Thrombotic Microangiopathy in a Transplant Recipient

Mundra, Venkat Ram Rakesh; Mannon, Roslyn B.

doi:10.2215/cjn.00020118

Cited by 5 publications

(5 citation statements)

References 10 publications

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“…In a renal transplant scenario, many TMA etiologies may represent a diagnosis challenge. There are three situations: recurrence, de novo TMA and associated to antibody mediated rejection (AMR) (11,17). One Brazilian cohort study with 1549 patients found 1.1% of de novo TMA after kidney transplantation, excluded AMR and recurrent HUS.…”

Section: Discussionmentioning

confidence: 99%

“…In C4d-negative AMR cases, increased expression of validated gene transcripts in the biopsy tissue could be an indicative of antibody interaction with vascular endothelium (22). The involvement of the entire vascular tree and endarteritis are features of AMR (17). The group of secondary TMA had 5 patients (41.6%) with AMR, all of them C4d-positive.…”

Section: Discussionmentioning

confidence: 99%

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Histopathological features of thrombotic microangiopathies in renal biopsies

et al. 2019

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Background: Thrombotic microangiopathy (TMA) is a morphologic lesion characterized by thrombi occluding microvasculature related to endothelial injury. Objectives: This study aimed to assess the association between histopathological findings and etiology of TMA. Patients and Methods: This cross-sectional study comprised a sample of 34 patients who underwent renal biopsy and received an initial TMA diagnoses resulting in 29 definitive TMA cases. We evaluated the TMA features and clinical histopathological correlation. Results: The most frequent etiologies were atypical hemolytic uremic syndrome (aHUS) (n= 10; 34.5%), hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli (STECHUS) (n=6; 24.1%) and secondary causes of TMA (n= 12; 41.4%). We found the following histological features; patients with aHUS had thrombi in 60% of biopsies, membranoproliferative glomerulonephritis (MPGN)-like pattern in 20% and ischemia in 20%; patients with STEC-HUS had thrombi (14.3%), MPGN-like pattern (14.3%), endothelial swelling (14.3%) and ischemia (57.1%); patients with secondary etiologies had thrombi (58.3%), endothelial swelling (16.7%), ischemia (16.7%) and MPGN-like pattern (8.3%). Conclusions: The distribution of classic TMA findings was not related to etiology in spite of microthrombi having been found mostly in aHUS and secondary etiologies, whereas ischemia was found mainly in STEC-HUS. We did not find a histopathological pattern to each etiology of TMA.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Histopathological features of thrombotic microangiopathies in renal biopsies

et al. 2019

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“…More severe thrombocytopenia is a risk factor for bleeding, and platelet transfusion may be necessary if invasive procedures, such as a renal biopsy, are required and the platelet count is <50 × 10 9 /L [61]. An important consideration, if thrombocytopenia is observed post-transplant, is to look for any other evidence of thrombotic microangiopathy (TMA, Table 7) [62]. TMA occurring after transplant may be due to recurrence of primary haemolytic uraemic syndrome, or a de novo problem.…”

Section: Haematological Biochemical and Metabolic Derangementmentioning

confidence: 99%

Perioperative Care for Kidney Transplant Recipients

Hultin¹,

Hawley²,

Johnson³

et al. 2019

Perioperative Care for Organ Transplant Recipient

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Transplantation carries significant mortality benefit compared to dialysis in end-stage kidney disease. Increased perioperative risk, however, results in a higher mortality in the first 3 months post-transplantation compared to remaining on haemodialysis. Consequently, optimal perioperative management is essential. Patients presenting for kidney transplantation require rapid assessment and preparation for theatre to minimise ischaemic times and improve mortality and graft outcomes. This task is often complicated by the presence of multiple medical comorbidities. Furthermore, early complications of hypotension, delayed graft function, renovascular and ureteric surgical complications and rejection render the perioperative phase of transplant challenging for the recipient and for the transplant team. In this chapter, we outline current practices in the assessment and management of kidney transplant recipients during the perioperative period, particularly focusing on their clinical application and the evidence underpinning them.

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“…Thrombotic microangiopathy (TMA) is a rare disease that presents with arteriolar and capillary thrombosis [1][2][3]. TMA is a clinicopathologic diagnosis [4].…”

Section: Introductionmentioning

confidence: 99%

Primary Hyperaldosteronism: A Rare Cause of Malignant Hypertension with Thrombotic Microangiopathy in a Kidney Transplant Recipient

Ormonde

Querido

Rombo

et al. 2021

Case Reports in Transplantation

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Thrombotic microangiopathy (TMA) is a rare disease that presents with haemolysis and organ damage. The kidney is one of the main affected organs, and TMA is associated with serious complications and increased mortality. In transplanted patients, TMA is even less common and has a variety of possible causes, including thrombotic thrombocytopenic purpura (TTP) and haemolytic-uremic syndrome (HUS), infections, drugs, autoimmune disease, tumours, and malignant hypertension. Transplant-related causes, such as antibody-mediated rejection, calcineurin inhibitors, and viral infections, need to be considered as well. The authors report a rare case of TMA in a kidney transplant recipient, whose investigation revealed malignant hypertension secondary to primary hyperaldosteronism.

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Thrombotic Microangiopathy in a Transplant Recipient

Cited by 5 publications

References 10 publications

Histopathological features of thrombotic microangiopathies in renal biopsies

Histopathological features of thrombotic microangiopathies in renal biopsies

Perioperative Care for Kidney Transplant Recipients

Primary Hyperaldosteronism: A Rare Cause of Malignant Hypertension with Thrombotic Microangiopathy in a Kidney Transplant Recipient

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