Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

21 cases are fully agreed with the diagnosis standard of Schonlein-Henoch nephritis. Biopsy on the kidney of 5 cases with resistant duration was made and all were diagnosed as mesenteric hyperplastic glomerular nephritis, among them, one with segmental sclerosis, one with segmental sclerosis and crescents in some glomerulus. 13 cases were treated with prednisone, cyclophosphamide and Traditional Chinese herbs. 8 cases with wilfordine adding and/or traditional Chinese herbs. The results showed that 15 of 21 cases were cured, one case perfect remission, 4 cases part remission. All of the cases were followed-up from 2 years and 10 months to 12 years and 4 months, average 7.34 years. The late results: Group A, 16 cases with symptom, physical exam, urine routine normal. Group B, 4 cases with microscopic hematuria and/or "a little-(+)" urinary protein. Group C, one case with "+2" urinary protein and/or hypertension, urinary creatinine clearance rate normal. Of 5 cases, whose biopsies of kidney were made, one with glomerular segmental sclerosis belonged to Group B. 13 of 21 cases had recurrence for 1-6 times, which was closed related with up respiratory tract infection.
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PMID:[Long-term effect of Schonlein-Henoch nephritis with nephritic-nephrotic syndrome in children by traditional Chinese medicine and Western medicine]. 142 73

From June 1987 to June 1991 at the Belgrade University Children's Hospital 10 patients, 5 males and 4 females, aged 2-16 years, with chronic glomerular disease, were treated with CyA. Seven patients had INS, 2 lupus nephritis and one IgA nephritis. Before initiation of CyA, all but one, were treated with classic immunosuppressive therapy, which had no effect (8/10) and/or had serious adverse effects (9/10). CyA dosage was initiated at 4-6 mg/kg/BW, and was subsequently adjusted to achieve CyA concentrations in blood at range 50-100 ng/ml. Treatment duration was 2-17 months. Patient compliance to CyA therapy was observed in 5/7 INSs: 2 cortico-sensitive (1 with FSGS was cortico-dependent and 1 had frequent relapses) and 3 cortico-resistant patients (2 with FSGS and 1 with minimal histologic changes). After drug withdrawal, only one of the patients who responded, had no relapse. One of the two patients with SLE showed improvement during CyA administration, while no response was observed in the patient with IgA nephritis. Adverse experiences with CyA therapy involved decreased renal function (2/10), arterial hypertension (1/10), hyperbilirubinaemia (1/10), transient LDH increase and hyperuricaemia (1/10).
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PMID:[Cyclosporine in the treatment of glomerular diseases in children]. 146 61

The case records and histopathology of 42 adults with the characteristic light and electron microscopic features of Acute Postinfectious Glomerulonephritis (APGN) were studied. The biopsies were divided into three subtypes depending on the form and distribution of subepithelial "humps" and other immune-complex deposits on electron microscopy (EM): the "starry sky", "garland" and "mesangial" patterns. There was no significant difference between the three subtypes with regard to age, hypertension, creatinine, anti-streptolysin 0 titer and low serum complement levels on presentation. The "garland" subtype had significantly more proteinuria than both the "starry sky" (p = 0.04) and "mesangial" (p = 0.003) subtypes. The "mesangial" pattern had a lesser degree of cellular proliferation and leukocytosis in the glomeruli than the other subtypes. The "starry sky" subtype was present in 4 of the 5 cases of crescentic nephritis and in 6 of the 7 patients with a chronic course. Our study suggests that the higher degree of proteinuria in the "garland" subtype and the chronic course of the "starry sky" subtype are the main clinical features that distinguish the three histological subtypes. Our patients, from a developing community with poor socio-economic conditions, had a poor prognosis.
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PMID:Subtypes of acute postinfectious glomerulonephritis: a clinico-pathological correlation. 146 61

