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)

The proteinuria of fifteen patients treated with just aminoglycoside or aminoglycoside and either penicillin or cephalosporin was studied. The proteinuria was analysed by means of immunoelectrophoresis, acetate cellulose electrophoresis, thin-layer polyacrylamide gel electrophoresis and sodium dodecylsulphate acrylamide gel electrophoresis. We observed a urinary excretion of free immunoglobulin light chains and an increased urinary excretion of lysozyme in all cases. The increase in urinary excretion of beta-2-microglobulin and retinol-binding-protein appeared only in patients treated with aminoglycoside and cephalosporin. These disturbances disappeared a few days after the treatment was discontinued.
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PMID:Low molecular weight proteins as urinary markers of aminoglycoside nephrotoxicity in man. 9 49

The urine of patients with proteinuria of various etiologies was examined to determine if proteinuria alone was associated with significant glycosphingolipiduria. In all cases of proteinuria examined, the level of glycosphingolipids in the urine was found to be markedly elevated. There was no evidence of a glycosphingolipid storage disorder in any case. It was concluded that significant glycosphingolipiduria may occur in proteinuria as well as in the glycosphingolipid storage disorders.
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PMID:Increased glycosphingolipid excretion associated with proteinuria. 9 41

In 53 patients (19 women, 34 men), of them 41 patients with an intracapillary proliferative glomerulonephritis, 9 with membranous proliferative and 3 with a membranous glomerulonephritis under an indometacin therapy examinations concerning proteinuria were carried out, partly with determination of the index of selectivity and representation of the protein clearance. In patients with a moderate proteinuria of less than 3 g a day this treatment achieved a smaller antiproteinurie effect than in patients with a large proteinuria. When a large activity of the inflammatory process was present a therapeutic success was less frequently to be proved. An unequivocal correlation between the histological course of the disease and the change of the proteinuria could not be recognized. After cautious estimation of the findings the selectivity of the proteinuria may be regarded as a certain indicator for the application of indometacin. The protein clearance, however, proved less suitable for the judgment of the treatment performed.
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PMID:[Long-term treatment of glomerulonephritis with indomethacin with special regard to quantity and selectivity of proteinuria]. 9 29

Creatinine, total protein, albumin and beta2-microglobulin were measured in the urine of fifteen healthy women before and after strenuous short-term exercise. The heavy intermittent load produced an increased urinary excretion of total protein, albumin and beta2-microglobulin, while creatinine was unaffected. The renal clearance of albumin and beta2-microglobulin showed very high values after stopping the exercise. However, 45 min after the end of exercise, total protein returned to initial values while albumin and beta2-microglobulin remained high. The urinary ratio between beta2-microglobulin and albumin is higher in urine collected after exercise than in normal proteinuria. This implies that post-exercise proteinuria is of glomerular and tubular origin.
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PMID:Renal glomerular and tubular impairment during strenuous exercise in young women. 9 13

During a prospective screening for proteinuria in diabetic patients, isolated Bence-Jones proteinuria was detected in 2 cases. The first patient, a 52-year-old black female, was seen for evaluation of a slow but progressive weight loss which was attributed to poor adjustment of insulin therapy. The patient gained weight after an increase of the daily insulin administration. She had plasmocytosis in a bone marrow aspirate, but no other evidence of myelomatosis. The second patient, a 59-year-old black male who was seen for routine evaluation of his diabetes, had no clinical or laboratory evidence of myelomatosis. Although precise definition of these cases as "benign" or "idiopathic" Bence-Jones proteinuria is impossible without prolonged follow-up, at the time of presentation they appeared to fit this classification. This observation is one further example that isolated Bence-Jones proteinuria may be seen without any evidence of malignant B-cell dyscrasia.
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PMID:"Idiopathic" Bence-Jones proteinuria. 10 Oct 13

