危险因素.方法 选取2008年1月—2019年12月在郑州人民医院器官移植中心接受肾移植的149例原发病为IgA肾病的肾衰竭患者为研究对象.根据程序性肾活检结果,将肾移植后是否有IgAN复发分为复发组(40例)和未复发组(109例).分别记录两组患者的性别、年龄、供体类型、透析时间、...     

A case of superimposed renal lesions of IgA and membranous nephropathy with diabetic nephropathy]

A 64-yr-old man presented with diabetes mellitus, proteinuria, hypertension and moderate renal dysfunction. Renal biopsy revealed diabetic glomerulosclerosis (diffuse lesion), IgA nephropathy and membranous nephropathy (stage 2). Both mesangial IgA and subepithelial IgG deposits were demonstrated by immunofluorescence and immunoelectron microscopy. Electron microscopic studies by immunogold method showed localization of IgA (diameter 15nm gold particles) within mesangial dense deposits and IgG (diameter 15nm gold particles) within subepithelial dense deposits. Overlapping IgA and membranous nephropathy was revealed in the same diabetic glomeruli with functional and biochemical alternations.     

A case of non-Hodgkin's lymphoma presenting with acute renal failure diagnosed by renal biopsy]

We report a case of non-Hodgkin's lymphoma (NHL) presenting with acute renal failure. A-56-year-old male was admitted to our hospital on October, 1997 with fever and renal dysfunction. Physical examination showed no abnormality except for hepatomegaly. Body surface lymphadenopathy was not observed. Computed tomography (CT) of the abdomen showed markedly enlarged kidneys bilaterally and a mass of soft tissue density, which was considered as a swelling lymph node, around the aortic artery. The renal biopsy revealed parenchymal involvement of the NHL cells without normal tubulo-interstitial structure, but the glomeruli were almost intact. Our case rapidly fell into oliguria and acute renal failure, hence needed hemodialysis. After chemotherapy was performed, his renal function gradually improved and the kidney became smaller on subsequent CT. Unfortunately, the patient happened to suffer from methicillin-resistant staphylococcus aureus (MRSA) infection in a neutropenic state and died. Necropsy revealed recovery of the renal interstitium without residual NHL cells. Renal lymphoma without any other organ or nodal involvement is a rare type of NHL, which considered primary renal lymphoma (PRL). However, we believe this case to have been a result of lymphomatous infiltration of the kidneys in disseminated lymphoma.     

Treatment of subclinical rejection diagnosed by protocol biopsy of kidney transplants

BACKGROUND: Subclinical rejection (SCR) causes chronic allograft damage, which may be prevented by antirejection therapy. METHODS: A pilot study of the effect of routine treatment of SCR was performed in 88 recipients of either a kidney (n=59) or combined kidney-pancreas transplant (n=29) undergoing protocol biopsy (PBX) surveillance at 1 and 3 months, using calcineurin inhibitors, mycophenolate mofetil, and corticosteroid therapy. RESULTS: SCR was seen in 46.6% (41/88 patients), as 30 borderline and 11 acute SCR. From 279 transplant biopsies, the prevalence of SCR was 25% (22/88) at 1 month, 10.2% (9/88) at 3 months, and 8.3% (2/24) at 12 months PBX. Treatment included bolus intravenous or oral corticosteroids (n=20) and augmented immunosuppression, either by conversion to tacrolimus (n=6) or increased doses of maintenance therapy (n=14), whereas OKT3 was used in one case of subclinical vascular rejection. Borderline episodes were not treated in 12 patients. In biopsies taken to assess therapeutic response, persistent SCR was present in 46.1% (6/13). Treatment of SCR at 1 month was followed by lower acute Banff sum scores at 3 months PBX (P<0.01-0.0001). Early chronic damage was already present in the 1 month PBX, associated with SCR (P<0.0005 versus without SCR), although by 3 months these differences were lost. Rates of opportunistic infections and BK nephropathy were not increased by SCR treatment. CONCLUSION: Early chronic allograft damage was associated with SCR and therapy appeared to ameliorate further immune-mediated injury, although the efficacy of corticosteroids alone may be inadequate. A controlled trial of therapy for SCR is warranted.     

Recurrence of IgA nephropathy with nephrotic syndrome after kidney transplantation.

Two patients on maintenance hemodialysis after terminal renal failure due to mesangial glomerulonephritis with IgA deposits and the nephrotic syndrome, received cadaver renal allografts. After several years of functioning transplants, both patients developed slowly progressive proteinuria and finally the nephrotic syndrome, 1 of them with renal function deterioration. Renal biopsies revealed findings indicating recurrence of the original disease.     

The clinical course of IgA nephropathy after kidney transplantation and its management

Immunoglobulin (Ig) A nephropathy is one of the most common primary glomerulonephritides worldwide causing end stage renal disease in up to 20–40% of affected patients, nearly two decades post diagnosis. Kidney transplantation is the treatment of choice for patients with renal failure, secondary to glomerular diseases. However, IgA nephropathy has a strong tendency to recur in the graft, and although initially thought to be a benign condition, several reports of graft loss, due to recurrent IgA nephropathy, there have been over the last three decades. Overall graft survival has been significantly improved in kidney transplantation, as a result of reduced incidence of acute rejection, as more potent and more specific immunosuppressive agents are now available in clinical practice. Thus, the rates of IgA nephropathy and other glomerulonephritides recurrence are expected to increase, since graft survival has been improved. However, the reported incidence of IgA nephropathy recurrence in the graft varies substantially across centers, as a consequence of different levels of interest, diverse biopsy policies and differing durations of follow up, of the published studies. Notably, recurrence rates of patients receiving graft biopsies by clinical indication only, ranges from 13% to 50% with graft loss being between 1.3% and 16%. The aim of this review is to underline important pathogenetic insights of IgA nephropathy, describe the clinical course of the disease after kidney transplantation, with emphasis on the incidence of recurrence and the associated risk factors, and finally provide all available options for its management in transplant recipients.     

肝、肾联合移植治疗肾移植术后移植肾功能衰竭并肝硬化一例报告

目的 报告1例移植肾功能丧失并肝炎后肝硬化者再次接受肝，肾联合移植。方法 给1例肾移植术后移植肾功能丧失并肝炎皇肝硬化患者先行失功能移植肾的切除。针对患者群体反应抗体（PRA）较高（66%），切除术后第5d开始每天给予环磷酰胺50mg。连服3个半月，并行血浆置换2次。PRA降至23%。3个半月后施行一期肝，肾联合移植，肝移植采用原位背驮式肝移植术式。供肾移植于左髂窝，肝血流开放后每间隔30min检测PRA1次，术后免疫抑制治疗采用他克莫司（FK506）。霉酚酸酯（MMF）和激素。结果 术后移植肝，肾立即发挥功能。肝动，静脉血流开放后，，PRA由23%降至5%。并维持在8%左右。术后乙型肝炎病毒表面抗原转阴，丙型肝炎病毒抗体阴性，随访3个月，移植肝，肾功能正常。结论 对于移植肾功能丧失，且合并有肝硬化，肝功能不良者，再次施行肝，肾联合移植是可行的。     

Sevelamer and pharmacokinetics of cyclosporin A after kidney transplantation

Sir, In their interesting article, Pieper et al. analysed prospectivelythe effect of sevelamer on the pharmacokinetics of cyclosporin(CsA) and mycophenolate mofetil (MMF) in kidney