Kidney Transplantation in C3 Glomerulopathy: A Case Series.

RATIONALE & OBJECTIVE: C3 glomerulopathy (C3G), a form of glomerulonephritis associated with dysregulation of the alternative complement pathway, occurs either as dense deposit disease (DDD) or C3 glomerulonephritis (C3GN). Few studies have reported outcomes of patients with C3G after transplantation since its formal classification and the advent of complement-targeting therapies such as eculizumab. STUDY DESIGN: Case series of C3G. SETTING & PARTICIPANTS: We reviewed laboratory testing, native and allograft biopsy reports, and clinical charts of the 19 patients (12, C3GN; and 7, DDD) from our C3G registry who underwent transplantation between 1999 and 2016. RESULTS: During a median follow-up of 76 months, 16 patients had recurrent disease (10 of 12, C3GN; and 6 of 7, DDD), with median time to recurrence of 14 months in C3GN versus 15 months in DDD. Graft failure was more frequent in patients with DDD (6 of 7) than in patients with C3GN (3 of 12), occurred at a median time of 42 months posttransplantation, and was attributed to recurrent disease in half the failures. A rare genetic variant or autoantibody associated with alternative complement pathway abnormalities was detected in 9 of 10 screened patients. Treatment of 7 patients (8 allografts) with eculizumab was associated with variable clinical outcomes. LIMITATIONS: Incomplete testing for complement pathway abnormalities and genetic defects, incomplete records of HLA antigen matching, lack of centralized biopsy review, and limited sample size. CONCLUSIONS: In a case series of C3G transplant recipients, the proportion of disease recurrence was high in both C3GN and DDD, although graft loss appeared to occur more frequently in DDD. In a small subset of study patients, eculizumab therapy was not consistently followed by salutary outcomes.

A long history of dense deposit disease.

BACKGROUND: Dense Deposit Disease is a rare condition affecting the Bruch's membrane and the glomerular basement membrane. We report the progression of the ocular manifestations over a 30 year follow up period, longer than any previous report. CASE PRESENTATION: A 44 year old male presented with pigmentary changes at the macula noted by his optician. Best corrected visual acuity at presentation was good in both eyes. Fundoscopy showed pigmentary changes and drusen, and investigation using intravenous fundus fluorescein angiography did not demonstrate any choroidal neovascular membrane. The patient subsequently developed renal failure and received a dual renal transplant. The transplanted kidneys also failed over the coming year. The patient's vision gradually deteriorated and comparison between the images in 2010 and 1985 demonstrated a clear progression of the macula changes. Optical coherence tomography showed multiple subretinal hyper reflective drusenoid deposits. These deposits were also noted to be autofluorescent on blue auto-fluorescence. The young age at presentation of drusen, combined with the history of recurrent kidney failure and progression of subretinal deposits led to a diagnosis of dense deposit disease. CONCLUSIONS: Dense deposit disease is a rare condition affecting Bruch's membrane, but should be considered in the differential diagnosis of any patient under the age of 50 years presenting with drusen.

A case of recurrent proliferative glomerulonephritis with monoclonal IgG deposits or de novo C3 glomerulonephritis after kidney transplantation.

Proliferative glomerulonephritis with monoclonal immunoglobulin (Ig)G deposits (PGNMID) is a rare disease with a treatment that is not well established. Several cases of recurrent PGNMID after kidney transplantation have been documented, but almost all cases reported symptoms such as elevated serum creatinine and/or urinary protein levels; subsequently, episode biopsies were performed and a diagnosis was made. This is the case of a 27-year-old man who underwent living-donor kidney transplantation. The aetiology of renal failure was membranoproliferative glomerulonephritis type III, which had been diagnosed at the age of 9 years. Protocol biopsy performed on postoperative day 62 revealed isolated granular C3 deposits in the glomerular capillaries and mesangium. We reviewed the native kidney biopsy and confirmed IgG3 deposition alone, with strong glomerular staining for lambda light chains and negative staining for kappa light chains. Accordingly, we re-diagnosed the aetiology of his renal failure as PGNMID and suspected recurrent PGNMID in the early stage; therefore, we administered plasma exchange therapy. Thereafter, protocol biopsies were performed twice, which revealed persistent isolated C3 deposition; therefore, we made a diagnosis of recurrent PGNMID or C3 glomerulonephritis. Currently, the patient has normal renal function, with negative urine findings for >1 year. Here, we present the histological findings of consecutive allograft biopsies performed in this patient.

