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 review of the medical records of 123 persons with Legionnaires' disease hospitalized in the 1976 Philadelphia epidemic showed that the manifestations of infection ranged from mild grippe to a severe pneumonia that also involved other organ systems. Early in the illness, constitutional symptoms predominated. Fever, malaise, myalgia, rigors, confusion, headache, and diarrhea were usually followed by nonproductive cough and dyspnea. Physical examination showed few abnormalities other than rales. Moderate leukocytosis with left shift, elevated erythrocyte sedimentation rate, elevation of serum levels of liver enzymes, and hematuria and proteinuria were characteristic. Chest radiograph showed patchy, often nodular, areas of consolidation. Progression of pneumonia led to respiratory failure and the need for mechanical ventilatory assistance for 19 patients; renal failure, primarily after shock, occurred in 18 persons. Twenty-six patients died. Treatment with erythromycin or tetracycline resulted in the lowest case-fatality ratios, but the associations were not statistically significant.
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PMID:Legionnaires' disease: clinical features of the epidemic in Philadelphia. 43 27

From 1960 through 1972, 236 cases of amyloidosis with histologic proof were found. The amyloidosis was primary (without evidence of preceding or coexisting disease) in 132 cases (group 1) and associated with multiple myeloma in 61 (group 2). Secondary amyloidosis appeared in 19 cases (associated with rheumatoid arthritis or osteomyelitis in two-thirds of them). There were 22 patients with amyloid localized to a single organ (bladder, lung, skin, or larynx in more than half of them). Two patients had familial amyloidosis. In group 1 and group 2, the most common presenting symptoms were fatigue, weight loss, edema, dyspnea, light-headedness or syncope, and paresthesias. Symptoms of the carpal-tunnel syndrome were frequent. The liver was palpable in almost 50% of the series, but splenomegaly was an initial finding in less than 10%. Macroglossia was recorded in 26% of group 2 and in 12% of group 1. Enlargement of submandibular structures was noted in about 10% of cases; and purpura, particularly around the eyes, was a significant feature. Substantial numbers of the patients had carpal-tunnel syndrome, nephrotic syndrome, congestive heart failure, sprue, peripheral neuropathy, or orthostatic hypotension. Approximately 50% of patients had renal insufficiency at the time of diagnosis. Proteinuria was found in more than 90%. A monoclonal protein was found in the serum of 49% of group 1 and in 74% of group 2. Monoclonal proteins were found in the urine of 35% and 81%, respectively. Only 12% of patients in group 1 had no monoclonal protein when both serum and urine were analyzed, and all patients of group 2 had a monoclonal protein in the serum or urine when both were analyzed. Lambda light chains were more common than kappa. None of the patients in group 1 had more than 15% plasma cells in the marrow, whereas more than half of group 2 had more than 15% plasma cells. Roentgenograms showed no evidence of skeletal disease in 94% of group 1, but 50% of group 2 had skeletal abnormalities. Rectal biopsy was positive for amyloid in 84% of cases. Kidney, liver, and carpal-tunnel biopsies were positive in 90% or more. Follow-up of all 193 patients in groups 1 and 2 revealed that 80% of group 1 and 97% of group 2 had died. The median survival was 14.7 months in group 1 and 4 months in group 2. Cardiac failure was the most common cause of death, accounting for 30% of the fatalities. We also reclassified all cases by the method of Isobe and Osserman (105), which is based on clinical patterns: pattern I--principal involvement of tongue, heart, gastrointestinal tract, muscle, nerves, skin, and carpal ligaments; pattern II--principal involvement of liver, spleen, kidneys, and adrenals; and mixed pattern I and II. This analysis failed to reveal predictive value in the clinical pattern classification, and did not discern the survival differences between primary amyloidosis (group 1) and amyloidosis with myeloma (group 2). Consequently, for the present we prefer the classification used in this study.
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PMID:Amyloidosis: review of 236 cases. 115 71

A 19-year-old man presented with dyspnea, cough and chest pains; he also complained of nausea, anorexia and postprandial vomiting and reported a 10-kg weight loss. Generalized lymphadenopathy and some rales over both lung bases were noted and a chest radiograph showed bilateral nodular lesions. Persistent leukocytosis, thrombocytosis, proteinuria and anergy to a series of natural antigens were found. The diagnosis of lymphoid interstitial pneumonia was made from material obtained at open lung biopsy. Rapid but incomplete clearing of the lung lesions resulted from steroid therapy; the other abnormalities were corrected gradually, except for the proteinuria, which persisted. The clinical improvement and the ability to work and play have been maintained for the past 20 months.
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PMID:Lymphoid interstitial pneumonia. 126 92

