Cases reported "Hemolytic-Uremic Syndrome"

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1/11. 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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2/11. adult hemolytic uremic syndrome with renal arteriolar deposition of IgM andC3.

    Two cases of idiopathic adult hemolytic uremic syndrome in which deposits of IgM and C3 were identified in renal arterioles showing fibrinoid necrosis are reported. Fibrin was also identified in the lumina of the involved vessels, but there was no laboratory evidence of disseminated intravascular coagulation. In both cases, serum C3 was decreased and C4 was normal, suggesting involvement of the alternate pathway of complement activation. These two cases suggest that in some instances the adult hemolytic uremic syndrome may be immunologically mediated, and that renal vascular thrombosis is a secondary phenomenon.
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3/11. The histopathology of the hemolytic uremic syndrome associated with verocytotoxin-producing escherichia coli infections.

    Verocytotoxin-producing Escherichia coli (VTEC) infection was present in three cases of hemolytic uremic syndrome (HUS), two fatal and one non-fatal, in which detailed histopathologic investigations were conducted. Two patients had a prodrome of bloody diarrhea, one of whom required a hemicolectomy for severe bleeding. The renal histopathology was characterized primarily by glomerular thrombotic microangiopathy (TMA) with greater than 95% of glomeruli showing changes of capillary wall thickening, endothelial cell swelling, and narrowing or thrombosis of the capillary lumen. Preglomerular arterioles were frequently thrombosed, and abnormalities of the medium-sized vessels, including endothelial cell damage and thrombosis, were also commonly observed. Gastrointestinal involvement was prominent in all three cases. The colon was most severely involved, with marked mucosal and submucosal edema and hemorrhage, in the absence of significant inflammation or widespread ulceration. Microvascular angiopathy was present in all cases, with changes ranging from endothelial cell damage to overt thrombosis. Similar pathology was seen throughout the small bowel, including the presence of TMA. In one patient, typical morphologic changes of pseudomembranous enterocolitis were found in the absence of infection with clostridium difficile. The nature of vascular involvement in the kidneys and intestinal tract supports the hypothesis that HUS is mediated by systemic toxemia, and that endothelial cells are the primary target cells for the action of verocytotoxin.
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4/11. mitomycin-induced hemolytic-uremic syndrome.

    Four patients who took the antitumor agent mitomycin manifested microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. At autopsy, kidneys from all four patients had a microangiopathy typical of the hemolytic-uremic syndrome (HUS), with thromboses in glomerular capillaries and arterioles, fibrin deposition in mesangium, and prominent cellular intimal proliferation of the interlobular arteries. Development of the HUS was an important factor contributing to death in all four patients. From a review of the literature and our initial results of a randomized chemotherapy protocol for metastatic adenocarcinoma of the colorectum, it appears that mitomycin was the most likely cause for the development of the HUS in these patients. As more patients are being treated with mitomycin, particular care must be taken to monitor them for development of a drug-induced HUS.
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5/11. Comparative immunopathologic studies of thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome and disseminated intravascular coagulation.

    The vascular lesion of thrombotic thrombocytopenic purpura was characterized by two distinct types of changes in the arteriole of the heart and brain: (1) multiple incomplete vascular occlusions due to the subendothelial deposits composed of a homogeneous fibrin fibrinogen-like substance and platelets without the formation of polymerized fibrin; (2) vascular wall thickening due to the intramural granular deposits of IGM and beta 1C. A patient with hemolytic-uremic syndrome 9 days after the onset of the disease, exhibited (1) the formation of fibrin-thrombi in the glomerular capillary lumens, and (2) the granular deposits of IgM and beta 1C along the glomerular capillary walls and in the mesangium. In contrast, the case in which the symptoms subsided five weeks after the onset exhibited neither fibrin-thrombus formation nor the deposits of IgM and beta 1C in the glomeruli. The vascular lesions of disseminated intravascular coagulation accompanied by pancreas carcinoma was located mainly in the capillaries, and were characterized by the formation of numerous fibrin-thrombi. Although the glomeruli contained numerous thrombi, there was neither endocapillary proliferation nor deposits of immunoglobulins and complement components.
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6/11. Morphologic aspects of Goldblatt hypertension in a newborn infant.