Clinicopathological analysis of proliferative glomerulonephritis with monoclonal IgG deposits in 5 renal allografts.

BACKGROUND: We present a case series of 5 patients with proliferative glomerulonephritis with monoclonal IgG deposits (PGNMID) of renal allografts to better define its natural history, presenting characteristics, pathological features and treatment outcome. RESULTS: These 5 patients presented 5 to 19 months post-kidney transplantation for complaints of serum creatinine (Scr) elevation, proteinuria or hematuria. Membranoproliferative glomerulonephritis (MPGN) pattern was the most frequently observed histological manifestation. Immunofluorescence showed monoclonal IgG3κin 3 patients and IgG3λ in the other 2 cases. Immunofluorescence staining helped to establish PGNMID in the absence of conspicuous microscopic changes in one case. Rituximab and bortezomib were effective in alleviating proteinuria in all 4 treated patients and decreasing Scr in 2 cases. Plasmapheresis treatment in another patient was not effective in preventing Scr elevation. At last-follow-up, 2 patients were in dialysis and 2 had improved kidney function with almost normal Scr and no proteinuria. The remaining one patient died of pulmonary infections. CONCLUSIONS: We conclude that PGNMID occurs early after kidney transplant. PGNMID should be included in the differential diagnoses of recurrent MPGN in renal allografts. Rituximab and bortezomib are helpful to decrease proteinuria and Scr in a subset of patients. Larger studies are needed to conclusively establish best treatment strategies for PGNMID in renal allografts.

Membranoproliferative glomerulonephritis recurrence after kidney transplantation: using the new classification.

BACKGROUND: Membranoproliferative glomerulonephritis (MPGN) is an uncommon glomerular disorder that may lead to end stage renal disease (ESRD). With new understanding of the disease pathogenesis, the classical classification as MPGN types I, II, III has changed. Data on post-transplant MPGN, in particular with the newly refined classification, is limited. We present our center's experience of MPGN after kidney transplantation using the new classification. METHODS: This is a retrospective study of 34 patients with ESRD due to MPGN who received 40 kidney transplants between 1994 and 2014. We reviewed the available biopsies' data using the new classification. We assessed post transplantation recurrence rate, risk factors of recurrence, the response to therapy and allografts' survival. RESULTS: Median time of follow up was 5.3 years (range 0.5-14 years). Using the new classification, we found that pre-transplant MPGN disease was due to immune complex-mediated glomerulonephritis (ICGN) in 89 % of cases and complement-mediated glomerulonephritis (CGN) in 11 %. Recurrence was detected in 18 transplants (45 %). Living related allografts (P = 0.045), preemptive transplantations (P = 0.018), low complement level (P = 0.006), and the presence of monoclonal gammopathy (P = 0.010) were associated with higher recurrence rate in ICGN cases. Half of the patients with recurrence lost their allografts. The use of ACEi/ARB was associated with a trend toward less allograft loss. CONCLUSIONS: MPGN recurs at a high rate after kidney transplantation. The risk of MPGN recurrence increases with preemptive transplantation, living related donation, low complement level, and the presence of monoclonal gammopathy. Recurrence of MPGN leads to allograft failure in half of the cases.

Clinical findings, pathology, and outcomes of C3GN after kidney transplantation.

C3 glomerulonephritis (C3GN) results from abnormalities in the alternative pathway of complement, and it is characterized by deposition of C3 with absent or scant Ig deposition. In many patients, C3GN progresses to ESRD. The clinical features, pathology, and outcomes of patients with C3GN receiving kidney transplantation are unknown. Between 1996 and 2010, we identified 21 patients at our institution who received a kidney transplant because of ESRD from C3GN. The median age at the time of initial diagnosis of C3GN at kidney biopsy was 20.8 years. The median time from native kidney biopsy to dialysis or transplantation was 42.3 months. Of 21 patients, 14 (66.7%) patients developed recurrent C3GN in the allograft. The median time to recurrence of disease was 28 months. Graft failure occurred in 50% of patients with recurrent C3GN, with a median time of 77 months to graft failure post-transplantation. The remaining 50% of patients had functioning grafts, with a median follow-up of 73.9 months. The majority of patients had hematuria and proteinuria at time of recurrence. Three (21%) patients were positive for monoclonal gammopathy and had a faster rate of recurrence and graft loss. Kidney biopsy at the time of recurrence showed mesangial proliferative GN in eight patients and membranoproliferative GN in six patients. All allograft kidney biopsies showed bright C3 staining (2-3+), with six biopsies also showing trace/1+ staining for IgM and/or IgG. To summarize, C3GN recurs in 66.7% of patients, and one half of the patients experience graft failure caused by recurrence.