We present a patient with pericardial tamponade due to amyloid heart disease. A 64-yr-old man was admitted to the hospital because of fatigue and the abrupt development of chest pain and dyspnea. Echocardiography showed severe pericardial effusion and total pericardiectomy was necessary. Ten months later laboratory studies revealed proteinuria and high serum creatinine. A rectal biopsy showed amyloid deposition that was also found in the pericardial tissue. Pericardial tamponade is an extremely rare complication of cardiac amyloidosis. To our knowledge, only one previous case of cardiac tamponade due to amyloid heart disease has been reported.
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PMID:Cardiac tamponade as presentation of systemic amyloidosis. 142 40

A 38-year-old man was hospitalized for proteinuria, and pitting edema. He had noticed Raynaud's phenomenon at about age fifteen. One month prior to admission, his urine contained protein and the serum creatinine was 3.0 mg/dl. On admission, sclerodactylia, digital pitting scar of fingertips, digital bone absorption and pulmonary fibrosis were observed and a diagnosis of progressive systemic sclerosis (PSS) was made. Laboratory investigations revealed: 24-hour urine protein excretion 3 g; serum creatinine 5.6 mg/dl; creatinine clearance 13.5 ml/min; antinuclear factor strongly positive in a speckled pattern; antibodies to nRNP positive with a titer of 1: 20, 480; antibodies to DNA, Sm, SS-A, SS-B, Scl-70, centromere and Jo-1 negative; serum complement normal. A renal biopsy revealed focal and segmental necrotizing glomerulonephritis with 70% crescents but no vascular changes. Circulating antiglomerular basement membrane antibodies were negative. Immunofluorescence disclosed granular deposits of IgM and C3 in the mesangium and along the capillary walls. Treatment was begun with methylprednisolone pulse therapy. After 5 month, serum creatine and creatinine clearance were 1.9 mg/dl and 35 ml/min, respectively. A year after the discharge, he was readmitted for hemoptysis and worsening of proteinuria and microhematuria. A chest radiograph demonstrated bilateral alveolar consolidation. Serum creatinine was elevated to 3.5 mg/dl. The continuous hemoptysis resulted in a severe dyspnea associated with a rapid fall in the hemoglobin. On the fourth hospital day, the PaO2 was 41 Torr on oxygen by mask that necessitated mechanical ventilation and pulse therapy was started. However, the patient died on the ninth hospital day of respiratory failure due to pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis complicated by crescentic glomerulonephritis and diffuse pulmonary hemorrhage]. 147 23

YK-176 is a newly isolated 2'-deoxycoformycin (DCF), a potent inhibitor of adenosine deaminase, produced by Aspergillus nidulans. In a cooperative phase I study, YK-176 was administered to 22 patients, comprising 18 with adult T-cell leukemia-lymphoma (ATL), two with cutaneous T-cell lymphoma (CTCL), one with lymphoblastic lymphoma of T-cell type and one with carcinoma of the uterine cervix. Doses of YK-176 ranged from 3.0 to 9.0 mg/m2 and were given intravenously for three consecutive days. General malaise, anorexia, nausea, vomiting and low grade fever were frequently encountered, but were transient and not dose-related. At all dose levels hematological toxicities were mild. Two of seven patients receiving 7.0 mg/m2 for three consecutive days developed hepatocellular enzyme elevations (grade 2) and one patient, proteinuria (grade 2). One of two patients given 9.0 mg/m2 for three consecutive days manifested a life-threatening (grade 4) disturbance of consciousness and dyspnea, presumably ascribable to the drug-related toxicity of YK-176. The results suggest that 7.0 mg/m2 i.v. for three consecutive days is the maximum acceptable dose of YK-176. Central nervous system, pulmonary and possibly renal toxicities appeared to be dose-limiting. Out of the 20 patients evaluable for therapeutic response, partial remissions were observed in four, three with ATL and one with CTCL, who received less than 7.0 mg/m2 for three consecutive days. We conclude that YK-176 is an active agent against ATL at doses that may not be associated with prohibitive toxicity. A starting dose of 5.0 mg/m2 for three consecutive days is recommended for further phase II studies on ATL.
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PMID:Phase I study of YK-176 (2'-deoxycoformycin) in patients with adult T-cell leukemia-lymphoma. The DCF Study Group. 151 64

