1. Recurrent Glomerulonephritis In Kidney Transplantation
Salwa S. Sheikh MD, FCAP, FASCP
Consultant Pathologist
Dhahran Health Center, Saudi Aramco

2. Kidney Transplant 43% - proteinuria >1g/24h 13% - nephrotic range
Causes:
Chronic allograft nephropathy /
Recurrent glomerulonephritis
Calcineurin-inhibitor toxicity
Transplant pathology is one of the most challenging fields for pathologists. Renal transplantation has become the preferred modality of renal replacement therapy for most pts. With ESRD. Once a pt receives renal allograft, all subsequent events involving changes in renal function are attributed to the process & natural h/o transplantation itself: acute & chronic rejection, immunosuppressive drug nephrotoxicity, graft vasculature thrombosis or stenosis, ischemia, infection, & lymphoproliferative disorders.
Despite advances in prevention of acute rejection and improved short-and long-term kidney graft survival, recurrent glomerulonephritis remains problEmatic and poorly characterized.

3. Recurrent Glomerulonephritis
3rd cause of renal allograft loss – 10 yrs
Cardiovascular morbidity & mortality
True prevalence –
Pts losing allografts due
to recurrent GN
Pts with recurrence &
functioning grafts
Accumulating evidence indicates that recurrent gn. Is the third most important cause of renal allograft loss at 10 yrs after transplantation (after chronic rejection, & death with a functioning kidney).

4. Limitations in Evaluating Epidemiology of Native & Recurrent GN
Studies
Relatively small & variable
Short follow up post transplant
An understanding of epidemiology of native kidney dse secondary to gn is critical to ch the epidemiology of recurrent gn.
For various reasons the prevalence of posttransplant gn is not accurately known. One important reason is lack of consensus regarding the clinical approach to late allograft dysfunction i.e. > 12 months after transplant.

5. Limitations in Evaluating Epidemiology of Native & Recurrent GN
Native Kidney Disease
Restrictive renal biopsies- 50% underlying dses- unknown in many ESRD pts
Black pts-often labeled to have hypertensive nephrosclerosis
Difficulty in determining the cause of native kidney dse when presenting at late stage
Difficulty in determining primary vs secondary FSGS
Native glomerular dse is not verified in a substantial proportion of pts who present with shrunken kidneys, so it is not known whether the biopsy proven gn that develops after tx is recurrent or de novo. As a result some investigators do not report separate data for these 2 types of dse, referring simply to post-tx gn.
Misdiagnosis or mislabelling of native kidney dse

6. Limitations in Evaluating Epidemiology of Native & Recurrent GN
Indications for Post-transplantation
Renal Biopsy
Lack of unified approach in diagnosis
Non-uniform indications for biopsy
Protocol vs clinical renal dse
Not adequately classified – EM / IF lacking
Lack of unified approach in diagnosing pts with posttransplant proteinuria, hematuria, & renal dysfunction. Proteinuria & hematuria are hallmark findings in detecting recurrence of gn. Many centers do not include a urinalysis for detecting proteinuria & hematuria as part of their routine transplant surveillance or even for some pts with worsening renal functions before transplant renal biopsy.
The reported prevalence is markedly influenced by diff in biopsy policy in the population studied- protocol bx may be performed, or pts may be subjected to bx only if proteinuria develops, or if there is elevation of serum creatinine &/ proteinuria. Routine evaluation of allograft biopsy which involves light microscopy with the use of special stains, & C4d to detect humoral rejection is not sufficient for the dignosis of posttransplant gn.
EM & IF are not routinely submitted, are essential in diagnosis of most GN. Pts with early / mild recurrence og IgAN, MN, &lupus nephritis thus easily receive a misdiagnosis.

