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 43 year old woman was admitted to our hospital in April 1987 due to shortness of breath and pedal edema. She had a history of sepsis associated with the crisis of hyperthyroidism 15 years prior to the admission. Physical examination revealed a badly nourished with ascites: weight was 56 kg and height 156 cm. The heart sounds were distant with mild holosystoric murmur (grade I/VI) at xiphoisternum. The chest X-ray showed cardiomegaly (CTR: 72.3%) with pleural effusion. The electrocardiogram showed atrial fibrillation, low voltage and right ventriculer hypertrophy. The echocardiogram showed marked dilatation of right atrium and ventricle with very short septal leaflet of tricuspid valve. The anterior and posterior leaflets were undetected. The tricuspid regurgitant doppler signal was recorded up to hepatic vein. No other abnormalities were noted in other valves. The white cell count was 4900 with lymphocytopenia (26%; T-cell 82%, B-cell 13%). Serum total protein was reduced to 3.4 g/dl with albumin 1.64 g/dl. Immunoelectrophoresis showed normal IgG, IgA and IgM. Proteinuria was not recognized. Fecal excretion of polyvinylpyrrolidone-131I (PVP) was elevated to 2.8%, The systolic pressure in pulmonary artery, right ventricle, right atrium, superior and inferior vena cave were almost equal as 26 mmHg. The pulmonary arterial scintigraphy disclosed multiple peripheral defects in both lungs. Two weeks after the operation of tricuspid valve replacement based on the diagnosis of protein-losing enteropathy due to isolated tricuspid regurgitation, serum total protein and albumin were normalized to 6.8 g/dl and 3.6 g/dl respectively, but the lymphocytopenia was persistent. She become very well, with free of ascites and edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of isolated tricuspid regurgitation associated with protein-losing gastroenteropathy]. 273 14

A case of primary myelofibrosis complicated with pericardial effusion and proteinuria is described. A 66-year-old female was admitted to our hospital because of abdominal fullness and shortness of breath. On admission, hepatosplenomegaly and pericardial effusion were observed. Blood examination revealed leukoerythroblastic anemia and thrombocytosis with tear drop cells and giant platelets. Bone marrow aspiration was dry tap and its biopsy showed remarkable myelofibrosis. Urinalysis indicated severe proteinuria. Although neutrophilic alkaline phosphatase score was low, no signs of acute blastic crisis of chronic myelogenous leukemia was found. The diagnosis of an atypical type of primary myelofibrosis was obtained. Administration of MCNU was started in August 1987. Hepatosplenomegaly, pericardial effusion and proteinuria were gradually improved after the administration. The etiology of the pericardial effusion and proteinuria were not obvious, however, these facts suggest that these abnormal findings might be related to PMF itself and MCNU was effective to PNF.
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PMID:[The use of MCNU to a patient of primary myelofibrosis complicated with pericardial effusion and proteinuria]. 276 70

Intravenous immune globulin (IVIg) is advocated as a safe treatment for immune-mediated neurologic disease. We reviewed the medical records of 88 patients who were given IVIg for a neurologic illness. Major complications in four patients (4.5%) included congestive heart failure in a patient with polymyositis, hypotension after a recent myocardial infarction, deep venous thrombosis in a bed-bound patient, and acute renal failure with diabetic nephropathy. Other adverse effects included vasomotor symptoms 26, headache 23, rash 5, leukopenia 4, fever 3, neutropenia 1, proteinuria (1.9 g/day) 1, viral syndrome 1, dyspnea 1, and pruritus 1. Fifty-two patients (59%) had some adverse effect of IVIg infusion, most commonly vasomotor symptoms, headaches, fever, or shortness of breath in 40 (45%), which improved with reduced infusion rate or symptomatic medications. Five (6%) had asymptomatic laboratory abnormalities and seven (8%) had other minor adverse effects. Adverse effects led to discontinuation of therapy in 16% and permanent termination of therapy in 10% of patients. There was no mortality or long-term morbidity. Although adverse effects were frequent, serious complications were rare except in patients with heart disease, renal insufficiency, and bed-bound state.
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PMID:Complications of intravenous immune globulin treatment in neurologic disease. 930 72