Recurrent Membranoproliferative Glomerulonephritis After Kidney Transplantation: Risk Factors and Impact on Graft Survival.

BACKGROUND Membranoproliferative glomerulonephritis (MPGN) is an uncommon cause of end-stage renal disease (ESRD). Recurrence rates after transplantation range from 11.8% to 18.9% after 5 and 15 years, respectively. This study aimed to assess the risk factors of MPGN recurrence after kidney transplantation and its impact on graft survival. MATERIAL AND METHODS This was a single-center retrospective cohort, including renal transplant recipients older than 18 years, with a diagnosis of MPGN in native kidneys. Data were obtained from medical records during the first 5-year post-transplant follow-up. Primary endpoints were graft function and survival. Secondary endpoints were MPGN recurrence risk factors and these cases' clinical, laboratory, and histological features. RESULTS Twenty-eight patients were included; the majority male (60.7%), with a mean age of 24.0±9.4 years. At MPGN native diagnosis, all patients presented proteinuria, with C3 consumption in 42.9%. Histological analysis showed 13 (42.9%) MPGN type I and 5 (17.9%) type II, with no cases of type III. MPGN recurrence occurred in 7 (25.0%) patients; 85.7% were male, 57.1% were recipients from a living donor, all presenting nephrotic syndrome and hematuria, with C3 consumption in 71.4%. The graft function was similar between the groups. Two (28.6%) patients progressed to graft failure in the recurrence group, and 1 died with a functioning graft. CONCLUSIONS The MPGN recurrence rate was 25%, most of them recipients of kidneys from living donors. Nephrotic syndrome and C3 consumption were frequent at recurrence. The graft function was similar between the groups, and the 5-year graft survival rate in the recurrence group was higher than in other studies.

Allograft failure in kidney transplant recipients with membranoproliferative glomerulonephritis.

BACKGROUND: Membranoproliferative glomerulonephritis types I (MPGN-I) and II (MPGN-II) are rare diseases that in limited case series have been reported to recur frequently in kidney transplants and have a negative impact on allograft survival. STUDY DESIGN: Retrospective database review. SETTING & PARTICIPANTS: 189,211 primary kidney transplants in the United Network for Organ Sharing (UNOS) database from September 1987 to May 2007. PREDICTOR OR FACTOR: MPGN-I (811 patients; 0.4%), MPGN-II (179 patients; 0.1%), other GN (58,129 patients; 30.7%), and all other diagnoses (130,092 patients; 68.7%). OUTCOMES: Death-censored and non-death-censored allograft survival. RESULTS: Compared with controls, patients with MPGN-I and MPGN-II were significantly younger at the time of transplant, with a median age of 36 and 27 years compared with 44 years in the GN group and 46 years in all other disease groups, respectively (all P < 0.001). Mortality in patients with MPGN-I (8.8%) was significantly lower compared with the GN (11.3%; P = 0.02) and other disease (16.6%; P < 0.001) populations and lower in those with MPGN-II (9.5%) compared with the other disease (16.6%; P = 0.01) population. Graft failure rates were significantly higher in the MPGN-I (44.5%) cohort, but not in the MPGN-II (45.3%) cohort compared with the GN (38.0%) population (P < 0.001 and P = 0.05, respectively); neither MPGN cohort differed from the other disease (43.0%) population (P = 0.4 and P = 0.5). Overall, 10-year death-censored graft survival was similar for MPGN-I (56.2%) and MPGN-II (57.5%); both were significantly worse than for GN (65.2%; P < 0.001 and P = 0.003, respectively), and only MPGN-I was significantly worse than the other disease (60.0%) population (P = 0.004). Of allograft failures with a reported cause, disease recurrence was the primary cause in 36 (14.5%) MPGN-I and 18 (29.5%) MPGN-II transplant recipients and was significantly higher compared with 879 (6.6%) GN and 1,319 (4.4%) all-other-disease recurrence failures (P < 0.001). LIMITATIONS: Limited pretransplant clinical and biopsy data. CONCLUSIONS: A diagnosis of MPGN-I or MPGN-II has a significant negative impact on overall primary allograft survival compared with other forms of glomerulonephritis, whereas only MPGN-I has a significant, but modest, negative effect compared with other causes of end-stage renal disease.

