Cases reported "Hemolytic-Uremic Syndrome"

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1/68. Basic fibroblast growth factor in hiv-associated hemolytic uremic syndrome.

    Endothelial injury is the primary pathogenic event leading to the renal thrombotic microangiopathic lesions typical of the hemolytic uremic syndrome (HUS). Basic fibroblast growth factor (bFGF) is an angiogenic growth factor released by injured endothelial cells. In a previous study we have found a significant accumulation of bFGF in human immunodeficiency virus (hiv)-transgenic mice with renal disease. Here we investigated whether bFGF was accumulated in the circulation and kidneys of two children with hiv-associated HUS (hiv-HUS), and studied the mechanisms involved in this process. The plasma levels of bFGF in children with hiv-HUS (124 /-20 pg/ml) were increased compared with five children with hiv nephropathy (49 /-6 pg/ml) and twenty hiv-infected children without renal disease (26 /-4 pg/ml, P<0.001). immunohistochemistry and receptor binding studies showed that bFGF was accumulated bound to heparan sulfate proteoglycans in renal glomeruli and interstitium surrounding renal tubules in hiv-HUS kidneys. Basic FGF stimulated the proliferation of mesangial and urinary renal tubular epithelial cells isolated from both patients. These findings support the hypothesis that bFGF and its low-affinity binding sites may play a relevant role in modulating the process of glomerular and renal tubular regeneration during the acute stages of hiv-HUS. A follow-up study in a larger sample population is required to confirm these results.
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2/68. Hemolytic uremic syndrome in small-bowel transplant recipients: the first two case reports.

    Post-transplant hemolytic uremic syndrome (HUS) is an uncommon but well-described complication in solid organ transplant recipients. Believed to be secondary to immunosuppressive therapy, it has been reported after kidney, liver, pancreas, heart, and lung transplants. In all reported cases, the primary organ affected was the kidney (transplant or native). But until now, no cases after small-bowel transplants and no cases in which the kidney was not the primary organ affected have been reported. We report two cases of HUS in small-bowel transplant recipients. In our first case, clinical presentation was with renal failure; biopsy of the native kidney demonstrated the typical histological changes seen with HUS, namely occlusion of the microcirculation by thrombi and platelet aggregation. immunosuppression was changed from tacrolimus to cyclosporin, but with no improvement in renal function. In our second case, the transplanted bowel was the primary organ affected. This recipient presented with ulcers in the bowel mucosa, which were believed to be ischemic in origin, secondary to occlusive vascular lesions affecting the small vessels in the transplanted bowel. Her tacrolimus dose was decreased with resolution of ulcers and no evidence of rejection. These two cases represent the first reports of HUS after small-bowel transplants; in addition, our second case represents the first report of an extrarenal graft as the primary organ affected. When caring for small-bowel transplant recipients, physicians must be alert to the possibility of HUS and its various presentations.
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3/68. Thrombotic microangiopathy with renal failure in two patients undergoing gemcitabine chemotherapy.

    Described here are 2 patients who developed thrombotic microangiopathy of the kidneys after receiving high cumulative doses of the new anticancer drug gemcitabine. The first patient, who received gemcitabine for treatment of a carcinoma of the pancreas, required hemodialysis for 6 months. In the second case, a woman suffering from a cholangiocellular carcinoma, end-stage renal disease was irreversible. Clinical awareness, timely detection and discontinuation of gemcitabine are mandatory to prevent this rare but disastrous complication of gemcitabine therapy. copyright copyright 1999 S. Karger AG, Basel
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4/68. cyclosporine-induced hemolytic uremic syndrome and hemorrhagic colitis following renal transplantation.

    Nephrotoxicity remains one of the most common side-effects of cyclosporine in the setting of transplantation. Acute reversible decreases in glomerular filtration rate and chronic irreversible renal damage are the most common manifestations, but hemolytic uremic syndrome and thrombotic thrombocytopenic purpura have been reported. prognosis of cyclosporine-associated de novo hemolytic uremic syndrome (CyA-HUS) is poor, with nearly half of affected patients losing function in the transplanted kidney. Therapeutic options are limited, but good outcomes have been reported by switching patients from cyclosporine to tacrolimus. We report an unusual presentation of CyA-HUS associated with hemorrhagic colitis following renal transplantation. The patient was successfully managed by switching from cyclosporine to tacrolimus.
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5/68. A case of late onset cyclosporine-induced hemolytic uremic syndrome resulting in renal graft loss.

