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

It is suggested that patients with the haemolytic-uraemic syndrome and related disorders (such as thrombotic thrombocytopenic purpura) lack a plasma factor which stimulates prostacyclin (P.G.I2) activity. Normal plasma would supply the missing factor and is a rational treatment for some life-threatening symptoms (thrombocytopenia, haemolytic anaemia, hypertension) of this syndrome.
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PMID:Haemolytic-uraemic syndrome: deficiency of plasma factor(s) regulating prostacyclin activity? 8 15

Angiographic and histological studies of the intrarenal circulation have been undertaken in 20 patients following complicated pregnancies: 12 patients had had hypertension of pregnancy (group 1); 7 acute renal failure due to either ante- or post-partum haemorrhage and 1 patient post-partum renal failure (group 2). 3 months after delivery all patients had angiographic evidence of structural and functional abnormalities involving intrarenal blood vessels and cortical blood flow. The severity of the structural changes was related to the degree of microangiopathic haemolytic anaemia noted in the acute obstetric complication but not to the height of the blood pressure at this stage. Histological abnormalities of the cortical blood vessels were minimal. At the time of the renal angiogram and biopsy, 3 of the 12 group 1 patients were hypertensive and 3 had impaired renal function, compared with 5 and 1, respectively, in the 8 group 2 patients. Although during the follow-up period (mean 5 years) no further deterioration in renal function in either group has been observed, hypertension developed in 50% of the group 1 patients compared with only 1 of the patients in group 2. The relationship between the late onset of hypertension and the intrarenal vascular and haemodynamic abnormalities is discussed.
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PMID:Structural and functional changes in the renal circulation after complicated pregnancy. 31 35

Three cases of postpartum hemolytic uremic syndrome (HUS) are presented. Symptoms of acute renal failure, hypertension and microangiopathic hemolytic anemia with thrombocytopenia occurred 10, 17 and 24 days after delivery. Despite early heparin therapy in all cases, one patient went into terminal renal failure needing chronic hemodialysis, with persistent hypertension which became uncontrollable requiring bilateral nephrectomy 6 months later. The second patient had diuresis one month after starting hemodialysis, but 3 months later developed malignant hypertension. Slight improvement in renal function with persistent hypertension occurred after hemodialysis for 20 months. The third patient showed complete clinical recovery after 2 months. Pathological examination of renal tissue showed the typical lesions of thrombotic microangiopathy (TMA). However, striking differences were observed in the lesion seen in early and late specimens. Early lesions could be differenciated from infancy TMA because the medium-dize arteries were more severely involved. Late lesions were variable, ranging from minor changes in glomeruli and blood vessels, via ischemic and sclerotic lesions in glomeruli with arteriolosclerosis, to the vascular and glomerular lesions seen in malignant nephrosclerosis. There was a good correlation between the renal pathology and the clinical outcome of the patients. HUS with renal TMA as a cuase of postpartum renal failure has been reported in 49 patients with a fatal outcome in 61%. The pathogenesis of the syndrome probably involves a primary endothelial damage. This causes local renal intravascular coagulation in the presence of the usual postpartum hypercoagulable state. This is shown by the presence of fibrin-fibrinogen in glomeruli and vessels, increased plasma fibrin degradation products, thrombocytopenia and lowered levels of coagulation factors. There is little hematological or pathological evidence fo disseminated intravascular coagulation or an immune-complex disease. Hypocomplementemia seen frequently is probably due to local C3 activation via the alternative pathway.
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PMID:Postpartum hemolytic uremic syndrome: a study of three cases with a review of the literature. 38 9

The haemolytic uraemic syndrome is an acute illness characterised by the occurrence of renal injury, haemolytic anaemia with red cell fragmentation and thrombocytopenia. Haemorrhagic diathesis, arterial hypertension and neurological manifestations often complicate the acute phase of the disease. In this article, we shall discuss in more detail the aspects of this phase. Data obtained in 72 patients treated at the Wilhelmina Children's Hospital in Utrecht, from 1964 to 1977, are used to illustrate the characteristics of the disease.
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PMID:Haemolytic uraemic syndrome. 39 9

Two patients with the hemolytic uremic syndrome were treated with plasma exchange an infusion: in both cases, the reduced platelet count reverted to normal values and the microangiopathic anemia ceased within a few days. Systemic blood pressure and requirement for antihypertensive drug therapy were also markedly reduced following treatment with plasma. Venousprostacyclin (antiplatelet aggregating) activity was undetectable in both patients before but was restored after treatment with plasma. The plasma samples collected before, but not those collected at various intervals after replacement therapy, had decreased capacity to stimulate prostacyclin activity in rat aortic rings. It is suggested that in patients with the hemolytic uremic syndrome or with other clinical conditions which can be included under this rubric (such as thrombotic thrombocytopenic purpura) a plasma factor is lacking which stimulates prostacyclin activity. Plasma would supply such a missing factor, thus representing a rational treatment for some of the life-threatening manifestations (thrombocytopenia, hemolytic anemia, hypertension) of this severe syndrome.
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PMID:Treatment of the hemolytic uremic syndrome with plasma. 39 47