A 44-year-old patient died from amyotrophic lateral sclerosis (ALS) after nine years of heavy exposure to cadmium (Cd) in a nickel cadmium (Ni-Cd) battery factory. Two years after starting work he and co-workers had experienced pruritus, loss of smell, nasal congestion, nosebleeds, cough, shortness of breath, severe headaches, bone pain, and proteinuria. Upper back pain and muscle weakness progressed to flaccid paralysis. EMG findings were consistent with motor neuron disease. Cd impairs the blood-brain barrier, reduces levels of brain copper-zinc (Cu-Zn) superoxide dismutase (SOD), and enhances excitoxicity of glutamate via up-regulation of glutamate dehydrogenase and down-regulation of glutamate uptake in glial cells. High levels of methallothionein, a sign of exposure to heavy metals, have been found in brain tissue of deceased ALS patients. The effects of Cd on enzyme systems that mediate neurotoxicity and motor neuron disease suggest a cause effect relationship between Cd and ALS in this worker.
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PMID:Amyotrophic lateral sclerosis in a battery-factory worker exposed to cadmium. 1137 40

A 60-year-old Swiss woman presented with a 1-year history of periorbital hemorrhagic papules, a tendency to develop hematoma due to minor trauma and shortness of breath. The personal medical history included surgery for bilateral carpal tunnel syndrome (CTS) 2 years ago. Clinical and laboratory findings included macroglossia, Bence-Jones proteinuria, reticular lung infiltrates, thickening of the ventricular walls in echocardiography and increase in atypical plasma cells in the bone marrow. The coexistence of the specific symptoms of CTS, macroglossia and cutaneous lesions should immediately alert the physician to the probable existence of plasma-cell-dyscrasia-related systemic amyloidosis.
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PMID:Bilateral carpal tunnel syndrome as a clue for the diagnosis of systemic amyloidosis. 1145 59

A 28-year-old female presented for evaluation of left flank pain and polyuria after having been exposed to cadmium in the jewelry manufacturing industry for approximately 3 years. This patient possessed both elevated 24-hr urinary ss2-microglobulin and elevated blood cadmium levels. Approximately 6 months after initial presentation, the patient resigned from her job due to shortness of breath, chest pain, and anxiety. Exposure to cadmium in the jewelry industry is a significant source of occupational cadmium exposure. Other occupational sources include the manufacture of nickel-cadmium batteries, metal plating, zinc and lead refining, smelting of cadmium and lead, and production of plastics. Cadmium is also an environmental pollutant that accumulates in leafy vegetables and plants, including tobacco. Major toxicities anticipated from cadmium exposure involve the renal, pulmonary, and, to a lesser extent, gastrointestinal systems. These include the development of renal proximal tubular dysfunction, glomerular damage with progressive renal disease, and respiratory symptoms including pneumonitis and emphysema. Low-level cadmium exposure has also been associated with increased urinary calcium excretion and direct bone toxicity, effects that recent research suggests may result in the development of osteoporosis. The body burden of cadmium, over half of which may reside in the kidneys, is most often measured through the use of urinary cadmium levels. Blood cadmium measurements generally reflect current or recent exposure and are especially useful in cases with a short exposure period and only minimal accumulation of cadmium in the kidneys. Both ss2-microglobulin and alpha1-microglobulin serve as organ-specific, early-effect biomarkers of tubular proteinuria and thus play a role in identifying early signs of cadmium-induced renal damage in those with potential exposures. In addition to ensuring workplace compliance with Occupational Safety and Health Administration-mandated monitoring and screening measures, it is prudent for those with cadmium exposure to maintain adequate intake of both iron and calcium, appropriate measures even in the absence of exposure.
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PMID:Cadmium exposure and nephropathy in a 28-year-old female metals worker. 1246 Aug 7

We report a 54-year-old woman with systemic sclerosis who presented alveolar hemorrhage. She noticed shortness of breath in May 1997. She was diagnosed having interstitial pneumonitis and systemic sclerosis with sclerodactylia of bilateral fingers in December. She developed bloody sputum and dyspnea suddenly on March 12, 1999. Bloody lavage fluid with hemosiderin-laden macropharge was observed by bronchial fiber scopic examination. The elevated level of MPO-ANCA was detected without anti-DNA antibody. Administration of intravenous methylprednisolone(1g per day, 3 days) followed by 40 mg per day of prednisolone achieved complete response, and MPO-ANCA level was decreased. Mild proteinuria and microhematuria was detected on admission, but renal biopsy revealed no findings of crescent formation or angiitis. With coadministration of oral cyclophosphamide she doesn't have any renal involvement or recurrence of alveolar hemorrhage during these four years. MPO-ANCA level remains negative. Alveolar hemorrhage, which is uncommon pulmonary event in systemic sclerosis, is often coexist with renal angiitis in the context of "pulmo-renal syndrome". MPO-ANCA is said to be related to pulmo-renal syndrome and is sometimes induced by D-penicillamine. This patient is really important in considering the pathogenesis of alveolar hemorrhage because she had no renal vasculitic lesions or D-penicillamine intake.
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PMID:[Case of systemic sclerosis presenting with alveolar hemorrhage and positive anti-neutrophil cytoplasmic myeloperoxidase antibody(MPO-ANCA) without pathological renal involvement]. 1459 64

