1/82. Thrombotic microangiopathy as a complication of long-term therapy with gemcitabine.Three patients with pancreatic carcinoma treated with gemcitabine for 1 year developed clinical and laboratory findings compatible with an indolent form of the hemolytic-uremic syndrome. Renal biopsy specimens in two of these patients showed the characteristic features of thrombotic microangiopathy, and a skin biopsy specimen from the third patient, who presented with livedo reticularis, showed intravascular fibrin deposition. Thrombotic microangiopathy may represent a toxic effect of long-term gemcitabine therapy.- - - - - - - - - - ranking = 1keywords = microangiopathy (Clic here for more details about this article) |
2/82. Postpartum hemolytic-uremic syndrome associated with lupus anticoagulant. A case report.BACKGROUND: Hemolytic uremic syndrome is a rare thrombotic microangiopathy characterized by acute renal failure, thrombocytopenia and hemolysis. The underlying abnormality is currently thought to involve enothelial injury within the microcirculation. CASE: A 30-year-old woman, gravida 2, para 1, underwent emergency cesarean delivery at 36 /- 2 weeks' estimated gestational age for repetitive late decelerations and presumed severe preeclampsia. Postoperatively, the blood pressure remained persistently elevated despite multigent hypertensive therapy. By postpartum day 4 the patient continued to display acute oliguric renal failure, persistent severe thrombocytopenia and worsening hemolysis. Percutaneous renal biopsy was consistent with the clinical diagnosis of hemolytic uremic syndrome. Lupus anticoagulant was present, corroborated by markedly abnormal tissue thromboplastin inhibition and platelet neutralization procedures. With supportive therapy and daily plasmapheresis, the patient was discharged 22 days after delivery, with full recovery of renal function and resolution of the hemolytic process. CONCLUSION: Hemolytic uremic syndrome can be associated with lupus anticoagulant. This autoantibody may promote localized platelet aggregation, causing endothelial damage.- - - - - - - - - - ranking = 0.16666666666667keywords = microangiopathy (Clic here for more details about this article) |
3/82. Thrombotic microangiopathy associated with interferon therapy for patients with chronic myelogenous leukemia: coincidence or true side effect?BACKGROUND: interferon-alpha (rIFN-alpha) is an established therapy for patients with myeloproliferative disorders. Unusual immune-mediated side effects have been associated with rIFN-alpha therapy. The association of rIFN-alpha therapy with hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) has been reported infrequently. methods: Two patients with chronic myelogenous leukemia (CML) treated with rIFN-alpha-based regimens at the University of texas M. D. Anderson Cancer Center developed thrombotic microangiopathy (HUS/TTP). The course of their disease is described. A third patient who developed renal failure while receiving rIFN-alpha therapy and had no other causative factor for his renal failure is also described. RESULTS: The patients were ages 24, 49, and 36 years, and they had received rIFN-alpha therapy for 37, 67, and 92 months, respectively, prior to the development of the disorder. One patient had discontinued rIFN-alpha 1 month before the event because of presumed rIFN-alpha-related cardiomyopathy. Two patients received hydroxyurea and cytarabine as part of their therapy. No patient was receiving any medication known to be associated with HUS/TTP. None had a history of diarrheal illness, but escherichia coli OH157.H7 was grown from the stool of one patient. Two patients responded to plasmapheresis with normalization of counts and other indices, but both developed renal failure and became dependent on dialysis. One patient had evidence of disease progression and died of multiorgan failure. The third patient required dialysis for 18 months but is currently off dialysis; this patient has some residual renal impairment. CONCLUSIONS: Although no definitive association between rIFN-alpha therapy and thrombotic microangiopathies can be concluded from these data, these and other previously reported cases suggest that HUS/TTP is a rare side effect of rIFN-alpha therapy that should be managed in the standard fashion. Hypotheses regarding the mechanism underlying this association are discussed in this article.- - - - - - - - - - ranking = 0.83333333333333keywords = microangiopathy (Clic here for more details about this article) |
4/82. De novo hemolytic uremic syndrome postrenal transplant after cytomegalovirus infection.After renal transplantation, hemolytic uremic syndrome (HUS) may occur as recurrent disease or de novo. Here, we describe the de novo occurrence of HUS immediately after the onset of primary cytomegalovirus (CMV) disease in two renal allograft recipients. Patient no. 1 had primary CMV disease with biopsy-proven CMV esophagitis 2 months after transplantation. Patient no. 2 experienced primary CMV disease with fever and leukopenia 8 years after transplantation. Both patients were treated with intravenous ganciclovir. Both patients developed HUS with biopsy-proven thrombotic microangiopathy in the renal allograft only a few days (3 to 5 days) after the onset of CMV disease. The short interval between the onset of CMV disease and HUS, as well as the parallel course of CMV viremia and HUS in both patients, indicate there may be a pathophysiological link between both diseases. However, because antiviral therapy with ganciclovir was started before the onset of HUS in both patients, we cannot definitely rule out that HUS was triggered by ganciclovir.- - - - - - - - - - ranking = 0.16666666666667keywords = microangiopathy (Clic here for more details about this article) |