A patient with chronic granulocytic leukemia, neutrophilic type, was followed for 28 months. A paraproteinemia, IgA type K, and Bence Jones proteinuria (K) appeared without prior chemotherapy with alkylating agents.
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PMID:Chronic granulocytic leukemia, neutrophilic type, with paraproteinemia (IgA type K). 10 Oct 17

Acidic hydrolases were assayed in urines of 19 normal children, 33 children with idiopathic nephrotic syndrome of childhood (INS), 21 children with glomerulonephritides (GN) and 7 children with persistent proteinuria/hematuria, and in plasma of 10 children each with INS or GN. Both plasma and urinary acidic hydrolases were studied in intermittent orthostatic proteinuria. Cbeta-galactosidase and Cbeta-N-hexosaminidase were done in normals and children with active renal disease. Significantly (P less than 0.01) elevated urinary acidic hydrolases excretion in active renal diseases, both in INS and GN, returned to a normal range with regression of the diseases. Increased postural proteinuria was associated with normal urinary acidic hydrolases. Both beta-galactosidase and beta-N-hexosaminidase excretion was higher than similar mol wt proteins in normals and increased further in active renal diseases. The data suggests that increased urinary acidic hydrolases is related to the activity of the renal disease, and not to urinary WBC, hematuria or proteinuria. The likely source of urinary acidic hydrolases thus appears to be the injured renal parenchyma itself.
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PMID:Urinary acidic hydrolases in renal diseases in children. 10 80

In a series of 100 adult patients with definite rheumatoid arthritis of at most 3 years' duration and with no previous penicillamine, gold or systemic corticosteroid treatment, 50 patients were treated with D-penicillamine and 50 with gold for one yar. The dose of penicillamine was 600 mg daily. Sodium aurothiomalate was given 50 mg weekly up to a total of 13 mg/kg and thereafter 50 mg once a month. In both treatment groups a statistically significant decrease in the number of painful and/or swollen joints, an increase in haemoglobin and a decrease in ESR, serum ceruloplasmin-, alpha1-acid glycoprotein-, IgG-, IgM- and IgA levels was observed. All the changes in these clinical and laboratory tests were of the same degree in both treatment groups. In the penicillamine group 12 out of 20 seropositive patients became seronegative and in another 5 the Waaler-Rose titre dropped clearly. In the gold group, 7 out of 16 seropositive patients became seronegative, and the Waaler-Rose titre dropped in another 5. An equal increase in the number of eroded joints in hands and toes was seen in the penicillamine and the gold group. Penicillamine was discontinued because of side effects in 13 patients (26%), and gold treatment in 15 (30%). Proteinuria and/or haematuria were the most common causes of discontinuation in the penicillamine group.
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PMID:Comparison of penicillamine and gold treatment in early rheumatoid arthritis. 10 90

A 2-year-old girl was treated with gold salts for juvenile rheumatoid arthritis. Treatment had to be discontinued when persistent proteinuria was detected. As this case report indicates, close monitoring of the urine is mandatory during treatment with gold salts to detect early signs of toxicity: hematuria followed by casts and then proteinuria as therapy is continued. Histologic examination with electron microscopy will help to differentiate the different forms of gold toxicity. When the findings are consistent with gold-induced renal involvement, therapy should be discontinued. The gold nephropathy usually resolves in time, with no permanent renal damage.
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PMID:Gold nephropathy in juvenile rheumatoid arthritis. 10 19

This report describes a case of macroglobulinemia in a six year old castrate male Collie cross dog with clinical signs of epistaxis, anemia, retinopathy and high serum viscosity. The highest total serum protein was 12 g/dl with approximately 60% monoclonal beta globulin. Proteinuria, Bence Jones protein and osteolytic lesions were not detected.Chemotherapy and partial removal of the plasma protein by withdrawal of whole blood and transfusion with packed red cells from a DEA negative donor resulted in transient clinical remission.
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PMID:Case report: Macroglobulinemia in a dog. 10 83


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