De novo Thrombotic Microangiopathy Induced by Cytomegalovirus Infection Leading to Renal Allograft Loss

Keyzer, Kristel De; Laecke, Steven Van; Peeters, Patrick; Vanholder, Raymond

doi:10.1159/000321328

Cited by 26 publications

(25 citation statements)

References 30 publications

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“…CMV infection can be a trigger for TMA in kidney-transplant recipients, and TMA can occur shortly after a transplant or even years later (53-55). A case of bilateral CMV retinitis presented as a floater was reported in a case study of a woman with systemic lupus erythematous who was undergoing hemodialysis.…”

Section: Miscellaneous Presentationsmentioning

confidence: 99%

Rare Presentations of Cytomegalovirus Infection in Renal Allograft Recipients

Ardalan

2012

Nephro Urol Mon

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Cytomegalovirus is the most common viral infection after kidney transplantation. Clinical presentations of cytomegalovirus infection range from asymptomatic infection to organ-specific involvement. Most symptomatic infections manifest as fever and cytopenia. The gastrointestinal tract is the most common site of tissue-invasive infection, often presenting as diarrhea or gastrointestinal bleeding. Gastrointestinal obstruction, perforation, thrombosis of large gastrointestinal veins, splenic artery thrombosis, and pancreatitis are rare gastrointestinal presentations of cytomegalovirus infection. Renal-allograft ureteral stricture and skin involvement are other rare presentations of cytomegalovirus infection. hemophagocytic syndrome, thrombotic microangiopathy, adrenal insufficiency, and renal allograft artery stenosis are other rare symptoms of cytomegalovirus infection.

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Section: Miscellaneous Presentationsmentioning

confidence: 99%

Rare Presentations of Cytomegalovirus Infection in Renal Allograft Recipients

Ardalan

2012

Nephro Urol Mon

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“…Согласно данным литературы, наиболее частыми причинами ТМА de novo после ТП служат нефротоксичность ИК и антитело-опосредованное отторжение, но могут встречаться и другие этиологические факторы по отдельности или в сочетании -инфекции, другие лекарственные препараты (не ИК), онкологические осложнения, беременность, наличие антифосфолипидных антител, генетические аномалии белков-регуляторов комплемента (как при возвратном атипичном ГУС) [1,3,4,6,8,9,12,[19][20][21][22]. В нашем исследовании ведущими причинами ТМА также выступали нефротоксичность и антитело-опосредованное отторжение, однако к ним добавился еще один важный фактор -донорская (предсуществующая) хроническая ТМА.…”

Section: Discussionunclassified

Thrombotic microangiopathy after kidney transplantation: causes, clinical specifics and outcomes

et al. 2020

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Background: Thrombotic microangiopathy (TMA) is a clinical and morphological phenomenon characterized by specific microvascular injury, microangiopathic hemolytic anemia, and damage of various target organs. TMA after kidney transplantation (post-renal transplant TMA) is a serious complication affecting the recipient and graft survival.Aim: To analyze the timing, causes, specifics of the clinical course and outcomes of TMA in renal transplant recipients.Materials and methods: This one-center study was based on a comprehensive examination and follow-up of 697 patients who had undergone 728 kidney transplantations (KT) from deceased donors in 2003–2019. Post-transplant TMA of the renal graft was confirmed morphologically in all cases.Results: We identified 32 episodes of post-transplant TMA in 32 patients; thus, the incidence of TMA was 4.4%. All cases developed after KT de novo; no recurrent TMA was observed. TMA was systemic in 37.5% and locally renal in 62.5% of the patients. The median time to the development of post-transplant TMA was 0.55 (range, 0.1 to 51.6) months. The patients with TMA did not differ from those without by gender, age, body mass index, underlying disorders, type and duration of dialysis before KT, protocols of immunosuppressive therapy, incidence of surgical, urological, infectious, cardiovascular and oncological complications. The patients with TMA were significantly more likely to have graft rejection (25.0% vs 11.2%, p = 0.035) and a never-functioning transplant (28.1% vs 4.9%, p < 0.001). The presence of TMA negatively affected the transplantation outcomes. The cumulative 1-year graft survival in the patients without and with TMA was 91% and 44%, respectively, whereas their 5-year survival rates were 68% and 25% (p < 0.001). The leading causes of TMA were: donor pathology (31.2%), antibody-mediated rejection (28.1%), and cyclosporine/ tacrolimus nephrotoxicity (21.9%); the proportion of other causes was 18.8%. A combination of TMA etiological factors was identified in 68.7% of the recipients. The recipients with of calcineurin inhibitors nephrotoxicity had a more favorable prognosis compared to those with other causes of TMA.Conclusion: Post-renal transplant TMA is an infrequent but serious complication that worsens the graft survival and often is life-threatening for recipients. In most cases, TMA develops in the early post-operative period; however, it can occur any time thereafter. To improve the outcome of TMA, early diagnosis is necessary based on clinical suspicion and a prompt biopsy of the renal graft with suspected TMA. Treatment should be started quickly with consideration of the cause of the complication.

