Cyclosporine withdrawal in post‐renal transplant thrombotic microangiopathy

Manzoor, K.; Ahmed, Ejaz; Akhtar, F.; Kazi, Javed Iqbal; Naqvi, Syed Arsalan Ahmed; Rizvi, Syed Adibul Hasan

doi:10.1111/j.1399-0012.2005.00438.x

Cited by 11 publications

(13 citation statements)

References 24 publications

(32 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…reported to be the most common cause of posttransplant de novo TMA (5,(9)(10)(11). One explanation may be that a vast majority of renal allograft recipients receive CNI containing immunosuppressive regimen.…”

Section: Usually De Novo Tma Occurs In the Early Posttransplant Periomentioning

confidence: 99%

De novo Thrombotic Microangiopathy in Renal Allograft Biopsies—Role of Antibody-Mediated Rejection

Satoskar

Pelletier

Adams

et al. 2010

American Journal of Transplantation

105

161

View full text Add to dashboard Cite

The most common cause of thrombotic microangiopathy (TMA) in renal allografts is thought to be calcineurin inhibitor toxicity. Antibody-mediated rejection (AMR) can also cause TMA, but its true impact on de novo TMA is unknown. In a retrospective review of renal allograft biopsies from January 2003 to December 2008 at our institution, we determined the prevalence of TMA in patients with C4d positive (n = 243) and C4d negative (n = 715) biopsies. Over 90% of patients received cyclosporine in both groups. De novo TMA was seen in 59 (6.1%) patients; most of them (55%) with C4d positive biopsy. Among patients with C4d positive biopsies, 13.6% had TMA, as compared to only 3.6% patients with C4d negative biopsies (p < 0.0001). Incidence of graft loss between C4d positive and C4d negative TMA groups was not significantly different, but 70% of patients with C4d positive TMA who received plasmapheresis had slightly lower graft loss rate. In biopsies with AMR-associated TMA, glomerulitis and peritubular capillaritis were significantly more prominent. AMR is the most common cause of TMA in renal allografts in our patient population. It is important to recognize AMR-related TMA because plasmapheresis treatment may be beneficial.

show abstract

Section: Usually De Novo Tma Occurs In the Early Posttransplant Periomentioning

confidence: 99%

De novo Thrombotic Microangiopathy in Renal Allograft Biopsies—Role of Antibody-Mediated Rejection

Satoskar

Pelletier

Adams

et al. 2010

American Journal of Transplantation

105

161

View full text Add to dashboard Cite

show abstract

“…Therapeutic guidelines for de novo TMA are not well defined. Complete withdrawal of the offending CNI is essential [61], although not all patients respond [62]. In a few cases, reversal of TMA was obtained by switching from cyclosporin to tacrolimus [63] or from tacrolimus to sirolimus [64].…”

Section: De Novo Post‐transplant Tmamentioning

confidence: 99%

Thrombotic microangiopathy after kidney transplantation

Ponticelli¹,

Banfi²

2006

Transplant Int

View full text Add to dashboard Cite

Summary Two forms of post‐transplant thrombotic microangiopathy (TMA) may be recognized: recurrent TMA and de novo TMA. Recurrent TMA may occur in patients who developed a nondiarrhoeal form of haemolytic uraemic syndrome (HUS) being particularly frequent in patients with autosomal recessive or dominant HUS. The recurrence is almost the rule in patients with mutation in complement factor H gene. Most patients eventually lose the graft. Treatment with plasma infusions or plasmapheresis is often disappointing, but few cases may be rescued. Intravenous immunoglobulins and rituximab have also been successful in anedoctic cases. De novo TMA is rarer. A number of factors including viral infection may be responsible of de novo TMA, but in most cases TMA is triggered by calcineurin inhibitors or mTOR inhibitors. The clinical presentation of de novo TMA may be variable with some patients showing clinical and laboratory features of HUS while others showing only a progressive renal failure. The prognosis is less severe than with recurrent TMA. Complete withdrawal of the offending drug may lead to improvement in many cases. The addition of plasma exchange may result in graft salvage in about 80% of cases.

