Cases reported "Hemolysis"

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1/28. Severe haemolysis after an ABO unmatched kidney transplant - a nonsecretor transplanted from a donor with high anti-A titre.

    A case of severe haemolysis following an ABO unmatched renal transplant is reported in a group A nonsecretor who received a kidney from a group O living related donor. Following the haemolytic episode, group A donor units were incompatible and the patient was transfused with group O blood. Serological investigation of the recipient revealed anti-A present in the serum and on the red cells. Investigation of the donor revealed the presence of high-titre anti-A. The association of such high-titre donor antibody with haemolysis in ABO unmatched grafts has not been reported before. We discuss the risk factors for developing haemolysis in an ABO unmatched organ transplant and explore the possible relevance of such high donor antibody titre to recipients who are nonsecretors.
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2/28. Development of black gallstones after the nonsurgical management of splenic injury: report of a case.

    A 22-year-old man was admitted to our Emergency Department after suffering splenic injury in a traffic accident. His intraabdominal bleeding was treated nonsurgically by the administration of total parenteral nutrition (TPN) and blood transfusions of packed red cells. He presented again 2 months after his discharge, being 3 months after the injury, for right hypochondralgia, at which time a gallstone was demonstrated on ultrasound (US) and computed tomography (CT). After endoscopic laparoscopic cholecystectomy, his symptoms disappeared and he has remained well since. The clinical course of this patient indicates that hemolytic hyperbilirubinemia can cause black gallstones as a late complication of the nonsurgical management of abdominal blunt trauma.
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3/28. Alloimmune hemolysis after renal transplantation.

    A 35-year-old patient with blood group AB developed hemolysis 1 week after receiving a blood group B cadaveric kidney transplant. The patient's serum was shown to contain anti-A antibody, which was likely to have been derived from passenger lymphocytes transplanted concurrently with the graft. The alloimmune hemolysis subsided spontaneously without treatment. The present case underscores the potential complication of ABO blood group-compatible but nonidentical organ transplantation. Clinical vigilance is important to differentiate from other more sinister causes of posttransplant hemolysis.
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4/28. Donor-derived alloantibodies and passenger lymphocyte syndrome in two of four patients who received different organs from the same donor.

    BACKGROUND: Reported here is the occurrence of RBC alloimmunization in two of four patients who received different organs from an immunized donor. STUDY DESIGN AND methods: The donor, a 58-year-old woman, was group O D , K-, and Fy(a-). Initially, her serum contained only a K antibody. After blood transfusion, a second antibody (anti-Fy(a)) could also be identified. The liver was given to a group O D , K-, Fy(a ) patient; the pancreas and one kidney to a group O D , K-, Fy(a ) patient; the heart to a group A D , K-, Fy(a-) patient; and the other kidney to a group B D , K-, Fy(a ) patient. RBC grouping and antibody screening were performed by standard techniques. Lymphoid microchimerism in the peripheral blood of the recipients was analyzed by flow cytometry and nested PCR. RESULTS: None of the recipients had irregular RBC alloantibodies at the time of transplantation. After the transplant, anti-K became detectable in the serum of the liver recipient, and anti-Fy(a) could be eluted from the RBCs of the liver recipient and the pancreas-kidney recipient. The latter patient also developed mild hemolysis, and his Hb dropped to 8 g per dL on posttransplant Day 9. Donor-derived lymphocytes were detectable by flow cytometry in the peripheral blood of the liver recipient and the pancreas-kidney recipient until Days 8 and 63, respectively, whereas no lymphoid chimerism could be demonstrated in the heart recipient. PCR chimerism analyses were positive in all three recipients over the whole observation period of 97 postoperative days. CONCLUSION: The amount of cotransplanted lymphoid tissue may correlate with the extent of peripheral lymphoid microchimerism and the antibody-formation capacity in solid organ transplantation.
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5/28. cyclosporine-associated thrombotic microangiopathy during daclizumab induction: a suggested therapeutic approach.

