Cases reported "Hemolytic-Uremic Syndrome"

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11/68. Acquired glomerulocystic kidney disease following hemolytic uremic syndrome.

    Glomerulocystic kidney disease (GCKD) is a rare congenital condition that is usually reported in infants and young children. Only five cases of acquired GCKD after an acquired renal disease have been reported. Among these, two patients have developed cystic glomerular lesions following hemolytic uremic syndrome (HUS). We report a third case in a 2-year-old patient with this association. Common features between these three cases include atypical HUS, development of GCKD after prolonged peritoneal dialysis treatment, severe hypertension, and normal-sized kidneys without development of macroscopic cysts. pathology findings in our patient include heavy expression of epidermal growth factor receptor in proximal tubules and evidence of obstruction of the glomerular outflow. We speculate that cystic dilatation of the Bowman's capsule may be secondary to ischemic lesions leading to proximal tubular obstruction.
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12/68. Combined kidney and liver transplantation for familial haemolytic uraemic syndrome.

    Recurrent haemolytic uraemic syndrome (HUS) is a genetic form of thrombotic microangiopathy that is mostly associated with low activity of complement factor H. The disorder usually develops in families, leads to end stage renal disease, and invariably recurs after kidney transplantation. We did a simultaneous kidney and liver transplantation in a 2-year-old child with HUS and a mutation in complement factor h to restore the defective factor H, with no recurrence of the disease. The operation was successful, and at discharge, the child had healthy kidney and liver function, with no sign of haemolysis.
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13/68. Fulminant recurrence of atypical hemolytic uremic syndrome during a calcineurin inhibitor-free immunosuppression regimen.

    recurrence of hemolytic uremic syndrome (HUS) after kidney transplantation is frequent, occurring almost exclusively in patients with atypical HUS, which is not caused by escherichia coli gastroenteritis and in which diarrhea is absent. calcineurin inhibitors are associated with recurrence of HUS. In two children who underwent living donor kidney transplantation for atypical HUS, we pre-emptively employed sirolimus in a calcineurin inhibitor-free immunosuppression regimen. Both children had excellent early graft function, yet both developed severe recurrent disease and subsequently lost their grafts. Avoidance of calcineurin inhibitors did not prevent recurrence of severe HUS and graft loss. Transplantation for severe atypical HUS remains problematic.
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keywords = kidney
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14/68. TTP/HUS occurring in a simultaneous pancreas/kidney transplant recipient after clopidogrel treatment: evidence of a nonimmunological etiology.

    BACKGROUND: One recently reported thrombotic thrombocytopenia purpura/hemolytic uremic syndrome (TTP/HUS) case involved a patient who underwent simultaneous pancreas/kidney (SPK) transplant followed by pancreas rejection and clopidogrel treatment, an antiplatelet agent that has been associated with immunologically mediated TTP/HUS. We present a second case of TTP/HUS developing in an SPK recipient who was also receiving clopidogrel. methods: After a stroke, a 48-year-old male SPK transplant recipient received clopidogrel. Four months later, thrombosis and rejection of the transplanted pancreas occurred. One week after a pancreatectomy, TTP/HUS developed that resolved with clopidogrel and sirolimus discontinuation and lowering of the tacrolimus dose. RESULTS: A plasma sample revealed von willebrand factor cleaving metalloproteinase activity, although no immunoglobulins to the protease were identified. The patient continues taking tacrolimus with normal renal function 1 year after the incident. DISCUSSION: Our findings suggest a nonimmunological etiology for TTP/HUS in clopidogrel-treated transplant recipients. Furthermore, mechanistic focused laboratory studies can facilitate interpretation of case report findings.
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keywords = kidney
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15/68. Withdrawal of interferon-alpha results in prompt resolution of thrombocytopenia and hemolysis but not renal failure in hemolytic uremic syndrome caused by interferon-alpha.

    This case report describes 2 patients with chronic myeloid leukemia in whom hemolytic uremic syndrome developed while being treated with interferon-alpha and hydroxycarbamide. Hemolytic uremic syndrome was recognized by progressive renal dysfunction, thrombocytopenia, microangiopathic hemolytic anemia, and histologic features of thrombotic microangiopathy in the kidney. Although renal dysfunction progressed to dialysis-dependent renal failure in one patient despite treatment with prednisolone and plasmapheresis but not in other, withdrawal of the treatment resulted in a prompt resolution of thrombocytopenia and microangiopathic hemolytic anemia in both patients.
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keywords = kidney
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16/68. Treatment of thrombotic microangiopathy in pregnancy with plasma exchange: a report of two cases.

