Acute renal allograft rejections with major interstitial oedema and plasma cell-rich infiltrates: high  -interferon expression and poor clinical outcome

Desvaux, Dominique; Gouvello, Sabine Le; Pastural, Myriam; Abtahi, Maryam Sadat; Suberbielle, Caroline; Boeri, N.; Philippe, Remy; Salomon, Laurent; Lang, Philippe; Baron, Christophe

doi:10.1093/ndt/gfh027

Cited by 79 publications

(130 citation statements)

References 23 publications

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“…The issue of plasma cellrich rejection has been studied in other solid organs, especially kidney and liver (18)(19)(20)(21)(22). As in our study, these rejection episodes tend to occur late after transplant, at a time acute cellular rejection was otherwise rare, and have a tendency toward steroid resistance.…”

Section: Adeyi Et Alsupporting

confidence: 55%

Rotavirus Infection in Adult Small Intestine Allografts: A Clinicopathological Study of a Cohort of 23 Patients

Adeyi

Costa

Abu‐Elmagd

et al. 2010

American Journal of Transplantation

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Rotavirus enteritis (RVE) is increasingly recognized as a cause of small bowel allograft dysfunction but its significance in adult patients is unknown. We have studied 23 adult small bowel transplant patients aged 19.8-59 years (mean = 38.2 years), who were presented with diarrhea and tested positive for rotavirus by enzymelinked immunosorbent assay methods. Serial followup biopsies, as well as clinical data, are documented and analyzed. These patients were followed up for an average of 168 days (range 33-534 days). Mean time of rotavirus diagnosis from transplant day was 794 days (range 38-2907 days). Self-limited diarrhea lasting 6-13 days (mean = 9 days) was the main presentation. Sixteen (69.6%) patients developed acute cellular rejection either concurrently with (i.e. six patients) or after (10 patients) RVE, often characterized by prominent mucosal plasmacytosis at an average of 22 days (range 0-94 days) from the day RVE was diagnosed. One-third of patients with acute rejection (i.e. five out of 16) required muromonab-CD3 rescue therapy. Two patients experienced graft loss (one from chronic rejection, another from sepsis). Rotavirus infection is a cause of diarrhea in adult small bowel transplant patients. The infection appeared to trigger cellular rejection that was associated with mucosal plasmacytosis, and sometimes required aggressive rescue therapy.

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Section: Adeyi Et Alsupporting

confidence: 55%

Rotavirus Infection in Adult Small Intestine Allografts: A Clinicopathological Study of a Cohort of 23 Patients

Adeyi

Costa

Abu‐Elmagd

et al. 2010

American Journal of Transplantation

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“…In previous studies, the response to antirejection therapy in PCAR, such as steroids, was less than satisfactory, with poor graft survival rates [105]. Some reports support the hypothesis that an antibody-mediated component participates in the graft injury of PCAR because it can be associated with both C4d staining and DSAs [99,103,106]. If there appears to be rapid progression of allograft dysfunction in the setting of significant plasma cell infiltration, then treatment modalities targeting both cellular and antibody-mediated pathways can be considered, although there are no data to support this line of treatment.…”

Section: Plasma Cell-rich Acute Rejection (Pcar)mentioning

confidence: 98%

“…PCAR is a morphological type of acute rejection with prominent plasma cells, which normally account for >10% of interstitial mononuclear cells [101][102][103][104] (Fig. 3c).…”

Section: Plasma Cell-rich Acute Rejection (Pcar)mentioning

confidence: 99%

Histopathological findings in transplanted kidneys

et al. 2017

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Improvements in immunosuppression have reduced acute kidney allograft rejection and clinicians are now seeking ways to prolong allograft survival to 20 years and beyond. The primary cause of kidney allograft loss is still chronic rejection, followed by death with a functioning allograft and primary kidney disease recurrence. Thus, overcoming kidney allograft rejection remains the most important issue. Kidney allograft rejection can be classified into two types: T cell-and antibody-mediated rejection. Both are diagnosed pathologically based on the Banff 2013 classification. Other important pathological features in addition to rejection include calcineurin inhibitor toxicity, polyomavirus nephropathy, and recurrence of the primary kidney disease. Here, we review the diagnosis and representative features of histopathological findings in transplanted kidneys.

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“…In PCAR, which is observed in 5% patients with biopsy-proven acute rejection, mature plasma cells comprise > 10% inflammatory cells in the graft 1,2 ; this syndrome often is observed in patients noncompliant with immunosuppressive therapy 3 and is associated with a poor outcome irrespective of the Banff score. The reason for the poor outcome of PCAR is unknown but might be related to the humoral component in graft injuries.…”

Section: Introductionmentioning

confidence: 99%

“…The reason for the poor outcome of PCAR is unknown but might be related to the humoral component in graft injuries. 1 Plasma cell infiltration also is observed in renal allograft biopsies from patients with PTLDs such as plasmacytic hyperplasia, polymorphous B-cell hyperplasia, or plasmacytomalike PTLD. 2 An association between plasmacytic infiltration into renal allografts and PTLD has been reported in a few studies.…”

Section: Introductionmentioning

confidence: 99%

Plasma Cell-Rich Acute Rejection With Monoclonal Gammopathy in a Renal Transplant Recipient

Sun

Cho²,

Hong³

et al. 2013

Exp Clin Transplant

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Plasma cell infiltration into a renal allograft comprises a spectrum of lesions from acute rejection to posttransplant lymphoproliferative disease. We report an unusual case of plasma cell infiltration into a renal allograft with monoclonal gammopathy. A 42-year-old woman was admitted because of graft dysfunction after noncompliance with immunosuppressive therapy for 5 months. A graft biopsy showed acute T-cell-mediated rejection and massive plasma cell infiltration. Despite initial treatment with steroids and antithymocyte globulin, there was persistence of graft dysfunction, monoclonal gammopathy, and plasma cell infiltration. Subsequent treatment with bortezomib improved graft function and caused the monoclonal gammopathy to resolve. Immunohistochemical evaluation of markers of B cells (CD20 and CD138) and the ratio of kappa-to-lambda light chain (15:1) showed that infiltrating cells were plasma cells producing kappa light chain. This suggested that plasma cell-rich acute rejection with monoclonal gammopathy in this patient might have been in an early stage of kappa light chain-producing posttransplant lymphoproliferative disease confined to the renal allograft, and that bortezomib may be effective in treating a patient with this condition.

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Acute renal allograft rejections with major interstitial oedema and plasma cell-rich infiltrates: high -interferon expression and poor clinical outcome

Cited by 79 publications

References 23 publications

Rotavirus Infection in Adult Small Intestine Allografts: A Clinicopathological Study of a Cohort of 23 Patients

Rotavirus Infection in Adult Small Intestine Allografts: A Clinicopathological Study of a Cohort of 23 Patients

Histopathological findings in transplanted kidneys

Plasma Cell-Rich Acute Rejection With Monoclonal Gammopathy in a Renal Transplant Recipient

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