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)

Acute glomerulonephritis is a distinct clinical entity, more frequently found in younger age. We report 69 patients with AcGN (25 female and 44 male) mean age 26 years (range 15-58). The disease is clinically characterized with hypertension (57%), edema (59%) and oliguria (35%). Urine analysis showed microhaematuria/proteinuria (36%) and micro/macrohaematuria alone in 89%, while azothaemia was observed in 16% pts, and decreased serum complement levels in one third of patients, more often decrease of C3 (33%) than C4 (15%). Initial infection of the upper respiratory tract was seen in 65%, pneumonia in 8%. In 25% of pts. there were no data of previous infection. Cultures of pharyngeal smear revealed. Streptococcus only in 2 pts. Elevated AST titer was found in 32% pts. Eleven kidney biopsies were made, and histological examination showed 2 normal findings, 6 mesangioproliferative GH, 2 endocapillary GN and 1 membranoproliferative GN. Follow ups have showed urinary abnormalities in 25% of pts., without developing renal failure.
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PMID:[Clinical and morphologic features in patients with acute nephritis syndrome]. 910 32

Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function. The commonest form of AGN in developing countries is that following a beta hemolytic streptococcal infection where the glomerular injury is mediated by deposition of immune complexes. In the usual patient with moderately severe poststreptococcal AGN (PSAGN) the above-mentioned features are present However, gross or microscopic hematuria may be the only abnormality. A similar picture may occasionally be produced by a variety of infections (when GN is referred to as post-infectious and the mechanism of glomerular damage and the renal histology are similar to that in PSAGN), primary renal glomerular disorders (e.g. membranoproliferative GN, IgA nephropathy), collagen vascular diseases (systemic lupus erythematosus), systemic vasculitis (Henoch Schonlein purpura) and hereditary nephritis and some nonglomerular conditions. PSAGN may also present with one or more of its complications such as profound volume expansion with heart failure and hypertensive encephalopathy. PSAGN resolves rapidly and has an excellent prognosis. Patients with severe renal involvement and life threatening complications need expert supportive management. AGN with associated systemic features or very pronounced azotemia, nonstreptococcal AGN and unresolving GN need prompt, appropriate evaluation that often includes a renal biopsy. If extensive crescentic changes are found (crescentic GN), aggressive immunosuppression will be necessary.
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PMID:Acute glomerulonephritis. 1079 62

Over a 31-year period, we have encountered 13 children with a disease entity not reported by other clinics that leads to rapidly progressive crescentic glomerulonephritis. Gross hematuria, rapidly declining renal function, and a serum C3 level at the lower limit of normal or slightly depressed usually characterized the disease onset; hypertension and nephrotic syndrome were absent. Glomerular IgG was absent, but large C3-containing subepithelial deposits on the paramesangial basement membrane (GBM) were always present. Because of these deposits and because dense alteration of the GBM was found in 3 patients, the disease may resemble membranoproliferative glomerulonephritis type II, but is distinguishable on other morphological and clinical grounds. The absence of anti-neutrophil cytoplasmic antibody, tested for in 5 of 13 patients, is one of several ways the disease differs from the pauci-immune glomerulonephritis of adults. Clinically and by glomerular morphology, it also differs from severe poststreptococcal acute glomerulonephritis. Treatment with high-dose corticosteroids has been highly successful. Because in this series the disease occurred only in children under age 12 years and the amount of silver-positive mesangial matrix was normal, indicating absence of mesangial proliferation, it has been designated juvenile acute non-proliferative glomerulitis.
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PMID:Acute non-proliferative glomerulitis: a cause of renal failure unique to children. 1095 28

Acute glomerulonephritis (AGN) is a representative disease of acute nephritic syndrome characterized by the sudden appearance of edema, hematuria, proteinuria, and hypertension. The prototype of AGN is acute poststreptococcal glomerulonephritis (APSGN). "Nephritogenic streptococci" are defined as organisms that are cultured from a patient who develops AGN. Although only a limited number of M-types of streptococci have been recognized as "nephritogenic streptococci", all M-types of streptococci may have nephritogenic potential because the genes for major putative nephritogenic antigens such as SPEB and NAPIr are found to be present in all group A streptococci thus far examined. Pathogenic mechanisms for APSGN involving both humoral and cell-mediated immunity have been recently proposed. The role of humoral immunity is presumed to be mediated by the in situ formation of nephritogenic streptococcal antigen-antibody complexes and circulating immune complexes. While in the cellular immune component a role for delayed-type hypersensitivity has been suggested to contribute to the pathogenesis of APSGN.
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PMID:Acute glomerulonephritis. 1096 98

A hypertensive emergency is a situation in which uncontrolled hypertension is associated with acute end-organ damage. Most patients presenting with hypertensive emergency have chronic hypertension, although the disorder can present in previously normotensive individuals, particularly when associated with pre-eclampsia or acute glomerulonephritis. The pathophysiological mechanisms causing acute hypertensive endothelial failure are complex and incompletely understood but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous vasodilator mechanisms, upregulation of proinflammatory mediators including vascular cell adhesion molecules, and release of local vasoconstrictors such as endothelin 1. Magnetic resonance imaging has demonstrated a characteristic hypertensive posterior leucoencephalopathy syndrome predominantly causing oedema of the white matter of the parietal and occipital lobes; this syndrome is potentially reversible with appropriate prompt treatment. Generally, the therapeutic approach is dictated by the particular presentation and end-organ complications. Parenteral therapy is generally preferred, and strategies include use of sodium nitroprusside, beta-blockers, labetelol, or calcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopathy. Novel therapies include the peripheral dopamine-receptor agonist, fenoldapam, and may include endothelin-1 antagonists.
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PMID:Hypertensive emergencies. 1105 14

