Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 40-year-old female had a history of fever, arthralgia, proteinuria, and dyspnea on effort twenty years ago, and was diagnosed as SLE, renal failure, and aortic regurgitation. She also suffered from pyelonephritis and sepsis due to the infection of E. coli. Preoperative examination revealed non-active phase of SLE. Echocardiography and aortography showed massive aortic regurgitation and operation was recommended. Operative findings showed fresh vegetation on the aortic leaflets, and aortic valve replacement (Tekna-Edwards 19 mm) was performed. Histological findings of the vegetation showed Libman-Sacks endocarditis and infectious endocarditis. Predonisolone was infused intravenously to prevent the acute deterioration of SLE after the operation. She was discharged from the hospital three weeks after the operation.
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PMID:[Aortic valve replacement due to Libman-Sacks endocarditis combined with infectious endocarditis]. 882 83

We report here a case of Cogan's syndrome associated with systemic vasculitis as well as myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA)-related glomerulonephritis. A 71-year-old woman with the diagnosis of aortitis syndrome and pulmonary fibrosis for 7 years, complained of vertigo and hearing impairment. A diagnosis of serous otitis media was made. Although steroid therapy was effective, the symptoms relapsed several times. Seven months after the first manifestation of aural symptoms, she developed painful red eyes bilaterally and proteinuria. On admission, perinuclear ANCA without cytoplasmic ANCA was detected by indirect immunofluorescence assay and MOP-ANCA was detected by enzyme linked immunosorbent assay using the 363 ELISA Unit. Renal biopsy showed necrotizing crescentic glomerulonephritis without immune deposits. A diagnosis of atypical Cogan's syndrome with systemic vasculitis and pulmonary fibrosis was made from the clinical and histological findings. As nephrotic syndrome progressed after admission, she was started on high-dose corticosteroid administration. Urinary protein and other symptoms, except for hearing acuity, improved in parallel with a decrease in the MPO-ANCA titer to normal values. While tapering the dose of corticosteroid, the MPO-ANCA titer increased again and dyspnea occurred. Although pulse methylpredonisolone therapy was performed, the patient died of respiratory failure complicated with sepsis. Postmortem lung biopsy showed pulmonary fibrosis and massive alveolar hemorrhage. The findings of this case study suggest that MPO-ANCA may be closely related to the pathogenesis of Cogan's syndrome.
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PMID:[A case of myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA)-related glomerulonephritis associated with Cogan's syndrome]. 891 96

A 33-year-old man presented malar rash in April, 1992. The rash had gradually developed and he was admitted to our hospital in February, 1994. Laboratory findings showed proteinuria of 0.5-0.8 g/ day, thrombocytopenia (4.8 x 10(4)/mm3), false positive serologic test for syphilis, anti-nuclear antibody with a speckled type at a titer of 1 : 80. Activated partial thromboplastin time was prolonged (41.3 s), and anti-beta 2-GPI antibody was strongly positive (56.6 U/ml on enzyme linked immunosorbent assay). The diagnosis of systemic lupus erythematosus with antiphospholipid syndrome was made and prednisolone 60 mg/day improved his manifestations. He could be discharged in July, 1994. Nine months after the discharge he developed dyspnea, and he was admitted to our hospital again. On admission the blood pressure was 212/170 mmHg, Levine III/VI systolic murmur was noted at the apex of heart. Significant laboratory findings showed as follows: WBC 15, 110/mm3 (Neu 73%, Lym 18%), RBC 380 x 10(4)/mm3, Hb 10.2 g/dl, Plt 20.0 x 10(4)/mm3, GOT 23 IU/l, GPT 21.
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PMID:[Acute cardiac failure due to dilated cardiomyopathy in systemic lupus erythematosus with antiphospholipid antibody]. 912 25