show abstract

“…In the setting of allograft dysfunction, TMA occurs in approximately 3.5% of all renal transplant patients on calcineurin inhibitor‐based immunosuppression (1). The mechanisms underlying TMA are not well established and several pathologic mechanisms have been proposed (9). Decreased production of activated protein C from endothelial cells and increased production of thromboplastin from mononuclear cells and of high‐molecular weight von Willebrand factor (VWF) multimers from endothelial cells can further sustain the thrombotic process (10).…”

Section: Discussionmentioning

confidence: 99%

“…The recommended initial treatment is cessation, replacement, or reduction in calcineurin inhibitors and administration of corticosteroids for concurrent GVHD (12). The reported long‐term outcomes after the above interventions have been variable (9). The substitution of another immunosuppressive drug for CsA, such as FK (13), may be one of the treatments of TMA.…”

Section: Discussionmentioning

confidence: 99%

Successful treatment of de novo thrombotic microangiopathy after minor ABO‐mismatched living donor kidney transplantation

Ushigome¹,

Sakai²,

Suzuki³

et al. 2008

Clinical Transplantation

View full text Add to dashboard Cite

We report a case of thrombotic microangiopathy developing after minor ABO‐mismatched living donor kidney transplantation. The patient was a 57‐yr‐old woman whose blood group was B‐positive. She received a kidney transplant from her husband whose blood group was O‐positive. The recipient human leukocyte antigen haplotype was entirely different from that of the donor and the direct lymphocyte cross‐match test was negative. The patient’s hemoglobin and platelet (Plt) count fell rapidly from 11.0 g/dL and 34 × 104/μL to 6.0 g/dL and 0.4 × 104/μL between days 10 and 15 after kidney transplantation, with no evidence of bleeding. On day 8, anti‐group B IgG and IgM antibodies were found in her serum. This anti‐B antibody was thought to be produced from passenger B lymphocytes in the donor’s kidney. Although in the case of hemolytic anemia after minor mismatched transplantation, the kidney function usually remains stable, the serum creatinine (s‐Cr) rose from 0.8 to 5.2 mg/dL. On day 16, the helmet cells appeared in the serum and a total of 20 units of group O packed red blood cells and 30 units of group O Plts were transfused. Biopsy of the transplanted kidney was performed, which revealed thrombotic microangio‐pathy, and appropriate therapy for DIC was administered, including anticoagulants, and cyclosporine A and mizoribine were replaced with tacrolimus and mycophenolate mofetil. Frequent plasma exchanges (PEX) with fresh frozen plasma were carried out. Furthermore, the anti‐CD20 antibody rituximab was administered, because PEX had no effect. Following the adoption of these measures, the anti‐donor antibodies disappeared to reduce the reaction on flow cytometric cross‐match test; an anti‐groupB antibody did not completely disappear but decreased in titer, and all the symptoms resolved immediately. The graft function recovered to a s‐Cr level of 1.6 mg/dL by 34 d after the transplantation and she was discharged by 36 d after the transplantation. At present, she is entirely healthy and the graft function remains good with a s‐Cr level of 1.1 mg/dL.

show abstract

Cyclosporine withdrawal in post‐renal transplant thrombotic microangiopathy

Abstract: The CsA withdrawal in cases with TMA at a stage when significant functional deterioration has not taken place can salvage the graft.

Cited by 11 publications

References 24 publications

De novo Thrombotic Microangiopathy in Renal Allograft Biopsies—Role of Antibody-Mediated Rejection

De novo Thrombotic Microangiopathy in Renal Allograft Biopsies—Role of Antibody-Mediated Rejection

Thrombotic microangiopathy after kidney transplantation

Successful treatment of de novo thrombotic microangiopathy after minor ABO‐mismatched living donor kidney transplantation

Contact Info

Product

Resources

About