Recurrent membranoproliferative glomerulonephritis after kidney transplantation.

On examination of the records of 1321 patients following kidney transplant over an 11-year period, we found that 29 patients had recurrent membranoproliferative glomerulonephritis (MPGN). We excluded from this analysis patients who had MPGN type II, those with clear evidence of secondary MPGN, and those lacking post-transplant biopsies. During an average of 53 months of follow-up, we found using protocol biopsies that 12 of these patients had recurrent MPGN diagnosed 1 week to 14 months post-transplant. In 4 of the 12 patients this presented clinically, whereas the remaining had subclinical disease. The risk of recurrence was significantly increased in patients with low complement levels. Serum monoclonal proteins were found in a total of six patients; appeared to be associated with earlier, more aggressive disease; and were more common in recurrent than non-recurrent disease. The recurrence of MPGN was marginally higher in recipients of living-donor kidneys. Some patients developed characteristic lesions within 2 months post-transplant, whereas others presented with minimal, atypical histological changes that progressed to MPGN. Of 29 patients, 5 lost their allograft and 2 patients remain on chronic plasmapheresis. Our study shows the risk of MPGN recurrence and progression depends on identifiable pretransplant characteristics, has variable clinical impact, and can result in graft failure.

Disease recurrence in paediatric renal transplantation.

Renal transplantation (Tx) is the treatment of choice for end-stage renal disease. The incidence of acute rejection after renal Tx has decreased because of improving early immunosuppression, but the risk of disease recurrence (DR) is becoming relatively high, with a greater prevalence in children than in adults, thereby increasing patient morbidity, graft loss (GL) and, sometimes, mortality rate. The current overall graft loss to DR is 7-8%, mainly due to primary glomerulonephritis (70-80%) and inherited metabolic diseases. The more typical presentation is a recurrence of the full disease, either with a high risk of GL (focal and segmental glomerulosclerosis 14-50% DR, 40-60% GL; atypical haemolytic uraemic syndrome 20-80% DR, 10-83% GL; membranoproliferative glomerulonephritis 30-100% DR, 17-61% GL; membranous nephropathy approximately 30% DR, approximately 50% GL; lipoprotein glomerulopathy approximately 100% DR and GL; primary hyperoxaluria type 1 80-100% DR and GL) or with a low risk of GL [immunoglobulin (Ig)A nephropathy 36-60% DR, 7-10% GL; systemic lupus erythematosus 0-30% DR, 0-5% GL; anti-neutrophilic cytoplasmic antibody (ANCA)-associated glomerulonephritis]. Recurrence may also occur with a delayed risk of GL, such as insulin-dependent diabetes mellitus, sickle cell disease, endemic nephropathy, and sarcoidosis. In other primary diseases, the post-Tx course may be complicated by specific events that are different from overt recurrence: proteinuria or cancer in some genetic forms of nephrotic syndrome, anti-glomerular basement membrane antibodies-associated glomerulonephritis (Alport syndrome, Goodpasture syndrome), and graft involvement as a consequence of lower urinary tract abnormality or human immunodeficiency virus (HIV) nephropathy. Some other post-Tx conditions may mimic recurrence, such as de novo membranous glomerulonephritis, IgA nephropathy, microangiopathy, or isolated specific deposits (cystinosis, Fabry disease). Adequate strategies should therefore be added to kidney Tx, such as donor selection, associated liver Tx, plasmatherapy, specific immunosuppression protocols. In such conditions, very few patients may be excluded from kidney Tx only because of a major risk of DR and repeated GL. In the near future the issue of DR after kidney Tx may benefit from alternatives to organ Tx, such as recombinant proteins, specific monoclonal antibodies, cell/gene therapy, and chaperone molecules.

Transitory lupus anticoagulant antibodies leading to a quickly resolvable left ventricular thrombus in a young female patient on peritoneal dialysis.