A full-term neonate with a history of umbilical venous catheterization followed by coagulase-negative staphylococcal sepsis is presented. The infant developed a solitary hepatic abscess with saprophytic organisms. Her liver abscess resulted in acute glomerulonephritis characterized by hypertension, proteinuria, oliguria, and azotemia. Surgical drainage and antibiotic treatment of the abscess was associated with resolution of the glomerulonephritis. Glomerulonephritis due to solitary liver abscess in a neonate has not been reported previously. Acute onset of glomerulonephritis should prompt a search for occult sources of infection.
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PMID:Solitary hepatic abscess with associated glomerulonephritis in a neonate. 1100 79

In 1998 there was a large outbreak of acute glomerulonephritis (GN) in Nova Serrana, Brazil, caused by group C Streptococcus zooepidemicus and linked to the consumption of contaminated cheese produced with unpasteurized milk. This study describes the follow-up of these patients after a mean of 2 years following the acute episode. Of 134 patients identified in 1998, 69 patients were reexamined and underwent measurements of blood pressure, 24-hour creatinine clearance, microalbuminuria (radioimmunoassay), and urine sediment analysis. Of the original group of 134 patients, 3 patients died in the acute phase and 5 patients (3.7%) required chronic dialysis. Of 69 patients reevaluated, 65 patients (94%) were adults (mean age, 39 +/- 2 [SE] years) and 47 patients (68%) were women. At the follow-up examination, we found arterial hypertension in 42% of subjects (27 of 64 subjects), serum creatinine levels greater than 1.2 mg/dL in 12% (10 of 68 subjects), reduced creatinine clearance (<80 mL/min/1.73 m(2)) in 30% (20 of 67 subjects, 2 of them on chronic dialysis therapy), and increased microalbuminuria (>20 microg/min) in 34% (22 of 65 subjects). Increased microalbuminuria and/or reduced creatinine clearance were detected in 48% of the subjects (31 of 65 subjects). Patients with microalbuminuria had greater diastolic blood pressure than those without microalbuminuria (mean, 98 +/- 4 versus 88 +/- 2 mm Hg; P = 0.02). In conclusion, after a mean of 2 years, patients with epidemic poststreptococcal GN caused by S zooepidemicus present a high rate of hypertension and frequent abnormalities of renal function, with some having reached end-stage renal disease. Longer follow-up will be important to define the prognosis of these patients.
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PMID:Follow-up of patients with epidemic poststreptococcal glomerulonephritis. 1147 49

Acute glomerulonephritis (AGN) trends in the last 3 decades in the Novosibirsk Region have been analysed basing on the data from 308 AGN case histories. The results of the analysis demonstrate that AGN occurs not often but with stable rate. It is encountered more frequently in young men. The last decade is characterized by higher morbidity after streptococcal infection, high percentage of women at reproductive age, aggravation of the clinical course with marked edemas, severe arterial hypertension, renal dysfunction (acute renal failure in 10.4%), cases of left ventricular failure (5.2%) and eclampsia (1.7%) not registered earlier.
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PMID:[Evolutionary trends in symptoms of acute glomerulonephritis in adult population of the Novosibirsk region]. 1158 87

A 23-year-old man was admitted with macrohematuria and systemic edema appearing after an acute upper respiratory tract infection. He had been diagnosed 6 years earlier with IgA nephropathy (IgA-N). On admission, hypertension, nephrotic syndrome and hypocomplementemia were evident together with a high titer of anti-streptokinase (ASK). Renal biopsy showed severe glomerular mesangial proliferation, segmental endocapillary proliferation and crescent formation. Immunofluorescence microscopy (IF) showed strong deposition of C3 and reduced deposition of IgA. Electron microscopy showed a so-called "hump" on the epithelial side of the glomerular basement membrane. These features were consistent with post-streptococcal acute glomerulonephritis (PSAGN) superimposed on IgA-N. Following 2 weeks of observation, blood pressure, C3 level and ASK titer returned to normal ranges, although nephrotic syndrome was still evident, which necessitated oral prednisolone (30 mg/day) therapy. Another biopsy taken 2 months later demonstrated regression of endocapillary proliferation and IF showed decreased deposition of C3. Immunohistochemical staining of the specimen taken on admission revealed the presence of numerous T cells and macrophages in the interstitium. Macrophages were also seen in the glomerular tuft. Many interstitial infiltrating cells were positive for interferon-gamma, but their number diminished after treatment. Our findings suggest that PSAGN complicating pre-existing IgA-N activates cellular immunity and augments renal tissue injury.
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PMID:Superimposition of post-streptococcal acute glomerulonephritis on the course of IgA nephropathy: predominance of Th1 type immune response. 1235 93

The clinicopathological features of rapidly progressive glomerulonephritis (RPGN) were studied in 4 young adult Nigerians who presented with acute GN. There was a predilection for males with a male to female ratio of 3:1. Hypertension. nephrotic-range albuminuria, haematuria granular and cellular urinary casts, and a rapid progression to severe renal failure or death were the findings in all four patients. Renal biopsy revealed histological features compatible with findings in RPGN in all the patients, including the presence of crescents and epithelial cellular proliferation. The study shows that the early development of hypertension and deterioration of renal function in patients with features of acute glomerulonephritis should arouse suspicion of a rapidly progressive GN whose course could be altered by appropriate therapeutic measures, some of which are highlighted.
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PMID:Rapidly progressive glomerulonephritis in adult Nigerians: a report of 4 cases. 1251 36


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