7. Limitations in Evaluating Epidemiology of Native & Recurrent GN
Diagnosis of Post-transplant GN
Lack of histological features in early dse.
Difficulty in differentiating GN from other causes.
Difficulty in determining primary vs secondary.
Recurrent or de novo gn. Often coexists with glomerular manifestations of acute or chronic rejection so establishing the diagnosis is frequently a challenge.
Diagnosis of posttransplant GN:
Difficulty in determining primary vs secondary (FSGS, IgAN, MPGN vs Transplant / allograft glomerulopathy)
Lack of histologic features- early (in FSGS in early stages of recurrence)
Difficulty in differentiating cause of HUS/TTP (primary vs drug toxicity vs humoral rejection)

8. Recurrent GN
Differential Diagnosis Of Recurrent Disease After Kidney Transplantation
De novo glomerulonephritis
Transplanted glomerulonephritis
Chronic rejection
Cyclosporine toxicity
Acute rejection
Allograft ischemia
Cytomegalovirus infection
DD-difficult -Transplant glomerulopathy, de novo Gn., transplanted Gn, & real recurrence
Acute cellular rejection and cyclosporine toxicity usually can be distinguished easily from recurrent glomerular disease. Recurrent hemolytic uremic syndrome, however, can cause a microangiopathy similar to cyclosporine toxicity, with erythrocyte fragments visible both in blood films and within glomerular capillary loops. The major diagnostic difficulty lies with chronic rejection, especially in the form of transplantation glomerulopathy, and de novo or transplanted glomerulonephritis. Chronic transplantation glomerulopathy occurs in 4% of renal allografts and usually is associated with proteinuria of more than 1 g/d, beginning a few months after transplantation. Chronic glomerulopathy shares some features with both recurrent mesangiocapillary glomerulonephritis type I and hemolytic uremic syndrome: glomerular capillary wall thickening, mesangial expansion, and double contour patterns of the capillary walls with mesangial cell interposition [13]. Thus, a definitive diagnosis of recurrent nephritis may require histologic characterization of the underlying primary renal disease and a graft biopsy before transplantation.

9. Prevalence of Glomerulonephritis
Prevalence of GN as cause of ESRD: 10-25%
Prevalence of recurrent GN – 4%-20%
2-5% - graft failure
Higher prevalence:
Children
White population
Based on literature recurrent dse is observed in 4-20% of pts receiving a kidney transplant & will lead to graft failure in 2-5%. On the contrary it is the cause of renal failure for 20-upto 50% of those who receive a transplant. The proteinuria & elevated serum creatinine levels that result from recurrent gn are associated with cardiovasc morbidity & mortality.
Higher prevalence of gn in children is related to lower prevalence of diabetes as the cause of ESRD as opposed to in adults.
Prevalence of recurrent GN – 2.9%-12.1% & is inversely proportional to recipient age & directly proportional to the duration of follow-up. Prevalence is higher when pts with functioning grafts & recurrence are included

10. Definition & Classification
Clinical Classification
True recurrence
Transplant glomerulopathy with unknown primary disease
De novo disease
Recurrent & de novo gn can be classified according to clinical or histologic criteria.
In clinical practice transplant gn sometimes occurs in pts for whom the native kidney dse was not determined. In these cases true distinction between primary or recurrent gn can not be made. To circumvent this common problem some authorities recommend the term : Transplant glomerulopathy with unknown primary dse.
True recurrence (native & recurrent dse are same confirmed by histology)

11. Definition & Classification
Histological Classification
Recurrence of primary GN
Recurrence of secondary GN
Recurrence of metabolic
or systemic diseases
De novo diseases
1- Recurrence of primary GN (FSGS, MPGN, IgA, MN)
2- Recurrence of secondary GN (SLE, HSP, HUS/TTP, crescentric GN, anti-GBM dse)
3- Recurrence of metabolic or systemic dse.(diabetic nephropathy, oxalosis, amyloidosis, fabry”s dse, scleroderma, cystinosis, fibrillary GN)
4- De novo dses (anti-GBM dse in Alport syndrome, Memb N in pts with polycystic kidney dse.

12. Glomerulonephritis Recurrence- first few weeks
De novo- usually after 1 yr post transplant
GLOMERULONEPHRITIS
% RECURRENCE
FSGS, idiopathic
20-30%
IgAN
25%
MPGN-I
MPGN-II
80-almost 100%
Membranous GN
30%
Recurrences-tend to occur in the first few weeks after tx though there is a wide window of recurrence of days to yrs.
It would be beyond the scope of this short talk/review to discuss the relevance of recurrent dse in detail for every gn entity. Some specific aspects of individual forms of gn. & new findings published in literature in the last yrs will be highlighted.
Glomerular disease that recurs at the highest rate (95 to 100 percent) is dense deposit disease (membranoproliferative glomerulonephritis type II), although less than 15 percent of affected patients lose their graft to recurrent disease. Other conditions that commonly recur in the allograft include membranoproliferative glomerulonephritis type I (recurrence rate 40 to 70 percent), IgA nephropathy and Henoch-Schönlein purpura nephritis (30 to 50 percent), focal segmental glomerulosclerosis (30 to 40 percent), and hemolytic uremic syndrome (nonepidemic form; 30 percent). Lower rates of recurrence are reported for membranous glomerulopathy (10 percent), antiglomerular basement membrane (anti-GBM) disease (5 to 10 percent), and lupus nephritis (less than 5 percent). Most recurrences occur within the first 6 months post-transplantation. In some cases, as in recurrent focal segmental glomerulosclerosis, nephrotic syndrome may develop as early as several days post-transplantation.