A 14-year-old boy with persistent proteinuria (1.6-4.0 g/day), microscopic haematuria, moderate hypertension, macrothrombocytopenia (giant platelets, platelet number 30 x 10(9)/l) and a familial sensorineural hearing loss (the father and the brother were also affected) was studied. Kidney biopsy revealed a diffuse mesangial proliferation, and a focal thickening of the glomerular basement membrane was seen on electron microscopy. A normal number of megakaryocytes was observed in bone marrow aspirates. The aggregation response of the platelets to collagen, epinephrine and adenosine diphosphate (ADP) was decreased. The platelet number was slightly diminished, platelets were of normal size in both parents and the brother, and showed a decreased aggregability in response to collagen, epinephrine and ADP in the brother and mother. No functional abnormality of the platelets was observed in the father. Urinalysis and kidney function were normal in the family members. This boy with nephritis, platelet disorders and hearing loss corresponds to Epstein's syndrome.
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PMID:Hereditary nephritis, platelet disorders and deafness-Epstein's syndrome. 153 37

Data from 659 patients with a diagnosis of lupus nephritis were retrospectively collected among 32 nephrology centers in Italy, as a result of the collaborative effort of the Gruppo Italiano per lo Studio della Nefrite Lupica (GISNEL, Italian Lupus Nephritis Study Group). The overall probability of renal survival was 80% 10 years after the diagnosis. The probability of maintaining life-supporting renal function was evaluated according to several variables (clinical characteristics at presentation, World Health Organization [WHO] histologic classification). The presence at the time of diagnosis of hypertension and diffuse proliferative nephritis (WHO class IV) was associated with a worse prognosis.
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PMID:Lupus nephritis: prognostic factors and probability of maintaining life-supporting renal function 10 years after the diagnosis. Gruppo Italiano per lo Studio della Nefrite Lupica (GISNEL). 158 37

In order to compare the protective effects of angiotensin converting enzyme inhibitors (ACEI) and calcium channel blockers (CCB) on the renal function in experimental nephritis, nephrotoxic serum nephritis was induced in male spontaneously hypertensive rats (SHR). The above drugs were then chronically administered to different groups, as follows: the ACEI-treated group (n = 7) received captopril (150 mg/kg/day), and the CCB-treated group (n = 6) was given both nifedipine (40 mg/kg/day) and nisoldipine (20 mg/kg/day). The control group (n = 8) received a placebo. Although the control group developed marked hypertension and proteinuria, the rats treated with either ACEI or CCB demonstrated a significant and equivalent decrease in mean arterial pressure and urinary protein excretion. At 15 weeks after the injection of nephrotoxic serum, all rats were anesthetized with Inactin, and the glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured. In the control group, GFR and RPF were markedly attenuated. However, both were preserved at much higher levels in the ACEI-treated group, and GFR was also maintained to a similar degree in the CCB-treated group. Histological studies were carried out after the clearance studies. As a result, it was found that the ACEI treatment significantly limited the development of glomerulosclerosis, whereas CCB modestly ameliorated the glomerular structural lesions. Moreover, ACEI significantly reduced the serum cholesterol, while CCB did not exert such an effect. These results suggest that both ACEI and CCB have a therapeutic effect in experimental glomerulonephritis models which are accompanied by hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of converting enzyme inhibitor and calcium channel blocker in SHR with nephrotoxic serum nephritis. 163 85

Frederick Akbar Mahomed was an Englishman of mixed Indian and Irish descent who made substantial contributions to the study of high blood pressure in a short professional life from 1872 to 1884. He was strongly influenced by the previous work of Richard Bright on kidney disease at his own hospital (Guy's Hospital in London) and by the contemporary pathological studies of Gull and Sutton on arteriolar changes in persons with high blood pressure. In detailed clinical studies, he separated chronic nephritis with secondary hypertension from what we now term essential hypertension. He described the constitutional basis and natural history of essential hypertension and pointed out that this disease could terminate with nephrosclerosis and renal failure. His clinical studies were done without the benefit of a sphygmomanometer but with the aid of a quantitative sphygmogram that he had initially developed while a medical student. He described characteristic features of the pressure pulse in patients with high blood pressure and in persons with arteriosclerosis consequent on aging. These pressure wave changes have recently been verified and explained. He contributed to a number of other advances in medical care, including blood transfusion and appendectomy for appendicitis. He initiated the Collective Investigation Record for the British Medical Association; this organization collected data from physicians practicing outside the hospital setting and was the precursor of modern collaborative clinical trials. Mahomed died from typhoid fever, almost certainly contracted from one of his patients, at age 35 at the height of his career.
Hypertension 1992 Feb
PMID:Frederick Akbar Mahomed. 173 55