    A case of late onset hemolytic uremic syndrome (HUS) associated with cyclosporine (CYA) is described in this report. A 50-yr-old man with end-stage renal failure due to immunoglobulin a (IgA) nephropathy received a renal transplant from his wife. Human leucocyte antigen was completely unmatched. Immunosuppressant was a combination of prednisolone, azathioprine, and CYA. He was discharged 1 month after transplantation, with no episode of acute rejection. Twenty-one months after transplantation, his platelet count and hematocrit began to decrease and lactate dehydrogenase began to increase. Graft biopsy showed thrombotic microangiopathy and recurrent IgA nephropathy. Graft function was rapidly deteriorated and methylprednisolone pulse therapy was not effective. Twenty-five months after transplantation, he returned to a regular hemodialysis. hemolysis was immediately improved after a reduction of the dose of CYA to 50 mg/d. The trough level of CYA was less than 200 ng/mL in most periods of his clinical course. blood pressure was high throughout the clinical course. Although acute vascular rejection or malignant hypertension could also cause a thrombotic microangiopathy, CYA was most likely a cause of HUS in the present case because of the following reasons: neither anti-acute rejection therapy nor an adequate control of his blood pressure was effective in improving clinical features of HUS; hemolysis and thrombocytopenia disappeared immediately after the reduction of the dose of CYA to 50 mg/d. It has been reported that HUS carried poor prognosis only when occurring shortly after transplantation in cadaver kidney recipients. The present transplant was from a living donor and HUS occurred 21 months after transplantation and was severe enough to result in graft loss. High blood pressure might be one of the predisposing factors of HUS associated with CYA in the present case. CYA should be stopped and other alternative immunosuppressants should be given in cases of acute graft deterioration with hemolysis and thrombocytopenia, irrespective of the interval from transplantation, CYA dose, or CYA trough level.
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6/68. Autosomal dominant hemolytic uremic syndrome: variable phenotypes and transplant results.

    Autosomal dominant hemolytic uremic syndrome (ADHUS) is a rare disorder with a poor prognosis that was considered to present mainly in adults. Recurrent episodes of ADHUS were also thought to be uncommon. However, increasing reports suggest that children are often affected, that recurrent episodes may occur pretransplantation, and that post-transplant recurrences occur in about 50% of cases. We describe the occurrence of ADHUS in two unrelated families with different outcomes. It is apparent that there are several types of ADHUS (with and without serum complement abnormalities) and that there may be variable expression of the phenotype. There was variable penetration of HUS in four (possibly five) adults and two children in four generations of one kindred. There was also one definite unaffected carrier. Two patients had successful renal transplants without recurrences; the HUS recurred in a third patient soon after transplantation. In a second family, the father had three episodes of HUS at 18, 26 and 29 years of age; his son had one episode of HUS at 5 years of age. Both recovered completely. Evaluation of these patients, previous reports, and follow-up contacts of previous reports suggests that post-transplant recurrence of ADHUS is more common than previously reported and may not be prevented by prior nephrectomy of native kidneys.
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7/68. Clopidogrel-associated thrombotic thrombocytopenic purpura/hemolytic uremic syndrome in a kidney/pancreas transplant recipient.

    BACKGROUND: We present a case report of thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS) developing in a kidney/pancreas transplant recipient after the initiation of treatment with clopidogrel for symptomatic coronary artery disease. methods: A 35-year-old male kidney/pancreas recipient developed unstable angina 5 years after transplantation. The patient was treated with clopidogrel as adjunct therapy. A TTP/HUS condition developed, was diagnosed early, and successfully reversed with the implementation of plasmapheresis and cessation of clopidogrel and cyclosporine A. RESULTS: The patient continues taking cyclosporine A with good renal function 6 months after the incident, and successfully underwent coronary artery by-pass grafting 3 months after the event. DISCUSSION: This case demonstrates that early identification and treatment can reverse the TTP/HUS process associated with thienopyridine-derived agents. We strongly recommend that drugs of the thienopyridine class be used cautiously in transplant recipients, especially those taking calcineurin-inhibitors.
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8/68. Hemolytic uremic syndrome associated with denys-drash syndrome.