13. Analysis of Allograft Loss due to Recurrence of GN, AR, CR & Death
Impact Of Glomerulonephritis OnGraft Survival / Outcome: The overall impact of posttx gn on graft survival is not easy to determine because such dse rarely the sole cause of graft failure. In majority of cases acute &/chronic rejection &/ calcineurin-inhibitor nephrotoxicity coexist with with posttx gn.
Controversial, Rate of recurrence-related graft loss varies according to the type of Gn ---table
Kaplen-Myeir analysis of allograft loss due to recurrence of GN, acute rejection, chronic rejection, and death with functioning kidneys
Immunosuppressive regimens do not influence rate of histologic recurrence or graft loss
E Briganti, G Russ, J McNeil, R Atkins, S Chadban. Risk of renal allograft loss from recurrent glomerulonephritis.
N Engl J Med, 347(2): , 2002.

14. Analysis of Allograft Loss due to Recurrence of GN, According to GN Types
E Briganti, G Russ, J McNeil, R Atkins, S Chadban. Risk of renal allograft loss from recurrent GN
N Engl J Med, 347(2): , 2002. 14

15. Cumulative Probability of Post-Transplant GN by Original Disease
Chailimpamontree, W. et al. Probability, Predictors, and Prognosis of Posttransplantation
Glomerulonephritis. J Am Soc Nephrol 2009;20:

16. Cumulative Probability of Post-Transplant GN by Histological Type
Chailimpamontree, W. et al. Probability, Predictors, and Prognosis of Posttransplantation
Glomerulonephritis. J Am Soc Nephrol 2009;20:

17. Cumulative Incidence of Recurrent Post-Transplant GN
Chailimpamontree, W. et al. Probability, Predictors, and Prognosis of Posttransplantation
Glomerulonephritis. J Am Soc Nephrol 2009;20:

18. Cumulative Incidence of De Novo Post-Transplant GN
Chailimpamontree, W. et al. Probability, Predictors, and Prognosis of Posttransplantation
Glomerulonephritis. J Am Soc Nephrol 2009;20:

19. Probability of Graft & Patient Survival with PTGN
Chailimpamontree, W. et al. Probability, Predictors, and Prognosis of Posttransplantation Glomerulonephritis. J Am Soc Nephrol 2009;20:

20. Focal Segmental Glomerulosclerosis

21. DDX Of Segmental Glomerular Scars On Transplantation Biopsy
Diagnosis
Features
Recurrent FSGS
Recurrent heavy proteinuria within 3 mo
Original disease caused renal failure <3y
Rejection
Insidious onset of proteinuria
Feature of chronic rejection on biopsy, especially vascular sclerosis and glomerulopathy
Cyclosporine-related
Previous thrombotic microangiopathy affecting glomeruli
De novo FSGS
Original disease not FSGS
Chronic rejection excluded
Other glomerulonephritis
Characteristics immunohistology and electron microscopy, especially in immunoglobulin A disease
Segmental glomerular scars in a functioning graft is a common finding. The interpretation of the biopsy requires knowledge of
the previous histology in the native kidneys and the clinical course after transplantation. Immunohistology and electron microscopy
can be particularly helpful in this setting. Recurrent focal segmental glomerulosclerosis is the most common cause of early massive
proteinuria. Both rejection and cyclosporine therapy, however, can cause segmental scars indistinguishable from those of focal segmental
glomerulosclerosis. Recurrent or de novo immunoglobulin A disease in an allograft also can cause segmental glomerular scarring, but with mesangial hypercellularity, immunoglobulin A detectable by immunostaining, and paramesangial deposits on electron microscopy.

