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)

We report a case of endstage renal disease due to simultaneous occurrence of membranous nephropathy and crescentic glomerulonephritis associated with anti-GBM antibodies. The patient was a 60-year-old male and was hospitalized for prolonged anorexia and general malaise. On admission, his body temperature was 38.5 degrees C. Urinalysis revealed 3+ proteinuria and the sediment contained abundant erythrocytes. The urea nitrogen was 142.4 mg/dl, the creatinine 19.5 mg/dl, the potassium 6.47 mEq/dl and CRP 10.1 mg/dl. Anti-GBM antibodies were 1000EU/ml. Immediately after initiating hemodialysis, pulse steroid therapy, plasma exchange and continuous heparinization were performed. However, renal function had been impaired and maintenance hemodialysis was required. Histological examination of the renal specimen revealed marked epithelial crescent formation, whereas thickening of basement membrane and mesangial proliferation were not observed. By immunofluorescent staining, both bright linear and fine granular fixation of IgG and fine granular fixations of C3 along the glomerular capillary walls were observed. Electron microscopy showed subepithelial electron lucent deposits and thickening of the glomerular basement membrane, diagnostic of the advanced membranous nephropathy (stage IV).
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PMID:[A case of anti-GBM nephritis (crescentic glomerulonephritis) associated with membranous nephropathy]. 147 22

A total of 99 cases of viridans streptococcal endocarditis encountered during the period of 1973 and 1990 at the Veterans General Hospital-Taipei were reviewed to evaluate its prognostic factors. Applying strict clinical and laboratory criteria, 24 cases were categorized as definite, 44 probable, 23 possible and 8 likely. The symptoms were frequently subtle and atypical but initial laboratory tests gave useful indications: 69.1% with leukocytosis, 78% with anemia, 58.5% with elevation of LDH level, 88.9% with elevation of ESR value and 100% with elevation of CRP level. Furthermore, 32.4% of the cases demonstrated proteinuria and 67.4% microscopic hematuria. Seventy-three of the subjects had a history of underlying heart disease, predominantly rheumatic heart disease. Histological examination and echocardiography revealed that 51 patients suffered from vegetative endocarditis, 7 (13.7%) of whom were found to have anatomically confirmed vegetations without initial echocardiographic evidence, Vascular events were seen in 61 cases (61.6%): peripheral stigmata (32 cases), cerebral vascular accidents (17 cases), pulmonary embolism (10 cases) and others (2 cases). The overall mortality rate was 18.2%. Congestive heart failure with embolization was the most common cause of death in this group. The presence of vegetation was not well correlated with embolic events. There was no statistically significant association between the mortality and the following characteristics: age, sex, underlying heart disease, evidence of echocardiographically detected vegetations, major surgical intervention and recurrent cases except for embolic events (p less than 0.01). In conclusion, viridans streptococcal endocarditis complicated embolic events usually presented with a fulminant course and a grave outcome.
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PMID:Overview of viridans streptococcal endocarditis: clinical analysis of 99 cases. 165 35

The authors studied the activity of peripheral blood natural killer cells in 25 patients with rheumatoid arthritis by 51 Cr release assays with K-568 target cells. Data on the comparative clinico-immunological analysis by the cytotoxicity index are submitted. There is a relation between the nature of rheumatoid arthritis course and the presence of systemic manifestations such as nodules, polyneuropathy, proteinuria, carditis, levels of the rheumatoid factor, anti-DNA, CRP, cryoglobulinemia and changed activity of peripheral blood natural killer cells. Patients with rheumatoid arthritis having a combination of marked changes of humoral immunity with changed cytotoxicity of the peripheral blood natural killer cells activity can be referred to the group of risk.
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PMID:[Activity of natural killer cells of peripheral blood in patients with rheumatoid arthritis and their clinical significance]. 180 25

A 54 year-old woman who had had 4 years history of ulcerative colitis (UC) was admitted to our hospital because of recently developed proteinuria and leg edema. On admission, laboratory findings disclosed massive proteinuria, hypoalbuminemia, acceleration of ESR and elevated of CRP. Her abdominal symptom was remitted. Renal biopsy showed amyloid deposition in glomeruli and arteriole. Amyloid deposition was also found on rectal biopsy. She had no evidence of familial amyloidosis and multiple myeloma. In this case, amyloid deposition might be developed after UC. Secondary amyloidosis due to UC was extremely rare, only 3 cases including ours were reported in Japan.
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PMID:[A case of secondary amyloidosis complicated with ulcerative colitis]. 237 13

A 22-year-old woman, who had been diagnosed as having rheumatoid arthritis (RA) 2 years before, was admitted to our hospital complaining of watery diarrhea (several times/day). She had been treated with low dose prednisolone (PSL) and auranofin in out-patient clinic. On admission, laboratory data showed moderate proteinuria (0.3 g/day) and positive CRP (2.7 mg/dl). Although the activity of RA was controlled by the administration of low dose methotrexate (7.5 mg/week) in addition to PSL, watery diarrhea and proteinuria did not improve. The biopsy of the stomach, rectum and kidney revealed the deposition of AA type amyloid protein, resulting in the diagnosis of secondary amyloidosis. Secondary amyloidosis has been reported as one of the common complications in RA patients, especially in old patients with a long history of RA. To our knowledge, however, there have been few reported cases who developed secondary amyloidosis so early during the course of RA as our case. We should be careful for the development of secondary amyloidosis even in young RA patients with short history of RA, when the disease is active.
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PMID:[A young woman with rheumatoid arthritis who rapidly developed secondary amyloidosis]. 755 43