We present a 38-year-old female patient on peritoneal dialysis for 3 years due to mesangioproliferative glomerulonephritis since early adolescence and chronic failure of the right kidney transplants. In early 2006 she was treated with high-dose cortisone due to cryptogenic, organized pneumonia. During a routine echocardiographic examination performed because of occurrence of cerebral symptoms such as diminished visual and auditory acuity in the patient, we detected a mobile, left ventricular thrombus of unusual large size, along with serologically measured Lupus anticoagulant antibodies (LA). The thrombus could be completely lyzed within only 12 hours by urokinese and antithrombotic danaparoid sodium therapy without surgical intervention. Successful treatment was proven by negative LA antibody activity as well as by echocardiography. The general clinical health was greatly improved after rehabilitation 2 months after lysis. We assume that the patient may have had infection- or cortisone-triggered transitory LA antibodies causing the serious heart thrombus with hypokinesia in the apex cordis.

Recurrence of membranoproliferative glomerulonephritis post transplant - Is this mere recurrence of pattern or recurrence of disease?

Recurrence of membranoproliferative glomerulonephritis (MPGN) is seen in 1965% cases of postrenal transplant resulting in graft loss in up to 35-50% of cases. A 31-year-old female, after 1% years on maintenance hemodialysis, underwent ABO compatible deceased donor kidney transplantation with basiliximab induction. During the immediate posttransplant period, the patient had delayed graft function, but achieved nadir creatinine of 0.9 mg/dL by 10 days. Nine months posttransplant, the patient developed fever, anasarca, and decrease in urine output with albuminuria 3+, active sediments in urine, serum creatinine 3.5 mg/dL, 24-h urine protein 7.5 g, and low C3. The patient underwent graft biopsy. Subsequently, the patient received pulse steroid for three days and five sessions of plasmapheresis. Renal biopsy report was suggestive of MPGN with focal crescents and acute tubular necrosis. Immunofluorescence showed Ig G3+, C3 3+, к 3+, and negative for λ or other immunoglobulins or complements. As her native kidney disease was immune-complex-mediated MPGN with no light chain restriction, paraffin tissue of the native kidney was reexamined for light chain restrictions by immunoperoxidase method, but did not show light chain restriction. The patient underwent extensive workup for paraproteinemias, but results were negative. Subsequently, she received four doses of bortezomib. The patient's serum creatinine got reduced to 0.8 mg/dL and proteinuria reduced to 800 mg/day. Our case is unique as we were not able to demonstrate monoclonal deposits in native kidney sample although there was recurrence of MPGN with monoclonal light chain deposits post transplant. Our findings emphasize the need for thorough evaluation of paraproteinemias in patients with idiopathic MPGN even in the absence of light chain deposition in biopsy.

Renal transplant compartment syndrome: a case report.

An unusual case of early double kidney transplant dysfunction due to abdominal compartment syndrome is herein reported. A 62-year-old woman on peritoneal dialysis underwent dual kidney transplantation. The grafts were positioned extraperitoneally in both iliac possae using standard techniques. Surgical procedures and immediate postoperative period were uneventful. The urine output was immediate and the creatinine decreased, but in a few days she developed severe ascites with reduced urine output, increased creatinine, and progressive changes on Doppler ultrasound. The patient underwent paracentesis: the kidney function recovered as well as the Doppler ultrasound. Kidney biopsy was negative for rejection or renal pathology. Graft dysfunction was related to the presence of ascites. A catheter inserted in the abdomen measured intra-abdominal pressure (IAP) of 14 mm Hg. IAP correlated with renal function showing that IAP probably explained renal flow modifications.

Outcome of primary glomerular disease in pediatric renal transplantation: a single-center experience.

INTRODUCTION: The recurrence of primary disease in transplantation is a well-known problem. We report our single-center experience to assess the frequency of the recurrence of primary glomerulonephritis in children after renal transplantation. PATIENTS AND METHODS: Medical reports of 14 children with primary glomerular disease were evaluated. Among the 14 grafts were 10 from living related and four from cadaveric donors. Ten were diagnosed as focal segmental glomerulosclerosis (FSGS), two membranoproliferative glomerulonephritis (MPGN), and two polyarteritis nodosa (PAN). The original diagnosis was biopsy-proven in every case. All patients were treated with calcineurin-based immunosuppressive therapy. RESULTS: The mean age was 15.5 +/- 5.4 years. The median transplantation duration was 47 months; however, one of the FSGS patient had hyperacute rejection. Five years later she received a second graft with a serum creatinine of 0.7 mg/dL at 7 years after transplantation. Posttransplant recurrence of FSGS was confirmed in two patients (20%), who were treated with plasmapheresis with no improvement of proteinuria, two FSGS patients had thromboses after transplantation. One had a cardiac thrombosis with heterozygote MTHFR mutation and one, a renal artery thrombosis and loss of graft with prothrombin 20210A mutation. They all have functioning grafts except these two. We did not observe recurrence of PAN or MPGN in patients. CONCLUSION: Although the number of patients is quite small, our recurrence rate was compatible with the previous reports. Additionally, we strongly recommend evaluation of all risk factors for thrombosis and give appropriate anticoagulation.