5/82. Thrombotic microangiopathy associated with reactivation of human herpesvirus-6 following high-dose chemotherapy with autologous bone marrow transplantation in young children.Thrombotic microangiopathy (TMA) is a serious complication of BMT. Several factors are important in the etiology of TMA, such as cyclosporin A, GVHD, irradiation, intensive conditioning chemotherapy and infection, which cause damage to vascular endothelial cells leading to activation of these cells. We describe two young children with TMA following high-dose chemotherapy with autologous BMT. Development of TMA was accompanied by reactivation of HHV-6, which was identified by both an increase in the copy number of HHV-6 dna in the peripheral blood and a significant increase in antibody titers to HHV-6. Thus, it was suggested that reactivation of HHV-6 together with high-dose chemotherapy played an important role in the pathogenesis of TMA in these patients. Since HHV-6 is known to infect vascular endothelial cells, and CMV which is virologically closely related to HHV-6, has been reported to be a pathogen that causes TMA, infection with HHV-6 of vascular endothelial cells may induce TMA via damage and activation of these cells.- - - - - - - - - - ranking = 0.83333333333333keywords = microangiopathy (Clic here for more details about this article) |
6/82. hemolytic-uremic syndrome with involvement of basal ganglia and cerebellum.hemolytic-uremic syndrome is a microangiopathy often associated with neurologic symptoms. Several patients with persistent lesions in cerebrum and basal ganglia have been reported. We present two children with bilateral basal ganglia and additional unilateral cerebellar lesions in magnetic resonance imaging. These resolved completely in one child. In the other child there were still residuals after 11 weeks. The neurologic symptoms of both improved after several therapeutic plasma exchanges and disappeared after months.- - - - - - - - - - ranking = 0.16666666666667keywords = microangiopathy (Clic here for more details about this article) |
7/82. 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- - - - - - - - - - ranking = 0.83333333333333keywords = microangiopathy (Clic here for more details about this article) |
8/82. 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.- - - - - - - - - - ranking = 0.33333333333333keywords = microangiopathy (Clic here for more details about this article) |
9/82. Renal thrombotic microangiopathy associated with interferon-alpha treatment of chronic myeloid leukemia.Recent reports have documented the development of renal thrombotic microangiopathy in patients with chronic myeloid leukemia (CML) who have undergone treatment with interferon-alpha. The pathogenesis of the renal lesion in such cases remains unclear. We report the case of a patient with chronic myeloid leukemia who developed renal failure and nephrotic syndrome while being treated with hydroxyurea and interferon-alpha. The renal biopsy showed features of chronic thrombotic microangiopathy. The patient had serologic and functional evidence of anti-phospholipid antibody. interferon-alpha is known to cause induction of multiple autoantibodies. We propose that in the context of CML, interferon-alpha treatment can induce pathogenic anti-phospholipid antibodies that result in renal thrombotic microangiopathy. This has important implications for patients with CML receiving immune-stimulating therapy because it suggests that prospective monitoring of such patients for anti-phospholipid antibody might identify those at risk of developing thrombotic microangiopathy. Furthermore, patients with established anti-phospholipid antibody syndrome in this context might benefit from intervention such as early anticoagulation.- - - - - - - - - - ranking = 1.3333333333333keywords = microangiopathy (Clic here for more details about this article) |
10/82. Thrombotic thrombocytopenic purpura in pulmonary-renal syndromes.Thrombotic thrombocytopenic purpura pathologically consists of a thrombotic microangiopathy that classically spares lung tissues. We describe a case of TTP that presented as a pulmonary-renal syndrome. In reviewing the international literature, pulmonary involvement is not as rare as once was thought, and the diagnosis of TTP should be considered in the differential diagnosis of pulmonary-renal syndromes.- - - - - - - - - - ranking = 0.16666666666667keywords = microangiopathy (Clic here for more details about this article) |
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