    A woman on daclizumab developed thrombotic microangiopathy secondary to cyclosporine after a living-unrelated kidney transplant. Despite cyclosporine discontinuation, hemolysis persisted. The second dose of daclizumab was postponed 24 h, and after a maximum of two sessions of plasmapheresis (to avoid further modifications in daclizumab schedule) with plasma exchange, daclizumab was administered. Plasma infusions were prescribed until D-dimer and fibrinogen-degradation products normalized; thereafter, FK-506 was started without recurrence of the hemolytic picture and renal function restored. This observation suggests that in patients on daclizumab who develop thrombotic microangiopathy secondary to immunosuppressants, if discontinuation of the offending drug is unsuccessful, plasmapheresis with plasma exchange can be performed when the lowest levels of daclizumab exist, followed by daclizumab infusion. Plasma prescription must be continued thereafter until D-dimer and figrinogen-degradation products normalize. However, if hemolysis persists when daclizumab levels are high, plasma infusions are useful and plasmapheresis avoided. FK-506 administration did not result in recurrence of hemolysis during daclizumab induction.
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6/28. Prolonged hemolysis from overheated dialysate.

    A patient with chronic renal failure exposed to overheated dialysate (50 degrees C) for 20 minutes developed evidence of delayed and protracted hemolysis, which continued for several days. By contrast, in the only previously reported similar case, sudden gross hemolysis followed by cardiac arrest occurred. It is emphasized that the rapidity and severity of hemolysis due to thermal injury to erythrocytes are dependent upon the duration of exposure and the height of temperature to which extracorporeal blood is exposed. methods of preventing such incidents and therapeutic approaches are outlined.
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keywords = injury
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7/28. Acute renal failure following massive attack by Africanized bee stings.

    Bee venom is a complex substance, which acts in several tissues. Although severe allergic reactions have occurred after one or more stings, several deaths have been reported without allergic manifestations, emphasizing the toxic effects of massive poisoning. A number of about 500 stings have been considered necessary to cause death by direct toxicity, but as few as 30-50 stings have proved fatal in children. Among the major toxic effects are hemolytic anemia, acute renal failure (ARF), and shock. ARF may be due to a common toxic-ischemic mechanism with hypovolemic or anaphylactic shock, pigment tubulopathy (myoglobinuria and hemoglobinuria), or acute tubular necrosis (ATN) from a direct kidney toxicity of the venom. We present a case of rhabdomyolysis and hemolysis with consequent ARF which developed after about 800 bee stings. The patient recovered completely after peritoneal dialysis.
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keywords = kidney
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8/28. 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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9/28. Hyperlactatemia and hemolysis in G6PD deficiency after nitrofurantoin ingestion.

    A 69-year-old man with glucose-6-phosphate dehydrogenase deficiency was treated with nitrofurantoin for pyuria. Four days later he presented with metabolic acidosis due to excess lactic acid, a decline in curculating hemoglobin, reticulocytosis, elevated serum transaminase levels, and hyperbilirubinemia. The drug was withdrawn and the hyperlactatemia subsided in three days without specific treatment. in vitro, nitrofurantoin is capable of stimulating erythrocyte glucose utilization aand lactate production, and inhibiting the generation of reduced glutathione. In vivo, this drug is capable of producing hemolysis in susceptible subjects and hepatocellular injury. The temporal proximity of drug ingestion and hemolysis, increased glucose utilization, lactate excess, and hepatic insufficiency suggests that nitrofurantoin may have been responisble for precipitating the clinical and chemical abnormalities observed.
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10/28. Autoimmune hemolytic anemia occurred prior to evident nephropathy in a patient with chronic hepatitis c virus infection: case report.

    BACKGROUND: Renal involvement in patients with chronic hepatitis c virus infection has been suggested to be due to a variety of immunological processes. However, the precise mechanism by which the kidneys are damaged in these patients is still unclear. CASE PRESENTATION: A 66 year old man presented with the sudden onset of autoimmune hemolytic anemia. Concomitant with a worsening of hemolysis, his initially mild proteinuria and hemoglobinuria progressed. On admission, laboratory tests revealed that he was positive for hepatitis c virus in his blood, though his liver function tests were all normal. The patient displayed cryoglobulinemia and hypocomplementemia with cold activation, and exhibited a biological false positive of syphilic test. Renal biopsy specimens showed signs of immune complex type nephropathy with hemosiderin deposition in the tubular epithelial cells. CONCLUSIONS: The renal histological findings in this case are consistent with the deposition of immune complexes and hemolytic products, which might have occurred as a result of the patient's underlying autoimmune imbalance, autoimmune hemolytic anemia, and chronic hepatitis c virus infection.
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