The clinical syndrome of accelerated hypertension is a relatively rare complication of hypertensive disease. The syndrome is recognized by high blood pressures, progressive neurologic and visual symptoms, acute renal damage, cardiac failure, and microangiopathic hemolytic anemia. When diagnosed, it must be recognized as an acute medical emergency. The patient should be admitted to an intensive care unit, arterial lines should be placed, and the blood pressure lowered as soon as possible. Once blood pressure has been controlled, oral medications should be begun. Long-term results in the treatment of hypertensive emergencies are gratifying. It is anticipated that with more experience gained in the use of medications in this situation, an even better prognosis will be achieved.
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PMID:Hypertensive emergencies. 43 Nov 88

Renal biopsies obtained from 20 adult patients within 30 days after onset of acute renal failure with microangiopathic hemolytic anemia ("the hemolytic-uremic syndrome") were studied. Lesions were graded independently by two observers without knowledge of the clinical history. All patients who did not have refractory hypertension were treated with heparin. Ten of the patients died, and four developed end-stage renal failure requiring chronic dialysis. Six patients, however, had a relatively good outcome: two recovered completely and four developed mild-to-moderate chronic renal failure not requiring dialysis. The six patients with a good outcome had significantly less severe arterial intimal thickening on biopsy compared with the remaining patients with a poor outcome. The patients with a good outcome and those with a poor outcome did not differ in the severity of glomerular lesions. The clinical features did not allow a prediction of late outcome. These results suggest that early renal biopsies may be helpful in predicting prognosis in the "hemolytic-uremic syndrome." This clinical syndrome may occur either in apparently healthy people, or may complicate the course of a chronic essential hypertension.
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PMID:Prognostic importance of vascular lesions in acute renal failure with microangiopathic hemolytic anemia (hemolytic-uremic syndrome): clinicopathologic study in 20 adults. 48 Jul 87

A 4-year-old boy had hemolytic uremic syndrome (HUS) associated with depression of serum C3 level, a B-hemolytic streptococcal throat infection, and an elevated level of antistreptolysin O titer. In addition to the characteristic histologic changes associated with this syndrome, substantial infiltration of polymorphonuclear leukocytes and nodular deposits of C3 globulin were seen in the glomeruli of the first biopsy specimen. Two months after clinical remission, he had a recurrence of hemolytic anemia, thrombocytopenia, and acute renal failure. The serum C3 concentration had decreased again, and serum C3NeF was detected in the serum. The typical changes associated with HUS were still present on electron microscopy. Bilateral nephrectomy and renal transplantation were done because of the development of uncontrollable severe hypertension and increasing azotemia. This patient had three manifestations of HUS, but because of several differences, such as hypocomplementemia, serum C3NeF, a recurrence, and persistent glomerular deposits of C3 globulin, he appears to have had a different form of the syndrome.
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PMID:Hemolytic uremic syndrome with hypocomplementemia, serum C3NeF, and glomerular deposits of C3. 57 89

The hemolytic-uremic syndrome consists of microangiopathic hemolytic anemia, acute renal failure, and thrombocytopenia following a prodromal illness of gastroenteritis or upper respiratory infection. The syndrome can present in dramatic fashion with severe abdominal pain and signs of peritonitis suggesting an acute surgical crisis. In a series of 25 patients, 40% had abdominal pain, 25% had abdominal tenderness, and 20% had peritoneal signs. Clues to diagnosis in the early stages of the acute illness were mild to moderate hypertension, abnormal peripheral blood smear, anemia despite dehydration, and proteinuria. Significant abdominal pain and x-ray evidence of colitis may occur before development of typical laboratory findings, and these were evident in at least one case. Three patients underwent laparotomy for suspected bowel perforation. Colitis without perforation was found in all cases. In the absence of documented perforation, toxic megacolon, or intussusception, the decision to perform laparotomy in patients with hemolytic-uremic syndrome who have signs of peritonitis must be individualized. Failure to recognize the underlying renal problem can lead to serious errors in fluid and electrolyte management and delay of appropriate therapy.
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PMID:Hemolytic-uremic syndrome: a diagnostic and therapeutic dilemma for the surgeon. 73 58

A case of arteriovenous fistula of the major transplant vessels contributing to posttransplant hypertension hypertension and severe microangiopathic hemolytic anemia is reported. Improvement in blood pressure and correction of anemia followed ligation of the fistula. This case reinforces the need for diagnostic evaluation of all patients with sustained post-transplant hypertension.
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PMID:Arteriovenous fistula complicating renal transplantation. 78 95


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