The clinical picture of nephropathia epidemica (NE) among children is poorly understood. We made a retrospective analysis of 32 patients aged 4-15 years treated in hospital for serologically verified recent NE. The most common clinical findings were high fever (100%), nausea (81%), vomiting (72%), tenderness in the kidney area (63%), abdominal pains (59%) and headache (59%). A peculiar symptom of NE, transient visual abnormalities, was found in 25% of patients. Four children had clinical bleeding and 1 had encephalitis. 44% were transiently hypertensive. Renal function was impaired in 84%, proteinuria was present in 97%, hematuria in 73% and leukocyturia in 44%. Other common laboratory findings were thrombocytopenia (87%), leukocytosis (41%), elevated ERS (74%, up to 76 mm/h) and CRP level (89%, up to 97 mg/l), elevated liver enzymes (53%) and hypoalbuminemia (50%). No child needed dialysis therapy and all recovered. NE seems to be less severe in children than in adults.
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PMID:Clinical picture of nephropathia epidemica in children. 791 22

A 67-year-old woman, who had been diagnosed with classical rheumatoid arthritis (RA), was admitted to our hospital because of massive proteinuria. Biopsy of the kidney revealed deposition of amyloid fibrils in the subepithelial and subendothelial spaces of the glomerular capillary walls. Though the treatment with prednisolone and dipyridamole against nephrotic syndrome and amyloidosis due to RA was not effective, cyclophosphamide, which was added after tapering of prednisolone, was able to induce remission of nephrotic syndrome after two years. The levels of CRP and serum amyloid A protein (SAA) returned to within the normal limits. As the impairment of renal function is thought to be due to deposition of amyloid supplied from the precursors of amyloid fibrils filtered from the general circulation in RA patients, remission of nephrotic syndrome might result from the suppression of production of SAA or removal of amyloid fibrils. Cyclophosphamide, which has the potential both to suppress disease activity in RA and to produce degradation of amyloid fibrils in glomeruli, may be useful against renal or systemic amyloidosis complicated by RA.
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PMID:Combined treatment with cyclophosphamide and prednisolone can induce remission of nephrotic syndrome in a patient with renal amyloidosis, associated with rheumatoid arthritis. 792 63

Approach to the management of AA amyloidosis complicating RA. (A) In case of proteinuria or loss of renal function a rectal biopsy or a subcutaneous fat biopsy is a suitable screening method for the detection of amyloidosis. If in any doubt, try to ascertain the diagnosis by renal biopsy. Adequate staining with alkaline Congo red and preferably immunohistochemical staining with anti-AA antibodies should be performed. Beware of renal pathology other than amyloidosis even in the presence of a positive rectal biopsy. (B) A vigorous attempt to control disease activity of the RA should be made in order to eliminate the production of SAA, an acute phase protein. The response to treatment should be monitored by serial measurements of CRP and preferably SAA. (C) The function of some vital organs should be evaluated: (a) endogenous creatinine clearance and the extent of proteinuria; (b) electrocardiogram and optional echocardiography; (c) thyroid function and adrenocortical function; (d) intestinal absorption tests; (e) optional--SAP scintigraphy and turnover studies. (D) Attention should be given to adequate supportive treatment: (a) blood pressure control; (b) treatment of intercurrent infections; (c) corticosteroids during major surgical procedures; (d) pay attention to the possible effect of NSAID on proteinuria and renal function. (E) In case of total renal failure or uncontrollable proteinuria: (a) consider the possibility of primary renal transplantation; (b) otherwise regular haemodialysis is indicated.
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PMID:Clinical and therapeutic aspects of AA amyloidosis. 795 68

This study analyzed the interleukin 6 (IL-6) response in 114 children with suspected urinary tract infection (UTI). Urine and serum samples were obtained at the time of enrollment. There were 90 children with UTI, 41 with and 49 without a temperature > or = 38.5 degrees C. The remaining 24 children did not have bacteriuria; 11 were febrile and 13 were not. The urinary IL-6 concentrations were higher in the children with UTI (mean, 129 units/ml) than in the children without bacteriuria (mean, 7 units/ml, P < 0.01). In contrast the serum IL-6 did not differ between children with or without UTI or between children with or without a temperature > or = 38.5 degrees C. The urinary IL-6 response was higher in children who were infected with P fimbriated Escherichia coli than in other children with UTI (P < 0.05). There was a correlation of urinary IL-6 with the degree of proteinuria, hematuria and urinary leukocyte counts (P < 0.001, P < 0.05, P < 0.05, respectively) but not with serum IL-6, CRP or temperature, and of serum IL-6 to C-reactive protein (P = 0.053) and renal concentrating capacity (P < 0.05). The results demonstrate that infections of the urinary tract activate an IL-6 response in children and that the magnitude of the IL-6 response is influenced by the properties of the infecting strain.
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PMID:Interleukin 6 response to urinary tract infection in childhood. 797 Sep 49

We studied whether the low serum C-reactive protein (S-CRP) level in patients with inflammatory arthritis and proteinuria was due to the loss of CRP into urine. In 19 patients with secondary amyloidosis (14 with rheumatoid arthritis and five with juvenile chronic arthritis), S-CRP was measured with both immunoturbidimetric and radioimmunoassays. The concentration of urinary CRP was measured with a double-antibody radioimmunoassay. One patient with the most extensive proteinuria (12 g/24 h) excreted CRP at 14 mg/24 h, while in 18 of 19 patients only negligible, if any, amounts of CRP were found in 24-h urine samples. Proteinuria of < 8 g/24 h did not reduce the S-CRP level. Proteinuria exceeding this level may result in increased excretion of CRP into urine and consequently may result in a reduced S-CRP level.
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PMID:Serum C-reactive protein is rarely lost into urine in patients with secondary amyloidosis and proteinuria. 969 59


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