1/72. Cardiovascular consequences of renal anaemia and erythropoietin therapy.Cardiovascular disease is the leading cause of increased mortality in patients with renal failure and vigorous attention to cardiovascular risk factors is therefore required to improve patient outcome. The availability of recombinant human Epo has focused the interest on the role of chronic anaemia in the pathogenesis of cardiovascular disease. Severalfold evidence indicates that anaemia can contribute to cardiac volume overload and together with overhydration, fistula flow and the pressure overload secondary to arterial hypertension, it may play a significant role in the development of cardiac hypertrophy. As in the general population left ventricular hypertrophy is a severe adverse risk factor in renal patients. In addition, in the presence of ischaemic heart disease anaemia may further worsen cardiac oxygen supply. This dual effect of anaemia probably explains why epidemiological studies have shown that a 1 g/dl decrease in haemoglobin levels is an independent, statistically significant risk factor for the development of cardiac morbidity and mortality. Follow-up examinations have demonstrated that partial correction of anaemia with recombinant Epo can improve cardiac oxygen supply and partially reverse pathological changes in left ventricular geometry. However, although partial anaemia correction regularly reduces left ventricular volume, the effects on wall thickness are far less significant. Moreover, in patients with advanced cardiac disease it has recently not been possible to demonstrate that a normalization of haemoglobin levels provides further benefit. It is not unlikely therefore that the development of severe anaemia has to be prevented by early implementation of Epo therapy in order to achieve the maximum benefit with respect to the cardiovascular system.- - - - - - - - - - ranking = 1keywords = anaemia (Clic here for more details about this article) |
2/72. Renal transplantation for end-stage renal disease following bone marrow transplantation: a report of six cases, with and without immunosuppression.BACKGROUND. Over 12000 bone marrow transplantations (BMT) are performed in the USA each year. This procedure is associated with significant morbidity including acute and chronic renal failure (CRF). CRF after BMT is usually secondary to radiation nephropathy and,or cyclosporine (CsA) toxicity. survival on dialysis therapy for patients with radiation nephropathy is poor and renal transplantation may be a preferable form of renal-replacement therapy. methods: We report our experience with renal transplantation in 6 patients with end-stage renal disease (ESRD) following BMT: 4 as a result of radiation nephropathy; one secondary to hemolytic uremic syndrome; and 1 as a result of antitubular basement membrane nephritis. Ages at the time of BMT ranged from 26 to 40 yr. ESRD developed after a mean period of 94 months (range 42-140 months) after BMT. The kidney source was from a living donor in 5 patients, and a cadaveric donor (CAD) in 1 patient. In 3 recipients, the bone marrow and kidney were from the same donor. They are managed without any immunosuppressive therapy. The other 3 were initiated on triple therapy (prednisone, mycophenolate mofetil/azathioprine and cyclosporine/tacrolimus). RESULTS: These patients have been followed for up to 31 months (range 3-30 months) after kidney transplant, and 5 out of 6 are alive with functioning bone marrow and renal transplants. Their plasma creatinines range from 70 to 160 micromol/L (mean 97 micromol/L). One patient died following metastatic squamous cell cancer of the genital tract. CONCLUSIONS: 1) Renal transplant is a feasible alternative for patients with ESRD following BMT: 2) if bone marrow and kidney are from the same donor, the recipient requires little or no maintenance immunosuppression; 3) short-term results show good survival, but long-term follow-up is needed: 4) infections and malignancy post-renal transplantation were seen in recipients who needed immunosuppression; and 5) reduction in immunosuppression may be needed in such post-BMT patients who undergo kidney transplants.- - - - - - - - - - ranking = 0.13537697692321keywords = hemolytic (Clic here for more details about this article) |
3/72. endoscopy as a tool for diagnosing and treating gastrointestinal angiodysplasia in haemodialysis patients.Gastroenteric angiodysplasia is an important cause of haemorrhage in chronic renal failure patients. This paper reports on 2 patients on maintenance haemodialysis with upper gastrointestinal bleeding due to different manifestations of angiodysplasic lesions (sudden appearance of haematemesis and melaena in one case, progressive anaemia with apparent resistance to erythropoietin in the other case). Exploratory endoscope examination of the first digestive tract showed in both cases the presence of bleeding angiodysplasic lesions. Both patients were there and then submitted to surgical endoscopy, during which the bleeding angiodysplasic lesion was sclerosed with physiological salt solution plus adrenaline 1/10000 and 1% polydocanol. In one patient, bleeding occurred again ten days later, making renewed surgical endoscopy necessary. In the course of this an elastic ligature was made to the superangular angiodysplasia. A year later in both cases there were no direct or indirect signs of further bleeding; an endoscopic check-up showed the treated lesions to be sclerosed. endoscopy offers the unique possibility of being used for both diagnostic and therapeutic purposes in a single session. In expert hands, endoscope therapy is effective and markedly reduces the risk of side effects.- - - - - - - - - - ranking = 0.090909090909091keywords = anaemia (Clic here for more details about this article) |
4/72. 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 = 0.67688488461604keywords = hemolytic (Clic here for more details about this article) |