We retrospectively reviewed 34 consecutive patients with serologically confirmed leptospirosis admitted during years 1992-2002. Nine patients (26.5%) had respiratory symptoms on admission including cough (n = 4), shortness of breath (n = 4), cyanosis (n = 2), and hemoptysis (n = 1). Six patients had pulmonary radiographic findings including (1) diffuse, ill-defined, ground-glass density (n = 3); (2) diffuse alveolar opacities (n = 2); and (3) small nodular density (n = 1). Male/female ratio was 8/1 and mean age was 47 years. Seven patients reported their exposure source including hunting (n = 2), fishing (n = 2), fresh water swimming (n = 2), and canoeing (n = 1). All patients had fever (mean = 40.1 degrees C). Other common symptoms were headache (n = 4), vomiting (n = 3), and myalgia (n = 3). Biological abnormalities included elevated liver enzymes (n = 8), proteinuria (n = 7), lymphopenia (n = 6), hematuria (n = 5), renal failure (n = 4), anemia (n = 4), and elevated neutrophil count (n = 4). PaO(2 )was measured for 3 patients while they were breathing room air (32, 55, and 66 mmHg). Suspected diagnosis on admission included leptospirosis (n = 2), bacterial pneumonia (n = 2), intoxication, influenza, viral hepatitis, biliary tract lithiasis, and rapidly progressive glomerulonephritis (one patient each). The first serologic testing for leptospirosis was positive for 5 patients (55%). Serovar was presumptively identified for 7 patients: Australis (n = 3), Grippotyphosa (n = 2), and Icterohaemorrhagiae (n = 2). Seven patients were treated with penicillin; two patients received no antibiotics. All patients were cured. In conclusion, patients with leptospirosis may present predominantly with nonspecific pulmonary symptoms. In these patients, leptospirosis must be suspected when there is a potential exposure to rats, especially in case of high-grade fever, myalgia, hepatitis, and renal abnormalities.
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PMID:Respiratory manifestations of leptospirosis: a retrospective study. 1621 64

A severely ill 65-year-old man presented with symptoms of shortness of breath, edema and vasculitidic purpura over his lower extremities. He had severe mitral regurgitation which had not been surgically treated. Hematologic examination demonstrated leukocytosis with profound anemia. Other blood tests revealed impaired renal function, hypoalbuminemia, hypocomplementemia and mixed-type cryoglobulinemia. Urinalysis showed proteinuria, hematuria and pyuria, typical of a nephritic sediment. Renal biopsy indicated diffuse proliferative glomerulonephritis and a "full house" deposition in immunofluorescence study (positive for C3, C4, C1q, IgG, IgA and IgM), resembling the pathologic findings in class IV lupus nephritis. Although subacute bacterial endocarditis was initially suspected owing to a history of a predisposing valvular heart disease, probable vegetation shown by cardiac sonography and a clinical picture suggestive of a chronic infection, it was thought unlikely due to the entire afebrile course and initial sterile blood cultures. However, the blood cultures repeated 2 weeks after admission grew 3 sets of viridans streptococci. Following a course of penicillin and gentamicin treatment, his renal function, anemia and abnormal urine sediments improved gradually. Diffuse proliferative glomerulonephritis is well known to occur in infective endocarditis. However, the "full house" immunostaining in immunofluorescence study has never been reported. This case adds a new entity to the differential diagnosis of "full house" immune complex-related glomerulonephritis and exemplifies the need to maintain a high index of suspicion for underlying infectious disorders when facing glomerulonephritic or vasculitic syndrome.
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PMID:"Full house" proliferative glomerulonephritis: an unreported presentation of subacute infective endocarditis. 1804 78

Takayasu arteritis (TA) is a rare chronic large-vessel vasculitis of unknown etiology. Although commonly thought of as an adult disease, initial manifestations frequently appear during adolescence. This is a case discussion of an 11-year-old boy with a recent history of fever who presented with shortness of breath, sore throat, chest pain, hypertension, and a new murmur. He had a markedly elevated antistreptolysin O titer, had a prolonged PR interval, and was initially evaluated with acute rheumatic fever. After admission, he had persistent hypertension, proteinuria, and hemoptysis, which prompted a magnetic resonance angiography that revealed aortic enhancement and thickening, and he was evaluated with TA. To our knowledge, this is the first case report in the pediatric literature of TA presenting with heart block. This case highlights the recondite nature of the systemic vasculitides and emphasizes the importance of keeping a broad differential diagnosis when seeing patients who present with common complaints.
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PMID:The heart of the matter: an atypical presentation of Takayasu arteritis in the Pediatric Emergency Department. 2192 85


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