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)

Spontaneous thymoma rats, Buffalo/Mna (B/Mna), in which nephrotic syndrome (NS) has recently been observed, have notable features in connection with muscle diseases; they exhibit muscle fatigability and weakness. Some biochemical measurements used for diagnosis of muscle diseases and NS were performed in these rats. ACI strain served as a reference strain. Urinary creatinine level and serum enzyme activities such as CPK, aldolase, GOT and GPT in the B/Mna rats did not differ from those in the ACI rats. On the other hand, urinary creatine level, the ratio of urinary creatine to creatinine and serum total cholesterol level in the B/Mna rats were significantly greater than those in the ACI rats. B/Mna rats also showed proteinuria and hypoalbuminemia. These results indicate the possibility of some pathological change of skeletal muscles which may result at least partially from abnormal lipid metabolism and hypoproteinemia as a consequence of NS, differing from the typical muscular dystrophy.
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PMID:Biochemical study on spontaneous thymoma rats with motor dysfunction. 662 Jan 16

A 66-year-old female was admitted to our hospital in January, 1998, complaining of low grade fever and muscle weakness of her legs. Physical examination revealed muscle weakness of her neck (4/5) and proximal skeletal muscles of her bilateral legs (3/5-4/5). She showed proteinuria and microhematuria. Her serum levels of ureanitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, creatinekinase, aldolase and myoglobin were all within the normal ranges. Antinuclear antibodies were negative, but her serum levels of pANCA (743 EU) and C reactive protein (18.0 mg/dl) were elevated. Neuroconduction velocity of her left common peroneal nerve was decreased to 40.8 m/sec and electric myograph showed neurogenic changes. Magnetic resonance images (MRI) of her bilateral thigh depicted high signal intensity in quadriceps by T 2 weighed images, but the signals were not enhanced by gadolinium injection. Muscle and renal biopsies revealed necrotizing vasculitis of the small arteries. Crescentic glomerulonephritis was also observed by renal biopsy. These findings supported the diagnosis of microscopic PN. On 16 th admission day, she developed acute cardiac and respiratory failures due to cardiac and respiratory muscle involvements with PN, and was assisted by mechanical ventilation. She was treated with methylprednisolone pulse therapy (500 mg/day, three consecutive days) on 18 th admission day, followed by 40 mg of oral prednisolone daily. However, her symptoms deteriorated, and herserum creatinine levels increased to 2.4 mg/dl. On 24 th admission day, intravenous cyclophosphamide pulse therapy (500 mg/day) was instituted. Her cardiac wall motion on echocardiography and serum creatinine levels gradually improved, but her skeletal and respiratory muscle weakness did not improve. On 38 th admission day, she was complicated with respiratory infection by methicillin resistant Staphylococcus aures. On 62 th admission day, she died of endotoxic shock. This is the first report describing respiratory muscle involvement with PN, and the second report describing MRI findings of muscle involvement by PN. Therefore, our case provides important clinical information for the diagnosis and treatment of the disease.
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PMID:[A case of microscopic polyangiitis with severe cardiac and respiratory muscle involvement]. 1061 70

We report the case of a 27-year-old African American man who presented with 6 months of generalized lymphadenopathy and nothing in his history or examination to suggest systemic lupus erythematosus (SLE). He was thought to have lymphoma, syphilis, or tuberculosis, and an extensive workup was done. Laboratory investigation finally revealed leukopenia (4.0), proteinuria (1.87 g), antinuclear antibodies (640 speckled), anti-double-stranded DNA (640), anticardiolipin immunoglobulins G and M, anti-Smith, Coombs, anti-Ro, anti-La, CK (531 U/L), aldolase (8.5 U/L), high erythrocyte sedimentation rate (130 mm/h), and low complement (C3 15 mg/dL and C4 3 mg/dL). A kidney biopsy showed diffuse proliferative glomerulonephritis, International Society of Nephrology class IV. Generalized lymphadenopathy as the first and only manifestation for 6 months made the diagnosis of SLE challenging. Generalized diffuse lymphadenopathy has been associated with SLE but is much less frequent now than in the past. The differential diagnosis of lymphadenopathy relevant to rheumatologists includes Kikuchi histiocytic necrotizing lymphadenitis, Castleman disease, syphilis, tuberculosis, sarcoidosis, and lymphoma.
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PMID:Diffuse lymphadenopathy as the presenting manifestation of systemic lupus erythematosus. 2404 14