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“…However, de novo TMA is commonly related as a result of immunosuppression, renal allograft rejection, infections like cytomegalovirus, and other causes such as recurrent glomerulonephritis. 6,7,10,[17][18][19] The reported rates of de novo TMA vary from 1.1% to 14%. [4][5][6][7][8][9][10][11][12][13][14][15] As we observed, the incidence of Escherichia coliassociated typical hemolytic uremic syndrome is significantly low in renal transplant patients.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Özdemir

Atılgan²,

Akçay³

et al. 2018

Exp Clin Transplant

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Objectives: Thrombotic microangiopathy is a form of renal capillary injury possibly associated with calcineurin inhibitor toxicity, acute humoral rejection, infections, and recurrent diseases. Here, we examined its incidence in patients diagnosed with acute and chronic active humoral rejection, polyomavirus nephropathy, acute cellular rejection, and immunoglobulin A recurrence. Materials and Methods: In total, 272 renal allograft recipients who met the inclusion criteria were reevaluated for presence of renal thrombotic microangiopathy. Thrombotic microangiopathy diagnosis was established by clinical, laboratory, and histologic features. C4d expression in peritubular capillaries was determined. Clinical data were collected from medical records. Results: Of 272 patients (mean age of 42.8 ± 12.7 years), only 74 patients (27.2%) had de novo thrombotic microangiopathy, which was found in 30/90 patients (33.3%) with acute humoral rejection, 9/51 (17.6%) with acute cellular rejection, 22/53 (41.5%) with chronic active humoral rejection, 10/55 (18.2%) with polyomavirus nephropathy, and 3/23 (13%) with immunoglobulin A nephropathy. Significant differences were shown between therapy type and thrombotic microangiopathy development (P = .02). Patients who received cyclosporine (38.5%) tended to show higher incidence of thrombotic microangiopathy than patients who received tacrolimus (20.7%) or sirolimus (7.7%). Patients with C4d-positive acute humoral (97.6% vs 2.4%) and chronic active humoral rejection (68.2% vs 31.8%) had greater incidence of thrombotic microangiopathy versus those who were C4d-negative. Graft loss was significantly higher in C4d-positive than in C4d-negative thrombotic microangiopathy groups (P < .001). Overall 1-, 3-, and 5-year graft survival was 94%, 85%, and 85% versus 83%, 51%, and 51% in thrombotic microangiopathy-negative versus thrombotic microangiopathy-positive patients (P < .001). Conclusions: Acute humoral rejection and chronic active humoral rejection were the most common and therefore most important causes of de novo thrombotic microangiopathy in renal transplant patients. Its presence in the renal allograft biopsy should arouse suspicion for underlying acute or chronic active humoral rejection. Key words: Acute cellular rejection, Acute humoral rejection, C4d expression, Chronic active humoral rejection, IgA nephropathy, Polyomavirus nephropathy, Renal allograft biopsy IntroductionThrombotic microangiopathy (TMA) describes a pathologic lesion in which abnormalities in the vessel wall of arterioles and capillaries lead to microvascular thrombosis. The clinical features of TMA result from the obstruction of the microcirculation and ultimately depend on the distribution of involved vascular beds. Microangiopathic hemolysis is the hallmark feature of this obstructed microcirculation. Thrombotic microangiopathy is a pathologic diagnosis, but its presence is commonly inferred from observations of thrombocytopenia and microangiopathic hemolysis in the appropriate clinical setting. [1][2]...

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De novo Thrombotic Microangiopathy Induced by Cytomegalovirus Infection Leading to Renal Allograft Loss

Cited by 26 publications

References 30 publications

Rare Presentations of Cytomegalovirus Infection in Renal Allograft Recipients

Rare Presentations of Cytomegalovirus Infection in Renal Allograft Recipients

Thrombotic microangiopathy after kidney transplantation: causes, clinical specifics and outcomes

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