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)

To assess toxicity of D-penicillamine a retrospective chart review was performed on 63 patients with rheumatoid arthritis receiving penicillamine. These patients had a total of 83 courses of therapy. The mean age of patients was 52 years and the mean duration of disease was 10.07 years. Laboratory data showed an increase in hematocrit values from 36 per cent to 40 per cent and a decrease in the erythrocyte sedimentation rate from an average of 50 to 29 mm/hour. The platelet count also decreased with treatment from 394,000 to 267,000/mm3. The over-all complication rate was 53 per cent. Life-threatening complications occurred in two patients including one case of aplastic anemia and one case of nephrotic syndrome. One additional patient was referred with aplastic anemia. Minor complications include rash in 18 per cent, loss of taste in 6 per cent, dyspepsia in 11 per cent, oral ulceration in 7 per cent and proteinuria of less than 3 g/day in 8 per cent. In summary, 53 per cent of the courses of penicillamine were associated with toxicity including one episode of aplastic anemia and one case of nephrotic syndrome. Therapy was stopped due to complications in 39 per cent of the patients in this series.
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PMID:Toxicity of D-penicillamine in rheumatoid arthritis. A report of 63 patients including two with aplastic anemia and one with the nephrotic syndrome. 62 27

Proteinuria and the nephrotic syndrome are well known to occur as complications of penicillamine therapy, but reports of penicillamine-induced pemphigus have been relatively few. This is the report of a case in which both complications occurred simultaneously.
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PMID:Penicillamine pemphigus and the nephrotic syndrome occurring simultaneously. 62 9

A microspectrophotometric study of sialomucins in human glomerular filter of the kidney in some diseases was carried out. Sialomucins were detected in paraffine sections stained after Haim, and examined on scanning microspectrophotometer. Lipid nephrosis, secondary amyloidosis, membranous-proliferative glomerulonephritis with the nephrotic syndrome were accompanied by a significant decrease in the amount of sialic acid. No reduction of sialomucins occurred in subacute glomerulonephritis with the nephrotic syndrome. A connection between the selective proteinuria and a decrease of the amount of sialomucins in the glomerulus is suggested.
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PMID:[Microspectrophotometric study of the sialomucin content of the glomerular filter in the nephrotic syndrome]. 65 13

Before and four weeks after immunization with a single 0.5-ml dose of influenza virus vaccine, sera from 36 children with renal diseases were tested for serum hemagglutinating-inhibiting antibody (HAI) titers to A/New Jersey/76, A/Victoria/75, and A/Port Chalmers/73. Before immunization, 1:40 HI antibodies to A/New Jersey were noted in one child only, to A/Victoria in ten children (27%), and to A/Port Chalmers in 25/34 children (68%). Serum HAI titers increased fourfold or more (P less than .01) in 31/36 children (86%) after immunization. Neither the type of the renal disease nor therapy with prednisone had any effect on the rise of serum HAI titers (P less than .05). Of the seven children with preimmunization proteinuria, four had a transient rise in protein levels following immunization. None required an increased prednisone dose for exacerbation of nephrotic syndrome. Children with chronic renal problems should be protected against influenza.
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PMID:Influenza virus immunization. Antibody response and adverse effects in children with renal disease. 66 Jul 87

We have made a blind retrospective analysis of 334 renal biopsies, each containing more than 10 glomeruli, from adults and children with glomerulonephritis, in order to assess the clinicopathological significance of segmental lesions. These were defined as endocapillary proliferation and/or sclerosis involving capillary loops, and a less than half the glomerular tufts. On optical microscopy of paraffin-embedded material, 57 biopsies containing segmental lesions were independently classified by two observes as "focal proliferative glomerulonephritis" or "focal segmental glomerulosclerosis". These results were then reviewed with immunofluorescence, electron microscopic and clinical data and an "executive" diagnosis reached. Scarred focal proliferative glomerulonephritis could not be reliably distinguished from focal segmental glomerulosclerosis by optical microscopy alone. Some cases of focal proliferative glomerulonephritis are not associated with systemic disease and may have negative immunofluorescence findings, and we were unable to distinguish scarring in these patients from the lesion of focal segmental glomerulosclerosis with any of the tools at our disposal. Some patients with scarred focal proliferative glomerulonephritis showed profuse proteinuria, a nephrotic syndrome and progression to renal insufficiency. These cases cannot therefore be differentiated from focal segmental glomerulosclerosis by their clinical features. It would seem that the morphological lesion of focal segmental glomerulosclerosis should be regarded as focal segmental glomerular scarring from a variety of insults, rather than a distinct disease entity.
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PMID:Focal segmental sclerosis or scarred focal proliferative glomerulonephritis? 66 23