This report describes a French Canadian family whose members exhibit a high incidence of allo- and autoantibodies to antigens present on both platelets and endothelial cells. This is correlated with various HLA specificities known to be associated with autoimmunity, such as A1, B8, DR3, and, in some cases, with clinical disorders, including nephritis, hypertension, and thrombocytopenia. Immunoblot analysis using platelet and endothelial cell lysates showed serum antibodies to a 75 kDa endothelial cell surface polypeptide and to polypeptides with apparent mass of 115 kDa and 26 kDa found on both platelets and endothelial cells. This 115 kDa internal platelet protein was also found in a variety of other cell types, such as mononuclear cells, and increased following cell activation. Monoclonal antibody immunobilization assays were used to characterize the 26 kDa polypeptide; in three of the four patients tested, an antibody to leukocyte differentiation antigen CD9 was identified. The asymptomatic child of the propositus also exhibited an autoantibody against an 80 kDa platelet protein which was sensitive to thrombin digestion, suggesting that this polypeptide may be platelet glycoprotein V. In addition, P1A1 alloantibody was identified in one sister who had given birth to a severely thrombocytopenic boy and who herself had a severe vascular rejection to a cadaver kidney 2 years prior to this study. The propositus also developed hypertensive renal disease following a pregnancy and became dialysis dependent. Thus, members of this family have developed a variety of antibodies, particularly to platelet and endothelial cell antigens. Some subjects have remained asymptomatic in spite of having autoantibodies. However, others have been seriously ill, and their immune response to these antigens is believed to have played a role in the pathogenesis of their neonatal alloimmune thrombocytopenic purpura, hypertensive renal disease, renal graft rejection, and thrombocytopenia.
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PMID:Characterization of novel platelet and endothelial cell target antigens in a family with genetic susceptibility to autoimmunity. 174 38

Various effects on renal function and factors which tend to cause aggravation in pregnancy and delivery in patients with renal diseases have been described previously. In the present study, the authors undertook personal and telephone inquiries to patients with renal insufficiency due to aggravated renal dysfunction occurring during the course of pregnancy and delivery, and to those showing a favorable course despite renal dysfunction before pregnancy. Sixty-four patients with IgA nephritis were investigated, covering 101 cases of pregnancy in them. The management of the pregnant women and their social and home (family/domestic) environments were taken into consideration, since these are important for giving guidance in their daily life to overcome various factors which influence the course of spontaneous pregnancy and delivery. The following findings were obtained. (1) In patients with hypertension, toxemia of pregnancy, abnormal delivery and abortion were frequently complicated. (2) Patients under greater mental and physical stresses during the course of pregnancy and after delivery showed a poorer prognosis for both mother and fetus. (3) Generally speaking, guidance should be given not to be overconfident or overdefensive in pregnancy. (4) Working women revealed a prognosis which was poorer than that of housewives.
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PMID:Study on the environmental background to aggravating factors for renal function related to pregnancy and delivery in IgA nephritis. 177 49

Primary IgA nephritis is the most frequent nephritis and represent half of the glomerular diseases. Its incidence is 2,7/10(5) inhabitants. The diagnosis is established on a renal biopsy, which shows typical IgA mesangial deposits: granular, predominant, and diffuse. A central pathogenic role is played by the IgA immune system, both from the mucosa and the bone marrow. The long term prognosis should no longer be considered as mild because, after 20 years of evolution, 1/3 of the patients are going into chronic renal failure, and 1/6 into end-stage renal disease. It is essential to delineate the risk factors predicting ultimate evolution towards chronic failure, to select patients who may benefit from aggressive treatment, such as high doses steroids. For all patients, it is essential to have a regular clinical and biological check up, and an adequate control of arterial hypertension, in order to avoid or delay progression.
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PMID:[IgA glomerulonephritis]. 180 52


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