22. Etiological Classification of FSGS

23. FSGS 7-10% in pts requiring transplant FSGS recurs – 20%-30%
Recur 6-12m post transplant
Heavy proteinuria, hypertension, &/ loss of graft function
Severe proteinuria in recurrent FSGS- thromboembolic complications
Majority – nonhereditary-
circulating permeability factor
Hereditary – mutations – NPHS2
Focal segmental glomerulosclerosis accounts for 7% to 10% of patients requiring renal replacement therapy. The overall recurrence rate is approximately 20% to 30% [1,4,31]. These numbers, however, may be an underestimate because of biopsy sampling errors. FSGS further stratified into primary, secondary, & familial, each incurring a different rate of recurrence. Denovo FSGS also recently has been related to sirolimus therapy in some tx pts
Recurrence manifests with proteinuria (often 10–40 g/d), developing hours to weeks after transplantation.
Recurrent cases reported as long as 5 yrs post tx. In pts with severe proteinuria in the course of recurrent FSGS an increased risk of thromboembolic complications has been noted (as in other recurrent gns with proteinuria exceeding 2g/day)
Majority – nonhereditary- & the role of an unidentified circulating glomerular permeability factor has been the focus of research into the pathogenesis of this dse since in pts with Hereditary – mutations have been identified in genes that encode podocyte proteins. Mutations in NPHS2 which encodes podocin are the most common cause of hereditary. Familal FSGS do not recur because defect is intrinsic to kidney

24. FSGS Proteinuria onset within weeks (80% nephrotic)
Acute graft dysfunction
Histologic changes- 4-6 wks post transplant
EM- changes within days after proteinuria onset- diffuse effacement of podocyte foot processes.
Recurrence- 20% - graft loss yrs
Living related donor- avoided with prior
allograft loss due to recurrent FSGS
Onset of proteinuria is frequently observed within weeks & 80% become nephrotic. Hypertension & hematuria are common & a considerable # of pts develop acute graft dysfunction.

25. Risk Factors For Recurrent FSGS after Transplantation
Recurrence rate, %
Age <5y 50
Age <15y with progression to ESRD within 3y
80-100
First graft lost from FSGS
75-85
Adults without risk factor
10-15
Patients at high risk for recurrence can be identified, particularly children with rapid evolution of their original disease and mesangial expansion
on biopsy [1,32]. In
children the mean time to recurrence is 14 days. Recurrence is not benign and leads to graft loss in up to half of patients. Patients at
highest risk for recurrence should not receive grafts from living related donors.
Graft loss occurs in half of all patients with recurrent FSGS and nephrotic syndrome.

26. FSGS Risk factors for clinically relevant recurrence
Childhood onset ( recurrence as high as 50%)
Recurrence of FSGS in prior allograft
Rapid progression (within 3yrs)
White race
Diffuse Mesangial hypercellularity (native)
Sirolimus therapy (de novo)
Graft failure - <20 yrs age – 24% of living related donors & 11% of cadavaric grafts
Onset under the age of <6yr is associated with recurrence rate of 50-80%
Rapid progression (within 3yrs) from diagnosis to ESRD
As per large study based on the US Renal Data System - Graft failure in recipients below 20 yrs age could be attributed to recurrent fsgs in 24% of living related donors & 11% of cadavaric grafts

27. FSGS Collapsing FSGS: Majority - De novo Higher rate of graft loss
Secondary & familial FSGS:
Do not recur
Collapsing FSGS can occur in HIV infected pts or as idiopathic form of fsgs. Both types are ch clinically by heavy proteinuria, progressive renal insufficiency & rapid evolution to ESRD. Same recurrence rate – 22%
Recurrent & de novo FSGS were each associated with higher rate of graft loss than was non-collapsing FSGS. No reliable clinical data exists on the rates of clinical correlates of other variants of FSGS
Secondary fsgs arising as a late complication of other native renal dses does not recur , as expected from its presumed hyperfiltration mechanism

28. FSGS
Plasmapheresis
Prophylactic plasmapheresis – more effective in preventing recurrence than after transplant
Children – majority respond
Adults – less effective
Recurrent FSGS seems to be mediated by a circulating factor. Removal of the permeability factor does seem to be the mechanism responsible for the success of plasma exchange in the therapy of recurrent FSGS. Although not assessed by a randomized , controlled, prospective trial, several series have reported success of plasma exchange in inducing remission in majority of pts treated within 2 wks of relapse. Relapse after cessation of plasma exchange has been encountered but may be prevented or reversed by chronic plasma exchange or concurrent tx e.g. cyclophosphamide, NSAID, ACE inhibitors, increasing dose of cyclosporin.
Cases – upto 6 yrs on plasmapheresis.