A 12-year-old boy was admitted to our hospital because of abnormal shadows on a chest radiograph, slight fever, and superficial lymphadenopathy. Laboratory examination showed anemia (Hb 9.9 g/dl) and hyperimmunoglobulinemia (IgG 5469 mg/dl) without M protein. A chest CT scan showed bilateral diffuse shadows and bilateral hilar lymphadenopathy. Biopsy specimens of an inguinal lymph node and a lung showed many lymphoid follicles with germinal centers, and marked infiltration of mature plasma cells in the interfollicular area without destruction of follicular structures. The polyclonality of the plasma cells was confirmed by immunohistochemistry. The patient was not treated because these results excluded malignant disease and he was asymptomatic. At the age of 17 years, he was admitted to our hospital again because of dyspnea and a tendency to bleed. Interstitial pneumonia, hyperimmunoglobulinemia (IgG 13900 mg/dl), and anemia (Hb 6.6 g/dl) were found, along with thrombocytopenia (2.5 x 10(4)/mm3) and proteinuria. The serum interleukin-6 level was high: 177 pg/ml. Bronchoalveolar lavage fluid contained many plasma cells. Therapy with corticosteroids and immunosuppressant medication was effective. Our diagnosis was plasma cell interstitial pneumonia as a manifestation of multicentric Castleman's disease.
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PMID:[Plasma cell interstitial pneumonia as a manifestation of multicentric Castleman's disease]. 934 Dec 83

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.
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PMID:[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome]. 939 74

A 22 year-old woman with a seven year history of (SLE) was readmitted because of oliguria, edema, dyspnea and arterial hypertension. She had a previous biopsy diagnosis of focal glomerulonephritis, (WHO III b), and had been treated with immunosuppressors and steroids. Laboratory data showed lupus activity, AHM with thrombocytopenia, nephrotic-range proteinuria and renal failure. A second renal biopsy was performed showing diffuse proliferative nephritis, (WHO IV), in association with noninflammatory necrotizing vasculopathy with luminal obliteration. She started with hemodialysis and was subsequently treated with methylprednisolone pulses, plasmapheresis, cyclophosphamide and oral steroids. During the inpatient period, she had generalized seizures, acute lung injury and pulmonary hemorrhage. These complications, the AHM and the thrombocytopenia receded totally. Renal function was never resumed. We emphasize that this association of diffuse proliferative nephritis with noninflammatory necrotizing vasculopathy is not infrequent and has a poor renal prognosis. The AHM with thrombocytopenia was interpreted as secondary to endothelial cell damage due to vasculopathy.
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PMID:[Renal vascular lesion and microangiopathic hemolytic anemia in systemic lupus erythematosus]. 953 30

In May 1984 a 58-year-old woman presented with a broad spectrum of clinical symptoms including malaise, arthralgia, hemoptysis and dyspnea, proteinuria and hematuria and a vasculitic necrotizing rash. Bronchial biopsies revealed subglottic granulomatous lesions and renal biopsies showed necrosis, extracapillary proliferation and crest formation, confirming the diagnosis of Wegener granulomatosis. Positive c-ANCA and anti-proteinase 3 subfraction (anti-PR3) titers were first analysed in 1991. Clinical remission was achieved by standard immunosuppressive therapy and renal function was stabilised. Several minor relapses were treated with pulsed intravenous cyclophosphamide but the symptoms could not be completely controlled. Eight years after the onset of disease, a dramatic increase in anti-PR3 titers was observed (34438 U/ml, normal range < 10, ELISA), followed 3 months later by a clinically apparent relapse. Immunosuppressive therapy was reinstituted without clinical improvement. At this point plasmapheresis resulted in an amelioration of clinical symptoms as well as a reduction in anti-PR3 titers. Concomitant immunosuppressive therapy was administered with oral corticosteroids. Forty days later anti-PR3 titers increased, reaching 75000 U/ml twelve months later, however this time without associated clinical symptoms. During the following months the patient had a further transient deterioration of pulmonary and renal function due to secondary bacterial infection which was successfully treated with antibiotics. A nephritic sediment was not present during these episodes. Curiously, the anti-PR3 titers have remained excessively elevated for the last three years.
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PMID:Dissociation between high anti-PR3 titers (c-ANCA) and the clinical course of disease in a case of Wegener granulomatosis. 982 23

