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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An unusual case of multifocused postpartum thrombotic microangiopathy was encountered in a woman with pregnancy-induced hypertension, which presented clinical features different from those generally seen in postpartum hemolytic uremic syndrome or thrombotic thrombocytopenic purpura. These changes included acute disseminated intravascular coagulation, severe elevations of liver enzymes, severe renal dysfunction, and hemolytic anemia. The patient was treated successfully with heparin, gabexate mesilate, furosemide, fresh whole blood, and large doses of corticosteroid with antibiotics, and she recovered completely without sequelae. The hypothetical pathogenesis of the complex symptoms of this catastrophic clinical condition is proposed.
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PMID:A case of postpartum hemolytic uremic syndrome with severe elevations of liver enzymes. 392 May 96

A syndrome, including microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and renal insufficiency, has been recognized to occur as a complication of antineoplastic therapy with mitomycin. The clinical presentation can vary from a chronic course with mild anemia and slowly progressive renal dysfunction to a fulminant course with severe anemia, rapid deterioration of renal function, and death. The optimal treatment of the mitomycin-associated MAHA syndrome is unknown. Therapy with steroids, antiplatelet agents, and heparin sodium has failed to reverse the MAHA. Plasmapheresis has improved the MAHA in a few patients without reversing the renal failure. We treated two patients who had MAHA and renal dysfunction during chemotherapy that included mitomycin; the MAHA and hypertension both objectively improved after treatment that included vincristine sulfate.
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PMID:Treatment of mitomycin-associated microangiopathic hemolytic anemia with vincristine. 395 31

A 14-year-old girl with postinfectious chronic hepatitis developed a life threatening autoimmune multisystemic illness with arthralgias, intracranial hypertension, Coomb's positive hemolytic anemia and hemorrhagic diathesis (due to antiplatelet and antifactor X antibodies). Mannitol and immunosuppressive therapy abolished acute symptoms. During the first year of follow-up, two attempts of decreasing prednisone below 15 mg/day caused recurrence of the hemolytic anemia and appearance of low titer antinuclear antibodies, while doses above 15 mg/day caused an increase in transaminase levels. Daily prednisone dose was therefore fixed at 15 mg. The patient was well and, although signs of mild hemolysis persisted, there was no anemia. Transaminases were found greatly elevated on two occasions. An autoimmune multisystemic steroid sensitive disease was seemingly initiated by a postinfectious steroid irresponsive chronic hepatitis.
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PMID:Multisystemic disease with intracranial hypertension and autoimmune cytopenia in chronic active hepatitis. 395 17

It is uncertain whether increased arterial pressure alone or increased arterial pressure combined with some other factor is responsible for the development of malignant-phase hypertension. Our object was to test this comparing two groups of rats with hypertension of different mechanism but of similar duration and degree. Two experiments were done in hypertensive rats. In the first blood pressure was measured in the tail, in the second by intra-arterial catheter and pressure transducer. In the first, hypertension was produced in 30 male Sprague-Dawley rats by unilateral nephrectomy followed by thrice-weekly injections of deoxycorticosterone (12.5 mg) and substitution of 1% NaCl and 0.2% KCl for their drinking water. After four weeks 28 rats survived and systolic blood pressure had risen to 220 mmHg. The survivors were paired by blood pressure and randomly allocated either to continued DOC and salt or to a regime in which DOC was stopped and tap-water was substituted for the NaCl-KCl solution (post-DOC rats). Blood pressure remained similar in the two groups thereafter, but in every case it was the DOC-salt animal of the pair which died first. Fibrinoid arteriolar lesions of malignant-phase hypertension were significantly commoner in DOC-salt animals and, before death, they had more pronounced features of microangiopathic haemolytic anaemia. The second experiment was the same in design as the first except that two weeks after randomization the similarity of blood pressure was confirmed by measurement of intra-arterial pressure in eight pairs of DOC-salt and post-DOC rats. We conclude that increased arterial pressure is not the only factor influencing development of malignant-phase hypertension.
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PMID:Similar blood pressure but different outcome in rats with DOC and post-DOC hypertension. 668 Oct 45

A 20-year-old black man with known sickle cell anemia was admitted to the hospital with the signs and symptoms of right middle lobe pneumonia. Because of a hemoglobin value of 3.9 g/dL, he received a transfusion of 3 units of packed erythrocytes. Seven days later, hypertension, headache, and one grand mal seizure occurred. Evaluation of his condition gave normal findings. Similar events, some terminating in cerebral hemorrhage and death, have been reported in patients with hemolytic anemia after they received multiple transfusions. To our knowledge, this patient represents the first adult with sickle cell anemia who had this syndrome. Prompt antihypertensive therapy may have been of benefit.
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PMID:Hypertension and a seizure following transfusion in an adult with sickle cell anemia. 670 31