29. De Novo FSGS Usually- 1yr post transplant
In association with arteriolar hyalinosis
Negative independent predictor of graft survival
Calcineurin-inhibitor toxicity
Sirolimus
The recipients with de novo FSGS and chronic allograft nephropathy had graft survival rate of 40% at 5 yrsafter diagnosis, compared with a rate of 60% in those with chronic allograft nephropathy alone

30. Membranous Glomerulonephritis
Overall frequency – 10%-30%
Graft loss – 50% of these pts
Recurrence within 1-2 wks – severe proteinuria
Histology – identical, early cases – EM, IF
28% develop recurrence within 4 months. Later cases can not be as reliably distinguished from de novo dse.

31. Membranous Glomerulonephritis
Risk factors (Not conclusive) :
Early recurrence & Massive proteinuria- progress rapidly to graft failure
HLA
Hepatitis B & C, autoimmune dse e.g. SLE.
Malignancy - lymphoma
No conclusive risk factors have been identified except for the possible role of HLA matching. Of those that recurred within 4 m 75% were in kidneys from living related donors. Hepatitis B & C, autoimmune dse e.g. SLE. However most are primary MN
In a subset of pts 3 lymphomas were described in 19 transplanted pts with membranous gn as the underlying dse. Whether this represented a consequence of immunosuppressive treatment of the original dse could not be determined but this implies that treatment of the recurrent dse with intense immunosuppression might further aggravate the risk of malignancy. 31

32. Membranoproliferative Glomerulonephritis- Type Il ( Dense Deposit Dse)
Recurrence - 80% - almost 100%
As early as 12 d after surgery
Crescent formation- negative correlation with graft survival
The presence of crescents in native kidney dse is also a risk factor for the recurrence rate of MPGN-II

33. Membranoproliferative Glomerulonephritis- Type I
Type I- Idiopathic / hepatitis C virus, cryoglobulinemia.
Recurrence: 36% in HCV +ve, 4% HCV –ve pts
Recurrence as early as 2 wks
20-50% of pts, proteinuria, usually within 4 yrs
Graft failure – 10-50%

34. IgA Nephropathy Recurrence – 20%-60% Frequency increases over time
13% of recurrent cases – recurrence related allograft dysfunction in 5 yrs
Allograft loss from recurrence – 45%-70%
With increasing graft survival time, recurrence of IgA deposits will become more common.

35. IgA Nephropathy Predictors of clinically relevant recurrence:
Function of time post transplantation
Young age
Living related – higher risk of recurrence & graft deterioration
At present it is controversial whether living related donor kidneys are at a higher risk of recurrence & graft deterioration than kidneys from non-related donors. Many studies failed to show a significant difference. However even in the studies where the risk was increased with living related donors, graft survival of living related and non-related grafts was identical at 5 yrs & failed to reach a significant difference at 10 yrs. In comparison to pts with other underlying gn or non-gn disorders, pts and graft survival up to 10 yrs after grafting in case of an underlying IgAN is not different

36. Systemic Diseases Recurrence rate – variable SLE – 2%-10%
Wegener’s granulomatosis – 17%
Anti-GBM -Recurrence - <5% (Anti-GBM titers -ve for 6-12m prior to transplant)
De novo anti-GBM in Alport dse
Recurrence rate – variable depends on the basis of specific dse
Anti-GBM Recurrence – rare, <5% as long as anti-GBM titers are negative for 6-12m prior to transplantation. De novo anti-GBM in Alport dse as a result of development of anti GBM ab in pts with genetic deficiency of type IV collagen proteins in their native kidneys.