We treated a 13-year-old girl who developed myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-related crescentic glomerulonephritis (GN) during propylthiouracil (PTU) treatment for Graves' disease. MPO-ANCA-related crescentic GN during PTU therapy has been described previously in only one recent report of 2 children. We report this case here and describe 15 (13 adult cases) more patients with MPO-ANCA-related GN associated with PTU found in a literature review. The mean age at onset was 41.3 years, and the length of PTU administration ranged from 2 weeks to 6 years (mean 3.5 years). Clinical signs and symptoms were hematuria (100%), proteinuria (100%), arthralgia (7 of 16 cases; 43.8%), fever (4 cases; 20.0%), purpura (2 cases; 12.5%), skin ulcer (1 case; 6.3%) and dyspnea (1 case; 6.3%). These patients were treated with steroid (15 cases; 93.8%), cyclophosphamide (8 cases; 50.0%), steroid pulse therapy (4 cases; 25.0%), or plasma exchange (1 case; 6.3%), or were not treated (1 case; 6.3%). Most patients revealed crescentic GN (15 cases; 93.8%) on renal biopsy, while one exhibited mesangial proliferative GN (6.3%). For 2 of the 16 patients (12.5%) irreversible renal dysfunction persisted and hemodialysis was started. Patients with Graves' disease treated with PTU should be observed carefully by urinalysis and monitoring of the serum creatinine level.
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PMID:[A pediatric case of myeloperoxidase-antineutrophil cytoplasmic (ANCA)-related crescentic glomerulonephritis associated with propylthiouracil treatment for Graves' disease]. 989 62

A 36-year-old woman, at the 17th week +5 days gestational age, who was already admitted to the nephrology department for gestational hypertension, proteinuria and legs oedema, was admitted to our Institute. About three weeks before her admission to the nephrology dept., the patient presented heart palpitations and exertional dyspnoea related to the first evidence of the legs oedema, weight gain (about 5 kg during only one month) and normal blood pressure values. During the following days, an antihypertensive therapy was made, but hypertensive crisis and strong headache were also persistent. Vulvar oedema was observed, the uterus was moderately contracted and its dimensions were similar to an uterus at the 21st week; beta-hCG serum values were more than 500,000 IU/lt. An echography confirmed the diagnostic suspicion of hydatidiform the presence of a fetus developed as much as the gestational time. beta-hCG serum values increased to 1,200,000 IU/lt; the molar abortion induction was made thru prostaglandins: fetal extrusion occurred after three hours. The placenta was instrumentally extracted and it showed evident hydatidiform moles a uterine curettage. Patient temperature was very high (39 degrees C) in the immediate postoperative period and three hematologic pockets were transfused. After a week, we made a second elective uterine curettage with the extraction of a little quantity of gestational material; the patient was still hospitalised for ten days: during this time there was a progressive decrease of the beta-hCG serum values (last value at discharge: 7,200 IU/lt). The patient had also positive beta-hCG serum values after about one year.
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PMID:[Partial hydatidiform mmole at the 17th week of pregnancy]. 1023 Feb 45

A 67-year-old female patient with biopsy proven AL systemic amyloidosis developed rapidly progressive dyspnea. Chest roentgenogram and CT scan revealed a large right pleural effusion in addition to nodular lesions with bilateral hilar lymphadenopathy. The patient's serum showed IgG lambda type monoclonal gammopathy and she also had Bence Jones proteinuria. The pleural effusion was an exudate that contained many mononuclear cells and a high concentration of protein. Cardiac function was not seriously disturbed. Except for amyloidosis, no other causes for the severe pleural effusion were found. This patient was treated with chemical pleurodesis using Picibanil and a low dose of prednisolone. Eighteen months after this treatment, her right pleural effusion did not recur. Bronchopulmonary tissues are known to be frequently involved by AL systemic amyloidosis, but a nodular pattern of pulmonary amyloid deposition and a unilateral large pleural effusion are rare clinical manifestations in this disease.
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PMID:Nodular lung disease with five year survival and unilateral pleural effusion in AL amyloidosis. 1061 52


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