    The denys-drash syndrome is defined by the occurrence of combinations of pseudohermaphroditism, nephrotic syndrome with diffuse mesangial sclerosis, Wilms' tumor, and constitutional mutations in the WT1 suppressor gene. Most patients develop end-stage renal failure. Atypical hemolytic uremic syndrome (HUS) is defined by onset of acute hemolytic anemia with fragmented erythrocytes, thrombocytopenia, and renal failure in the absence of a gastrointestinal prodromal illness of bloody diarrhea. The purpose of this report is to describe the occurrence of features of atypical HUS and denys-drash syndrome in two African-American boys aged 13 and 16 months. Each had nephrotic syndrome, diffuse mesangial sclerosis, and WT1 point mutations. Both had grade III hypospadias and undescended testes. They had normal serum creatinine concentrations and hematology a month before presenting with HUS. Stool cultures for escherichia coli o157:H7 were negative. Each patient has been transplanted with cadaver kidneys without recurrence of HUS.
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9/68. apoptosis of renal tubular cells in Shiga-toxin-mediated hemolytic uremic syndrome.

    In order to clarify the mechanism of unusual renal tubular dysfunction seen in a child with Shiga toxin (Stx)-mediated hemolytic uremic syndrome (HUS), we studied the renal biopsy specimens for Stx binding and apoptosis of renal tubular cells. A 7-year-old boy with Stx-2-mediated HUS demonstrated extensive renal tubular damage characterized by nonoliguric acute renal failure, increased urinary tubular enzymes and defective urine-concentrating capacity. His renal biopsy specimens were analyzed for Stx binding and apoptotic cell death. Seven kidney tissue specimens obtained from patients without HUS served as controls. Detection of Stx binding to renal sections and apoptotic cells were performed using mouse monoclonal anti-Stx 2 antibody and the TUNEL method, respectively. Positive staining was observed predominantly in renal tubular cells, while the 7 kidney tissue specimens from control patients did not show positive staining. To the best of our knowledge, this is the first case to show Stx binding and apoptotic cell death in renal tubules on biopsy specimens obtained from a child with Stx-mediated HUS. In conclusion, this case suggests that vascular endothelial cells are not the sole nor the consistent target for Stx-mediated cell injury and that significant renal tubular damage other than glomerular damage might occur in some children with Stx-mediated HUS.
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10/68. Localization of shiga toxins of enterohaemorrhagic Escherichia coli in kidneys of paediatric and geriatric patients with fatal haemolytic uraemic syndrome.

    Haemolytic uraemic syndrome (HUS) is characterized by haemolytic anaemia, thrombocytopenia and renal failure. infection with enterohaemorrhagic Escherichia coli (EHEC), mainly O157:H7, has been strongly implicated as the major cause of HUS in children. The pathogenesis of HUS caused by the infection is not well understood and the defined sites of Stx in kidney of EHEC-infected humans has not been clearly demonstrated. The aim of this study was to investigate and compare the locations of Stx deposition in kidneys of paediatric and geriatric patients who died from enterohaemorrhagic E. coli O157 (EHEC) associated HUS, using an immunoperoxidase staining of the tissues. The study revealed that binding of Stx was relatively less and limited only to the renal tubules of an adult case (81 years old), while more binding was found at both renal tubules and glomeruli of an infant case (21 months old). The Stx binding in the infant's glomeruli was at podocytes, mesangial and endothelial cells. It has been known that young children are more susceptible than adults to HUS. One possibility for this is that the more extensive binding of the Stx to the kidney tissue of the paediatric patient might be due to the higher synthesis and expression of Stx receptors, i.e. Gb(3), in infants and less so in the aged individuals. However, other alternatives are possible, for example, the difference in stage of HUS in individual patients. Thus it is too early to draw any conclusion on this enigma and further investigation is required.
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