    Thrombotic microangiopathy is a rare disease that can be induced and precipitated by pregnancy, and is associated with high maternal and fetal morbidity and mortality. It results from abnormal intravascular platelet aggregation that leads to transient ischemia in various organs, including the central nervous system, kidneys and placenta. plasma exchange is the most widely accepted method of treatment for this condition. delayed diagnosis is the main reason for morbidity and mortality, and results from difficulty in differentiating thrombotic microangiopathy from other obstetric emergencies. We report two cases of thrombotic microangiopathy that occurred antepartum and postpartum, respectively. The first patient was a 33-year-old woman who had two previous episodes of intrauterine fetal death in the 13th and 28th weeks of gestation, respectively. She received early plasma exchange at the 23rd week of gestation during this pregnancy and the fetus was delivered uneventfully. The second patient was a 28-year-old woman with progressive thrombocytopenia, anemia and deterioration of renal and liver function postpartum. She received early plasma exchange and it markedly improved her thrombocytopenia without sequelae. In conclusion, early diagnosis and early initiation of plasmapheresis may improve both maternal and fetal prognosis in thrombotic microangiopathy.
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keywords = kidney
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17/68. Recovery of renal function after long-term dialysis in hemolytic uremic syndrome.

    Long-lasting recovery of renal function of the native kidneys after prolonged renal replacement therapy is rare. An 8-year-old girl and a 3-year-old boy had suffered from acute atypical and diarrhea-associated hemolytic uremic syndrome (HUS), respectively, with subsequent apparent end-stage renal failure. Both recovered renal function after long-lasting anuria and dialysis of 8 and 16 months, respectively. After prolonged follow-up, i.e., 7 and 5 years after cessation of dialysis, they attained normal or slightly reduced renal function (plasma creatinine 84 and 90 micro mol/l, respectively). In addition, growth and cognitive development were normal. We conclude that caution is appropriate before offering early renal transplantation to pediatric patients with presumed end-stage kidney disease secondary to HUS.
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ranking = 0.2338632019518
keywords = kidney disease, kidney
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18/68. Successful treatment of hemolytic uremic syndrome after liver-kidney transplantation.

    INTRODUCTION: hemolytic-uremic syndrome (HUS) is a rare complication in organ transplantation, characterized by hemolytic microangiopathic anemia, thrombocytopenia, and severe renal failure. The syndrome is a well-recognized complication in bone marrow transplantation, and has been likewise described in several cases of solid organs transplantation, but never in patients receiving combined liver and kidney transplantation. CASE REPORT: We describe a case of HUS in a 59-year-old woman who underwent combined liver-kidney transplantation for hepato-renal polycystic disease. Clinical and laboratory manifestations of the syndrome were severe and included renal failure, hemolytic anemia, severe thrombocytopenia, hypertension, and neurological damage. The initial treatment consisted of withdrawal of cyclosporine, introduction of low-dose tacrolimus, and administration of fresh frozen plasma (FFP) transfusion and heparin. Since there was no improvement in clinical or biochemical features, plasmapheresis with FFP replacement (2000 mL/day) followed by intravenous immunoglobulin (0.4 mg/Kg/day) was started. A rapid improvement in renal function, platelet count, and hemolytic anemia was observed. CONCLUSIONS: Based on the good response observed in our patient, we feel that an aggressive treatment with plasmapheresis and intravenous immunoglobulin should be offered to organ transplant recipients with severe HUS.
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keywords = kidney
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19/68. Ischemic colitis as a manifestation of thrombotic microangiopathy following bone marrow transplantation.

    Thrombotic microangiopathy (TMA) is a microvascular disorder characterized by platelet aggregation and hemolytic anemia. In the setting of bone marrow transplantation (BMT), ischemic colitis due to TMA is difficult to differentiate from acute graft-versus-host disease. We report a 32-year-old man who presented ischemic colitis due to TMA after unrelated BMT for myelodysplastic syndrome. He suffered from treatment-resistant bloody diarrhea, and died of renal failure and aspergillus pleuritis on day 253 post-BMT. autopsy revealed endothelial injuries of arterioles and ischemic changes in the intestines and kidneys. Clinical and pathological characteristics of ischemic colitis due to BMT-associated TMA are described.
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20/68. Heterozygous and homozygous factor h deficiencies associated with hemolytic uremic syndrome or membranoproliferative glomerulonephritis: report and genetic analysis of 16 cases.

    Factor H (FH) is the major regulatory protein of the complement alternative pathway, with a structure consisting of a tandem array of 20 homologous units, called short consensus repeats (SCR). Reported are 16 FH-deficient patients. Among six patients with homozygous deficiency, four presented with membranoproliferative glomerulonephritis, and two with atypical hemolytic uremic syndrome (HUS). The ten other patients had heterozygous FH deficiency and developed atypical HUS. HUS onset occurred from birth to midadulthood, and disease progression was variable. Four children with homozygous or heterozygous FH deficiency and HUS underwent renal transplantation, which was successful in three but failed as a result of recurrence of HUS in one patient. All but one patient exhibited alternative pathway-mediated complement consumption, with no detectable FH antigenic levels or with 50% immunochemical or functional FH levels in the case of complete or partial deficiency, respectively. The molecular mechanisms of the deficiency were documented in all cases by exon-specific sequencing analysis. These mechanisms included nucleotide substitutions, insertion, or deletion located in SCR 2, 7, 11, 13, 15, and 20, leading to an amino acid substitution or to a stop codon. This report emphasizes the variability in the clinical progression of kidney diseases associated with FH deficiencies. Genetic analysis reveals the molecular abnormalities associated with FH deficiencies to be polymorphous.
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ranking = 0.19153419951205
keywords = kidney disease, kidney
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