5/72. How to improve survival in pre-dialysis patients.AIMS: This survey was performed to determine how anaemia in pre-dialysis patients is currently managed. methods: A random sample of 200 nephrologists attending the 1999 ERA/EDTA Congress participated in an interactive survey session. Participants were questioned on their current prescribing attitudes and preferences, and asked to select a preferred answer from a number of alternatives by means of an electronic key-pad. RESULTS: Three quarters of the audience treated their pre-dialysis patients with erythropoietin. However, approximately 50% treated patients and only 8% of respondents treated >/=75%. In addition, more than half of the respondents said that very few of their patients currently self-administer erythropoietin. Increased healthcare expenditure was the main reason given for limiting treatment. CONCLUSIONS: The survey highlighted important gaps in long-term treatment strategies for pre-dialysis patients. It indicated that new approaches to the treatment of renal anaemia are needed to minimise disease progression and to prevent cardiac dysfunction and associated mortality. erythropoietin has already been shown to significantly improve the survival of dialysis patients with renal anaemia, and new strategies might, therefore, include the prevention of anaemia in pre-dialysis patients by earlier initiation of erythropoietin therapy.- - - - - - - - - - ranking = 0.36363636363636keywords = anaemia (Clic here for more details about this article) |
6/72. tacrolimus-induced hemolytic uremic syndrome and end-stage renal failure after liver transplantation.BACKGROUND: Hemolytic uremic syndrome (HUS) is a rare complication in solid organ transplantation. It can be associated with severe hypertension. Several risk factors have been identified including immunosuppressive drugs such as cyclosporin A and, more recently, tacrolimus. methods: Here we report a case of tacrolimus-induced HUS in a 61-yr-old woman after liver transplantation. hypertension, microangiopathic anemia and end-stage renal failure occurred 2 yr after liver transplantation. RESULTS: At admission, she had malignant hypertension with a severe hypertensive retinopathy, renal failure (creatininemia: 800 micromol/L) and microangiopathic anemia (Hb: 7.3 g/dL, a low platelet count and elevated lactate dehydrogenase). At renal biopsy, histologic findings were ischemic and sclerotic glomeruli with hyaline thrombi, severe mesangiolysis and interstitial fibrosis. CONCLUSION: Despite steroid treatment, antihypertensive agents and fresh frozen plasma therapy, end-stage renal failure was observed and chronic hemodialysis treatment was required.- - - - - - - - - - ranking = 0.54150790769283keywords = hemolytic (Clic here for more details about this article) |
7/72. central nervous system involvement in a child with hemolytic uremic syndrome.We report a 20-month-old girl with postdiarrheal (shiga toxin) hemolytic uremic syndrome and severe encephalopathy. Magnetic resonance (MR) images were obtained in the acute phase of the disease and after 10 months. The first MR images showed widespread high signal intensity on T2-weighted and low signal intensity on T1-weighted images, in deep and subcortical white matter; the splenium of the corpus callosum was also involved, as well as cerebellar hemispheres. Neurological symptoms and signs gradually disappeared within 35 days. Follow-up MR imaging showed almost complete resolution of the previous findings, and the patient recovered without central nervous system impairment. The neurological lesions were probably due to hypoxia, although several other mechanisms could be involved, such as metabolic derangements and the action of shiga toxin. In spite of the dramatic clinical manifestations, we observed a good outcome, indicating that patients with similar lesions do not necessarily have a poor prognosis.- - - - - - - - - - ranking = 0.67688488461604keywords = hemolytic (Clic here for more details about this article) |
8/72. 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.- - - - - - - - - - ranking = 0.27075395384641keywords = hemolytic (Clic here for more details about this article) |
9/72. Hemolytic and uremic syndrome after heart transplantation.Two cases of hemolytic and uremic syndrome in heart transplant recipients are reported. Among solid organ transplantations, this complication mainly occurred in renal transplantation and only 1 case was reported in heart transplantation in the literature. cyclosporine was the only etiologic factor found. The renal outcome was severe with end-stage renal failure and no recovery of the renal function despite stopping cyclosporine, corticoids and plasma exchange.- - - - - - - - - - ranking = 0.13537697692321keywords = hemolytic (Clic here for more details about this article) |
10/72. Hyperhemolytic transfusion reaction in sickle cell disease.BACKGROUND: An atypical form of life-threatening hemolytic transfusion reaction (HTR) in patients with sickle cell disease (SCD) has been well described in the literature. Continuation of blood transfusion may be lethal, as it can further exacerbate hemolysis. The pathophysiologic mechanism of HTR is not well understood. case reports: Two cases of severe HTR in SCD after the transfusion of compatible RBC units are reported. hemolysis of both autologous and transfused cells was documented in Case 1 by urine Hb high-performance liquid chromotography. Multispecific HLA antibodies were identified in Case 1. Reticulocytopenia was noted in both cases during the acute hemolytic process. This was followed by a rise in reticulocyte count during receipt of IVIG and steroid therapy. bone marrow examination during reticulocytopenia in Case 2 showed erythroid hyperplasia. CONCLUSION: In SCD, both mature sickle cells and sickle reticulocytes adhere more readily to macrophages. In view of the bone marrow aspiration results, it appears that the recipients' HbS cells are destroyed by hyperactive macrophages and that the reticulocytopenia observed during HTR is likely to be due to peripheral consumption (i.e., destruction by macrophages), rather than suppression of erythropoiesis. Cessation of hemolysis during IVIG and steroid treatment may be due to IVIG's blocking of the adhesion of sickle cells and reticulocytes to macrophages, together with steroid suppression of macrophage activity.- - - - - - - - - - ranking = 0.81226186153924keywords = hemolytic (Clic here for more details about this article) |
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