This article presents six cases of hemolytic-uremic syndrome, defined as the combination of acute renal insufficiency, microangiopathic hemolytic anemia, and thrombocytopenia, in six adult patients, two men and four women, between 20 and 52 years old. Three of the cases were considered idiopathic, two secondary to the use of oral contraceptives, and one appeared after an abortion. All of the patients presented severe hypertension, frequently accompanied by increased renin levels; in no cases was there any important coagulation disorder. In all of the biopsies there were lesions denoting intravascular thrombosis in the arterioles and medium-sized arteries of the kidney, as well as thickening of the glomerular basal membrane. Immunofluorescence was positive for fibrinogen and C3 in the majority of biopsies examined. Two patients suffered acute pancreatitis, hypertension having perhaps been an important factor in this complication. One of the two patients died as a result of acute hemorrhagic pancreatitis and was the only death in the series. Of the five remaining subjects, three required periodic hemodyalisis and the other two presented a considerable degree of chronic renal failure, which confirms that the prognosis for the hemolytic-uremic syndrome is much worse for the adult than for the child.
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PMID:[Hemolytic-uremic syndrome in the adult (author's transl)]. 735 70

A hypercalcemic patient with adult T-cell leukemia was treated with deoxycoformycin (DCF) in a dose of 5 mg/m2 daily for three days. Several days later, severe thrombocytopenia appeared abruptly and then microangiopathic hemolytic anemia ensued. Subsequently, renal failure and hypertension developed, and the patient died seven weeks after DCF therapy. Needle necropsy of the kidney showed glomerular damage including swelling of endothelial cells, mesangiolysis and segmental collapse. This is the second reported case of hemolytic-uremic syndrome due to DCF.
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PMID:Hemolytic-uremic syndrome due to deoxycoformycin: a report of the second case. 754 51

We describe a patient with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes) who was found to have renal involvement with particular renal pathological findings. So far, 17 other cases, most of them from Japan, of POEMS syndrome with renal involvement, have been published. Clinical features are variable: acute renal failure with anasarca or moderate chronic renal insufficiency with mild proteinuria. This latter presentation often passes unnoticed. There is no severe hypertension, no microangiopathic hemolytic anemia. Renal biopsy shows prominent glomerular changes which are unusual and distinct from membranoproliferative glomerulonephritis (MPGN) and from glomerular thrombotic microangiopathy (TMA). Mesangial proliferation and thickening of the capillary wall with double contour on light microscopy suggest an MPGN. By immunofluorescent microscopy, no immunoglobulins or complement deposits were found. The occurrence of mesangiolytic lesions has led to the term of "mesangiolytic glomerulonephritis". The presence, on electron microscopy, of lucent subendothelial spaces could indicate TMA. But there are neither thrombi nor arteriolar changes. We are inclined to consider that the microangiopathic lesions are due to chronic injury of glomerular endothelial cells, exacerbated at outbreaks of the disease. Increased production of IL 6 could support the efficacy of corticosteroid therapy, particularly in acute clinical situations.
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PMID:Renal involvement in POEMS syndrome. 763 52

A 23-year-old female, gravida 0 para 0, underwent emergency cesarean section under general anesthesia, because of the complication of HELLP syndrome. Prostaglandin E1 (PGE1) was used to prevent hypertension and uterine atony just after the infant's delivery. The disorder was improved with the postpartum care. HELLP is the syndrome of hemolysis, elevated enzyme, and low platelets presented by a unique group of pre-eclamptic/eclamptic patients with or without the usual clinical findings of pregnancy-induced hypertension. PGE1 may be useful for microangiopathic hemolytic anemia, which might be related with the hemolysis, because of its inhibitory effect on both platelet aggregation and thrombus formation, and its ability to improve red cell deformability.
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PMID:[The use of prostaglandin E1 for emergency cesarean section in a patient with HELLP syndrome]. 769 14

A genetic model of malignant phase hypertension in rats is described which closely parallels the natural history of untreated human malignant phase hypertension. Although the factors initiating transition from essential hypertension to the accelerated phase in humans remain unknown, we report the characteristics of a genetically determined and reproducible phenotype which was found to result from a cross between hypertensive transgenic Ren-2 rats and normotensive Sprague-Dawley (Edinburgh) rats. Male F1 hybrids developed malignant phase hypertension with a penetrance of 73.5% (95% confidence limits 65.7 to 81.3%) by 100 days of age. Phenotypic features included an accelerated rise in blood pressure, fibrinoid necrosis, activation of the renal renin-angiotensin system and microangiopathic hemolytic anemia. In an analytical cross no significant difference in blood pressure was observed between malignant phase and non-malignant phase animals prior to transition, implying that a factor in addition to hypertension appears necessary for inducing transition to the malignant phase phenotype. Segregation of the malignant phenotype suggested that susceptibility is determined by at most two genetic loci.
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PMID:A genetic model of malignant phase hypertension in rats. 772 38


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