    hypertension (210 mm Hg), hyponatremia, hypochloremia, and hypokalemia were observed in an 11-day-old infant. After electrolyte repletion, blood pressure rose to 320 mm Hg in spite of administration of antihypertensive drugs. The child died of a massive cerebral hemorrhage on the 17th day of life. At autopsy, the left renal artery was partially thrombosed and the left kidney partially infarcted. The glomeruli in the preserved cortical areas were of normal size; the juxtaglomerular apparatuses markedly enlarged. The blood vessels were inconspicuous. Enlarged glomeruli, multiple ruptures in the mesangium, ectactic glomerular capillaries, and fragile capillary walls were found in the nonconstricted right kidney. Fibrinoid necrosis with occasional fibrin thrombi in the lumina was present in the arterioles. Pronounced intimal edema with fragmented cells and monocytes embedded in the intima were observed in the interlobular and larger arteries. The histologic findings in the blood vessels of the nonconstricted kidney resembled those found in the hemolytic-uremic syndrome (Gasser's syndrome).
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7/11. Haemolytic uraemic syndrome: report of a case and new pathogenetic concepts.

    Haemolytic uraemic syndrome (HUS) is a severe clinical condition characterised by thrombocytopenia, microangiopathic haemolytic anaemia and renal impairment [1]. At histological examination hyaline microthrombi occluding terminal arterioles and capillaries are generally found. Other syndromes share major clinical and histological diagnostic criteria with HUS. In particular, there is no method at present which clearly differentiates HUS from thrombotic thrombocytopenic purpura (TTP) [2]. We propose therefore the term thrombotic microangiopathy (TMA) to discuss both syndromes. The pathogenesis of TMA is unclear and many forms of therapy have been attempted without definitive proof of efficacy. The recently reported [3] successful results with exchange transfusion and plasma infusion represented a consistent advance in the management of these diseases. The beneficial effect of these procedures was attributed to replacement of an unknown 'missing' factor in plasma. This finding generated recent observations possibly relevant in understanding the pathogenesis of these diseases.
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8/11. Hemolytic uremic syndrome complicating postinfectious glomerulonephritis in the adult.

    Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura is known to occur as a secondary complication of primary renal diseases, specifically of lupus nephritis, membranous glomerulonephritis, and focal segmental glomerulosclerosis. In a patient without a family history of hemolytic uremic syndrome/thrombotic thrombocytopenic purpura we observed biopsy-confirmed postinfectious glomerulonephritis with humps, with simultaneous subendothelial hyaline deposits and fibrinoid thrombi in arterioles. The patient had a history of febrile pharyngitis with diarrhea 10 days prior to renal biopsy. He presented with transient elevation of serum creatinine, a nephritic sediment, and hypertension not exceeding 160/100 mm Hg. The patient also had purpura, transient thrombocytopenia, and signs of intravascular hemolysis. Results of verocytotoxin serology were negative. With the exception of isolated microhematuria, all findings reverted to normal within 8 weeks without any specific treatment. This case illustrates that hemolytic uremic syndrome/thrombotic thrombocytopenic purpura may complicate primary postinfectious glomerulonephritis in adults.
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9/11. Late changes of irreversible post-partum renal failure.

    The clinico-pathological data from a patient with irreversible post-partum renal failure (IPRF) are presented. The electron microscopy of the late changes are described for the first time and consists of: 1. Thickening of the basement membrane. 2. Interposition of mesangial cells and matrix between the thickened basement membrane and the endothelial cell encircling the periphery of the tuft. 3. Multiplication of basal lamina material between mesangial cells and endothelial cells. 4. Proliferation of endothelial cells. All of the above changes tend to obliterate the glomerular tufts and transform the vascular lumina into slit-like spaces. They explain morphologically why most patients with IPRF terminate in chronic renal failure, if they survive the early changes. The late occurring hypertension is regarded as a secondary stimulation of the renin-angiotension system caused by partial or complete occlusion of arteries and arterioles.
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10/11. Scleroderma renal crisis as a presenting feature in the absence of skin involvement.

    A 56-year-old man was admitted to the nephrology unit with a short (6-week) history of severe hypertension that necessitated renal replacement therapy within 7 days after admission. Renal biopsy showed features of thrombotic microangiopathy in arterioles and small arteries with occluding thrombi. The skin was unremarkable at the time of admission. Progressive skin lesions with scleroderma, telangiectasia, sclerodactyly, and generalized cutaneous sclerosis developed within 4 weeks and the specific skin changes were found on skin biopsy. On admission antinuclear antibody titers were high (1:10, 240) with a nucleolar pattern, and PM-Scl antibodies (1:5, 120) were present. In the present case the diagnosis of scleroderma renal crisis was made in vivo by renal biopsy. Renal and skin biopsies documented that renal lesions may precede the clinically manifest skin lesions of progressive systemic sclerosis.
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