70 cases of focal glomerulosclerosis (FGS) followed for periods ranging from 1 to 24 years are reported. 39 patients had a nephrotic syndrome. 31 patients had asymptomatic proteinuria. 97 renal biopsies were performed. At least one biopsy specimen from every patient showed focal and segmental involvement of glomeruli, but no lesions were observed on the first biopsy in 6 patients. 26 of the 35 patients with a nephrotic syndrome were treated with steroids alone and/or chemotherapy and/or indomethacin. Resistance to treatment was encountered in 21 patients. Complete remission was observed in 6 cases, despite persistence or accentuation of histological lesions on serial biopsies in 3 cases. Actuarial renal survival rate at 10 years was 45% in the group with a nephrotic syndrome versus 91% in patients with proteinuria. FGS with a persistent nephrotic syndrome represents the 'malignant' form of the disease. Recurrence of the disease was observed after transplantation in 2 cases and was absent in 1.
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PMID:Focal glomerulosclerosis: natural history and treatment. A report of 70 cases. 67 92

This paper describes the detection of a paraprotein in blood or urine in 12 of 260 patients with 'idiopathic' proteinuria, most of whom presented with the nephrotic syndrome. None had myeloma at presentation and only two have developed it. Initial clinical and biochemical findings did not suggest paraprotein-associated disease, total serum globulins and individual immunoglobulin levels usually being in the normal range. In seven of the 12 cases the paraprotein was detected only after repeated analysis of serum and urine specimens over months or years. Renal histopathology varied from case to case and is described in detail; amyloid deposition did not occur in patients who excreted kappa chain Bence Jones protein and was extensive in only three. One of these eventually developed myeloma. Patients were aged 27--69 years at onset and were observed without specific therapy for up to 56 months. Glomerular filtration rate tended to decline and proteinuria persisted. All patients have now been treated by a chemotherapeutic regimen consisting of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cyclophosphamide, melphalan, and prednisolone, in repeated short courses. In some patients, particularly those who had kappa Bence Jones protein, there was striking improvement. Overall survival is good, eight patients being alive 17--90 months after the onset of symptoms. The importance of repeated search for paraprotein in apparently idiopathic renal disease in adults is emphasized.
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PMID:Detection, significance and treatment of paraprotein in patients presenting with 'idiopathic' proteinuria without myeloma. 68 53

Antithrombin III (AT II/III) was determined immunologically and by means of a heparin cofactor assay in plasma samples and 24-hour urine of 15 patients with various degrees of proteinuria, being predominantly of glomerular origin. In urine the AT II/III concentrations were significantly correlated to the concentrations of albumin, plasminogen and IgG. One third of the patients had AT II/III plasma levels below the normal range. The plasma levels showed a significant inverse correlation to the AT II/III and albumin clearance rates. Similarily, the plasminogen concentrations in plasma were decreased in two thirds of the patients, being inversely correlated to the renal plasminogen clearance values. It is proposed that AT II/III deficiency in the nephrotic syndrome is an important pathogenetic factor in venous thrombosis.
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PMID:Acquired antithrombin III deficiency in patients with glomerular proteinuria. 68 89

We describe 11 patients whose renal biopsies showed minimal changes with focal segmental glomerulosclerosis. These patients, in contrast to the majority of patients with similar renal histology, went into renal failure within 2 1/2 years of clinical onset. All were young, severely nephrotic, most hypertensive, with microscopic hematuria, non-selective proteinuria and extreme hypercholesterolemia. Treatment with corticosteroids and cytotoxic drugs was without effect in any patient. Despite rapid decline in renal function, profuse proteinuria and a nephrotic syndrome persisted into terminal uremia and continued even after dialysis had begun. Seven patients were given nine allografts; four grafts failed because of immediate vascular complications, and a persistant nephrotic syndrome was evident in two of the five surviving grafts. This did not, however, lead to graft failure. Two patients died on dialysis because of myocardial problems. These patients with rapid decline in renal function constitute a distinct clinical subgroup amongst those with focal and segmental glomerulosclerosis; it is possible that they have a different primarily vascular pathogenesis in contrast to other patients with similar renal biopsy appearances.
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PMID:Focal segmental glomerulosclerosis with rapid decline in renal function ("malignant FSGS"). 69

Heavy proteinuria and/or the nephrotic syndrome rarely occur late in pregnancy. We report the clinical and renal biopsy findings on 11 patients with the nephrotic syndrome occurring during pregnancy in whom light and electron microscopic findings were characteristic of pre-eclampsia. Immunofluorescent microscopy revealed deposits of IgG, IgM, IgA, beta 1C globulin, and fibrinogen, predominantly in the subendothelial position. Only two patients were primigravid; three were in their second or third pregnancy; in six, pre-eclampsia first occurred in the fourth to eighth pregnancy. Clinical abnormalities appeared first between the 23rd and 39th week of gestation. All patients had marked elevation of blood pressure and of serum uric acid levels. Of the 12 infants, eight were alive and well, including one set of twins; four were stillborn. Following delivery, clinical resolution was similar to that in less severe pre-eclampsia. The findings suggest the possible importance of the role of intravascular coagulation in the genesis of pre-eclampsia.
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PMID:Pre-eclampsia with the nephrotic syndrome. 71 77


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