Anti-Fya antibodies as the cause of an unfortunate post-transplant course in renal transplant recipient.

BACKGROUND: Duffy glycoprotein, belonging to blood group alloantigens, is also recognized as chemokine-binding protein, therefore the role of Duffy antigen in chemokine distribution has been postulated. Duffy positive phenotype prevalent among Caucasians is associated with antigen expression on erythrocytes and endothelium of several organs including kidney. The role of anti-Duffy antibodies significant in transfusiology may be also important in kidney transplantation. CASE REPORT: The case of renal transplant recipient with Fy (a-b+) phenotype, possessing anti Fya antibodies, with unfortunate post-transplant course complicated with acute cellular and antibody-mediated graft rejections, with the presence of crescentic glomerular lesions, kidney graft insufficiency and recurrent urinary tract infections is presented. The role of anti-Duffy antibodies in acute antibody-mediated rejection is discussed. CONCLUSIONS: Fy(a )antibodies present in renal recipient with Fy(a-b+) phenotype may be the reason for unfavorable transplantation outcome resulting from reaction against Duffy antigen up-regulated on graft tissue during ischemia reperfusion injury and acute rejection episode. In renal transplant recipients with antibody-mediated rejection without antidonor specific antibodies, incompatibility in blood group antigens other than AB0 system could be considered.

A case of renal transplantation.

A 12-year-old boy was admitted in paediatric nephrology unit of Bangabandhu Sheikh Mujib Medical University (BSMMU) with massive proteinuria, hypertension, respiratory distress and anaemia and diagnosed as nephrotic syndrome. Percutaneous needle biopsy was consistent with diffuse endocapillary proliferative glomerulonephritis and initially managed conservatively with injection methyl prednisolone, cyclophosphamide, lisinopril etc. without any improvement. Living-related renal transplantation was done successfully from paternal uncle. Two episodes of acute rejection occurred, one immediately after transplantation and another after one month. These were managed with IV methyl prednisolone for 3 days. At present, he is on oral prednisolone, cyclosporine, azathioprine and antihypertensives with normal haemoglobin and stable serum creatinine level (pre-transplant level 12.5mg/dl to post-transplant level 1.5mg/dl). He has been maintaining his normal life including schooling for last few months. It is concluded that a patient with uncommon presentation of nephrotic syndrome should be confirmed by renal biopsy and renal transplantation may be considered if conservative measures fail.

[Successful renal transplantation following lung transplantation: a survey of the first Hungarian case]. / Sikeres vesetranszplantáció tüdoátültetés után: az elso magyarországi eset ismertetése.

The authors review the case of their young patient, who underwent a lung transplantation in Vienna because of an end stage idiopathic pulmonary fibrosis. During the prolonged postoperative phase renal failure full of complications developed, which necessitated haemodialysis. As the pulmonological rehabilitation was complete, but the regular dialyses considerably raised the risk of opportunistic infections, and also significantly reduced the quality of life of the patient, renal transplantation was performed in Debrecen four years after the lung transplantation. This is the first lung transplanted patient in Hungary who also underwent renal transplantation. Now, more than two years after the renal transplantation the patient lives a compensated, rehabilitated life, the respiratory function values have improved and the renal function values are also acceptable. The number of transplanted patients has significantly increased in recent years worldwide, and also in Hungary. However, due to immunosuppressive medications, calcineurin inhibitors mainly, numerous complications must be reckoned with. An outstanding one among them is the secondary renal failure which may occur both in acute and chronic form and may even necessitate renal transplantation. Renal transplantation is an excellent treatment option for end stage renal failure patients, who had received another organ transplant earlier. Kidney transplantation improves quality of life and increases expected survival, too.