Concomitant Thrombotic Microangiopathy and Rejection in a Recent Kidney Transplant: A Case Study

2020 ◽  
pp. 1-4
Author(s):  
Muhammad A. Bukhari ◽  
Abdulaziz Al-Thumali ◽  
El-Sadig Yousif ◽  
Muhammad A. Bukhari ◽  
Najla K Almalki ◽  
...  

Thrombotic microangiopathy (TMA) is an uncommon, life-threatening complication that adversely affects kidney transplant recipient and allograft survival. Post-transplantation TMA can occur as recurrence of the primary TMA or as a de novo condition. The latter can be triggered by numerous factors post-transplantation including calcineurin inhibitors, certain infections and antibody-mediated rejection. Rejection-associated TMAs carry a significantly lower graft survival rate compared with post-transplant TMAs that are not associated with rejection. In this case report, we present a rare case of rejection-associated TMA in a recently transplanted renal allograft that was managed in Al-Hada Armed Forces Hospital. Despite the poor expected outcome of this condition; the patient was successfully treated after early initiation of medical interventions. Transplantation teams may face many challenges managing such a combination of medical conditions, which may halt pursuing appropriate diagnostic and therapeutic measures in a timely fashion. This article highlights some of these challenges for better understanding of such a complex condition.

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Carolina Ormonde ◽  
Sara Querido ◽  
Nuno Rombo ◽  
Rita Roque ◽  
Belarmino Clemente ◽  
...  

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.


2015 ◽  
Vol 9 (4) ◽  
pp. 155-158
Author(s):  
Cengiz Bulut ◽  
Ebru Gok Oguz ◽  
Basol Canbakan ◽  
Deniz Ayli

2010 ◽  
Vol 10 (8) ◽  
pp. 1804-1811 ◽  
Author(s):  
A. A. Satoskar ◽  
R. Pelletier ◽  
P. Adams ◽  
G. M. Nadasdy ◽  
S. Brodsky ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Marta Crespo ◽  
Laura Llinàs-Mallol ◽  
Dolores Redondo-Pachón ◽  
Carrie Butler ◽  
Javier Gimeno ◽  
...  

BackgroundCorrelation between antibody-mediated rejection (ABMR) and circulating HLA donor-specific antibodies (HLA-DSA) is strong but imperfect in kidney transplant (KT) recipients, raising the possibility of undetected HLA-DSA or non-HLA antibodies contributing to ABMR. Detailed evaluation of the degree of HLA matching together with the identification of non-HLA antibodies in KT may help to decipher the antibody involved.MethodsWe retrospectively assessed patients with transplant biopsies scored following Banff’15 classification. Pre- and post-transplant serum samples were checked for HLA and non-HLA antibodies [MICA-Ab, angiotensin-II type-1-receptor (AT1R)-Ab, endothelin-1 type-A-receptor (ETAR)-Ab and crossmatches with primary aortic endothelial cells (EC-XM)]. We also analyzed HLA epitope mismatches (HLA-EM) between donors and recipients to explore their role in ABMR histology (ABMRh) with and without HLA-DSA.ResultsOne-hundred eighteen patients with normal histology (n = 19), ABMRh (n = 52) or IFTA (n = 47) were studied. ABMRh patients were HLA-DSApos (n = 38, 73%) or HLA-DSAneg (n = 14, 27%). Pre-transplant HLA-DSA and AT1R-Ab were more frequent in ABMRh compared with IFTA and normal histology cases (p = 0.006 and 0.003), without differences in other non-HLA antibodies. Only three ABMRhDSAneg cases showed non-HLA antibodies. ABMRhDSAneg and ABMRhDSApos cases showed similar biopsy changes and graft-survival. Both total class II and DRB1 HLA-EM were associated with ABMRhDSApos but not with ABMRhDSAneg. Multivariate analysis showed that pre-transplant HLA-DSA (OR: 3.69 [1.31–10.37], p = 0.013) and AT1R-Ab (OR: 5.47 [1.78–16.76], p = 0.003) were independent predictors of ABMRhDSApos.ConclusionsIn conclusion, pre-transplant AT1R-Ab is frequently found in ABMRhDSApos patients. However, AT1R-Ab, MICA-Ab, ETAR-Ab or EC-XM+ are rarely found among ABMRhDSAneg patients. Pre-transplant AT1R-Ab may act synergistically with preformed or de novo HLA-DSA to produce ABMRhDSApos but not ABMRhDSAneg. HLA epitope mismatch associates with ABMRhDSApos compared with ABMRhDSAneg, suggesting factors other than HLA are responsible for the damage.


Author(s):  
R. O. Kantariya ◽  
O. N. Vetchinnikova ◽  
A. V. Vatazin ◽  
L. A. Sherman

Background. Non-alcoholic Wernicke’s encephalopathy occurs in various somatic conditions with thiamine deficiency, excessive excretion of thiamine, or impaired thiamine metabolism. Very few cases of this pathology have been described in chronic kidney disease (CKD). We present a unique case of non-alcoholic Wernicke’s encephalopathy in a patient with a kidney transplant is presented.Past medical history. The patient underwent kidney transplantation in 2008. Outpatient follow-up by a nephrologist was irregular. Renal graft function remained relatively stable: blood creatinine 200–240 μmol/L, estimated glomerular filtration rate 40–30 mL/min, tacrolimus plasma concentrations tended to increase (5.7–7.6–8.4–10.4 ng/mL); repeated graft biopsy (in 2015 and in 2017) determined the chronic toxicity of calcineurin inhibitors. The patient’s condition worsened in late January 2020: body temperature increased to 38°C, nausea, vomiting, loose, watery stools for up to 5 times per day, 8 kg weight loss, decreased diuresis. A few days later, double vision, shaky gait and then immobility appeared. Biochemical examination results: potassium 3.8 mmol/L, sodium 139 mmol/L, alpha-amylase 159 units/L (norm 0–100 units/L), creatinine 242 mmol/L, urea 13.2 mmol/L; ultrasound signs of pancreatitis. Magnetic resonance imaging (MRI) of the brain: bilateral diffuse lesions of the midbrain, thalamus, and cerebellum. Based on the clinical picture and on brain MRI results, Wernicke’s encephalopathy was diagnosed. Parenteral administration of thiamine had a good effect.Conclusion. Possible mechanisms of the development of Wernicke’s encephalopathy in a patient were discussed. Vigilance is required regarding this disease when metabolic disorders occur in patients with CKD.


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