37. How to follow pts with underlying GN after transplant ??

38. Recommendations
Obtain exact diagnosis of primary dse wherever possible
Native kidney biopsy - when not contraindicated
Closely follow pts. peri- & post-operatively- abnormal lab findings- aggressive work up
Urinalysis/ visit
Early diagnosis - Biopsy – EM, IF
Nonfamilial FSGS- risk of recurrence depends –underlying dse. In all cases of Primary FSGS transplant should be offered as preferred choice of therapy.
Rate of recurrence in repeat transplant – very high as high as =>80% after the first loss of first graft as a result of recurrence, therefore living donor transplant should be discouraged after loss of primary graft due to recurrent gn.
Native kidney biopsy - when not contraindicated – should help clarify the true incidence of recurrent dse.
Urinalysis or simple dipstick check for protein & blood should be performed each visit. Simple intervention will lead to increased & earlier dx of recurrent gn. E.g. FSGS. Earlier dx & intervention will lead to remission & improved graft survival. Also abnormality should prompt biopsy

39. Investigating Recurrent Disease After Kidney Transplantation
Renal biopsy with immunofluorescence and electron microscopy
Cyclosporin A level
Urine microscopy and culture
24-h urine protein
Renal ultrasonogtraphy
Anti-glomerular basement membrane autoantibody and antineutrophil cytoplasm antibody
Cytomegalovirus serology and viral antigen detection
Hepatitis C virus serology and RNA detection
Confirming a diagnosis of recurrent disease requires a renal biopsy. Features that favor recurrence include an active urine sediment with erythrocytes and erythrocyte casts, heavy proteinuria, and normal cyclosporine levels. Serologic testing for anti–glomerular basement membrane antibody is important in patients with Alport’s or Goodpasture’s syndrome, and blood film examination for patients with previous hemolytic uremic syndrome. Immunofluorescence and electron microscopic studies are rarely performed routinely on transplantation biopsies but can be vital in making a diagnosis of recurrent nephritis.

40. Bilateral Pretransplant Native Nephrectomy
Bilateral pretransplantation native nephrectomy has been advocated to reduce the likelihood of recurrence of nephritis in renal transplantations.
The data shown here indicate that of 364 transplantations in patients with a diagnosis of primary glomerulonephritis,
an increased recurrence rate exists in those 61 patients with bilateral pretransplantation nephrectomies compared with the 303 patients
without nephrectomy (24.6% vs 12.2%; P < 0.02) [18]. Overall, 14% of patients having transplantation developed recurrent
glomerulonephritis (panel A), and 52% of grafts in these patients failed (panel B). Thus, pretransplantation nephrectomy has no
place in preventing recurrent nephritis. (From Odorico and coworkers [18].)

41. Conclusion Third cause of allograft loss at 10 yrs
With increasing graft survival- increase risk of recurrence
Bilateral nephrectomy prior to transplant does not prevent recurrence
Although short term and long term survival rates have improved markedly during the past 20 yrs, the introduction of immunosuppressive regimens has not influenced the natural h/o post tx gn (only limited advances made in tx gn). All forms of gn can recur but the likelihood of recurrence differs according to the type, FSGS, MPGN, IgAN often recur. Numerous uncontrolled reports reports of successful interventions for recurrent and de novo gns have been published but multicenter randomized controlled trials of such interventions are needed.

42. Conclusion No specific therapy – except for FSGS
Living related donors – particular attention
LRD - restricted e.g. FSGS
LRD - discouraged in repeat transplant (rate of recurrence =>80%)
At present in vast majority of pts with recurrent gn therefore no specific therapy has been established, with the exception of FSGS, and only good supportive care similar to that instituted in the primary dses can be offered.
Living related donors should be evaluated with particular attention & may require a renal biopsy prior to donation in cases of potential familial dse e.g. clinically unapparent familial cases of IgA nephropathy. In update/review living related donors are acceptable in pts with MPGN type I &II, membranous gn, IgAnephropathy, & anti-GBM nephritis. Even after an explicit discussion of the risk. Living related donor should be accepted in a restrictive fashion in pts with FSGS & a high chance of recurrence i.e. age < 15yrs, mesangioproliferative changes on bx, &/duration between dx & renal failure <3yrs. However it is not absolute contraindicated in these cases & in kids needs to be balanced against problems asoc with cont dialysis tx. If prior graft lost due to recurrent Gn- living donation to be discouraged in general & reserved for exceptional circumstances as the risk for a second recurrence & graft loss appears inappropriately high.

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