A 38-year-old female was admitted to our hospital because she was suffered from severe dyspnea on effort. She had a history of nasal bleeding, endocarditis, fever, proteinuria, and alopecia at the age of 16, and was diagnosed as SLE. She was suffered from recurrent cerebral infarctions at the age of 35 and 38, and then mitral regurgitation was pointed out. Preoperative examination revealed non-active phase of SLE and UCG showed massive mitral regurgitation. Operative findings showed thrombosed verrucca circumferentially on the mitral valve. Mitral valve replacement (B-S #27) was done with using a felt strip in order to reinforce the mitral annular tissues. Histological findings of the verrucca showed Libman-Sacks endocarditis. Postoperative course was uneventful. Surgical treatment for Libman-Sacks endocarditis is extremely rare.
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PMID:[A case of mitral valve replacement for Libman-Sacks endocarditis]. 156 50

The paper comprises 63 patients with diagnosed vasculitis of the skin who had abnormal findings in the urine. Thirteen of these patients had positive skin findings and abnormal findings in the urine, with concomitant attacks of dyspnea as seen in bronchial asthma. These patients account for 20% of the entire group, while there was an incidence of 37% of systemic manifestations. Skin findings: 45% had a maculopapular rash, 36% had urticarial findings, 13% had urticaria and angioedema and 6% had angioedema alone. Nonspecific biologic syndrome of evolution was statistically significant while no significant changes were found in the number of white blood cells and eosinophils. The degree of proteinuria ranged from 0.1 g/L to 1.16 g/L. Most patients with proteinuria above 0.25 g/L had microhematuria. Slightly over 50% of the patients had signs of complement activation by the alternative pathway, along with the presence of cryoglobulins. Increased histamine in the serum was found in over 50% of the patients although the values of histamine did not correlate with the degree of proteinuria. Proteinuria was not detected in patients with very high values of histamine (and without signs of vasculitis), which indicates that histamine itself responsible for changes in the glomeruli. There is a possibility that local tissue hyperhistaminemia is responsible for the increased permeability of the basal membrane of the glomeruli. According to the obtained results, the etiology of proteinuria and microhematuria should be pursued in the pathogenesis of vasculitis as signs of complement activation indicate. Other possible causes for proteinuria were excluded. The proteinuria was selective, benign according to its course and degree, occurred concomitantly with skin findings and was absent during remission of the disease.
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PMID:[Proteinuria in dermal vasculitis (incidence, degree and possible mechanisms of onset)]. 191 47

This article describes a case of Goodpasture's syndrome controlled by double filtration plasmapheresis (DFPP) combined with steroid and immunosuppressant therapy. A 48-year-old male, clerk, complaining of fever, dry cough and macroscopic hematuria, was admitted to our hospital. Microscopic hematuria was first pointed out at age 40 on an annual check up. His laboratory data on admission revealed severe anemia, azothemia, macroscopic hematuria and proteinuria. His chest radiograph and CT revealed diffuse nodular densities in bilateral lung fields. Specimens obtained by transbronchial lung biopsy and open renal biopsy revealed linear deposition of IgG by direct immunofluorescent antibody methods. Circulating antiglomerular basement membrane antibody level determined with radioimmunoassay was 1.8% on admission, but one week later it elevated to 5.6% with progression of dyspnea, hypoxemia, and renal failure. Steroid pulse therapy and a total of 6 double filtration plasmaphereses were performed in the first month. Subsequently hypoxemia and dyspnea disappeared, and the chest radiograph of the 40th hospital day showed no abnormal shadows. Two months later recurrence of pulmonary hemorrhage was noticed. Immunosuppressant administration (Cyclophosphamide 100 mg/day) and a total of 10 DFPP procedures were performed with success. By DFPP, circulating anti-GBM antibody fell rapidly to within normal ranges, and anti-GBM antibody level elevated in removed plasma. We think DFPP is effective to remove circulating anti-GBM antibody in Goodpasture's syndrome.
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PMID:[Double filtration plasmapheresis in case of Goodpasture's syndrome]. 221 5

In a serological survey among Dutch patients suspected of leptospirosis, using a recently developed enzyme-linked immunosorbent assay, a patient was traced with a high antibody titre to Hantaan virus. No anti-leptospira antibodies were detected in this 27-year-old man. Shortly before he had been admitted to the hospital with progressive dyspnoea and coughing, accompanied with high fever. An interstitial pneumonia was diagnosed. He subsequently developed a progressive renal failure with proteinuria and polyuria. Later a liver failure accompanied with thrombocytopenia, anaemia and coagulation disturbances occurred. Before an aetiological diagnosis was made, the patient was treated with erythromycin. The patient eventually recovered completely. Based on the clinical symptoms and the positive serology, it was concluded that the disease diagnosed had probably been caused by a Hantaan virus infection. The diagnostic value of Hantaan virus serology in patients with similar symptoms is stressed.
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PMID:[Another case of Hantaan virus infection in The Netherlands]. 257 78


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