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)

Thionamide drugs are widely used in the management of hyperthyroidism and are infrequently associated with adverse reactions. We report the development of the nephrotic syndrome during methimazole (Tapazole) therapy in a young man with Graves' disease. His proteinuria remitted promptly with discontinuance of the drug, and renal histologic features bore a striking resemblance to the toxic nephrosis induced in animals by the aminonucleoside of puromycin. In view of the histologic similarities, we propose that methimazole acted as a direct glomerular toxin, inducing the nephrotic syndrome in this patient.
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PMID:Nephrotic syndrome associated with methimazole therapy. 43 80

A 16-year-old male (S.F.) and his 21-year-old sister (D.H.) from a large family of Italian and Swedish descent had virtually identical lipoprotein pattern and complete absence of LCAT activity. Both had typical corneal opacities and mild anemia with target cells. S.F., but not D.H., presented with proteinuria, which has increased over three years of follow-up. His kidney biopsy revealed lipid deposits in the glomerular basement membrane. Ten relatives in 4 generations had normal LCAT activity and/or lipoprotein pattern. The patients and their relatives had haptoglobin type 2. Factors that might influence the different clinical presentation in our patients (previous renal disease, diet, abnormal lipoproteins), prognosis, and treatment (diet, enzyme replacement, cholestyramine) are discussed.
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PMID:Familial LCAT deficiency. Report of two patients from a Canadian family of Italian and Swedish descent. 74 43

A patient with Goodpasture's syndrome is described in whom pulmonary manifestations were dramatic, but in whom renal abnormalities were minor and only found on fluorescent and electron microscopy. His urine showed no proteinuria and no increase in cells in quantitative counts, and renal function was normal. It is suggested that there may be an indication for carrying out renal biopsies in patients with idiopathic pulmonary haemosiderosis and that this may lead to an early diagnosis of Goodpasture's syndrome.
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PMID:Goodpasture's syndrome: normal renal diagnostic findings. 109 Feb 23

Graves' disease was initially diagnosed in an 11-year-old Chinese boy in March 1989. After regular propylthiouracil (PTU) and thyroxine, he achieved a euthyroid state. Heavy proteinuria with class IV lupus glomerulonephritis, anemia, arthralgia, low serum complement and anti-dsDNA (+) appeared 15 months later. Thyrotoxicosis also relapsed at this time. His condition fitted the diagnostic criteria of systemic lupus erythematosus. His antimicrosomal antibody titer was 1:1,600 (+) thyroid-stimulating hormone receptor antibody level was strongly positive, and the titer of antiinsulin antibody was high as well. These clinical, laboratory and histological findings indicate that class IV lupus nephritis may be associated with Graves' disease.
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PMID:Class IV lupus nephritis associated with Graves' disease. 160 84

A 37-year-old male presented with primary plasma cell leukemia (PCL) with kappa-type Bence Jones proteinuria (BJP) and polyposis of the stomach and colon. His plasma cell leukemia was not preceded by a pre-existing multiple myeloma, and presented the complication of polyposis in both stomach and colon. Biopsy of mucosal lesions revealed marked accumulation of atypical plasma cells with positive cytoplasmic kappa-chain. No amyloidosis was present. His disease responded remarkably well to intermittent melphalan and prednisolone. This case represents an uncommon combination of primary plasma cell leukemia and polypoid gastrointestinal lesions with plasma cell infiltration.
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PMID:A patient with primary plasma cell leukemia accompanied by an extensive polypoid infiltration of the gastrointestinal tract. 177 Mar 27

A 54-year-old male patient with heterozygous Protein C deficiency associated with the nephrotic syndrome and deep femoral artery thrombosis is described. He was admitted to the hospital because of nephrotic syndrome. A few days later, severe pain appeared in his left leg and a diagnosis of deep femoral artery thrombosis was made. Thrombectomy was performed immediately. His proteinuria disappeared in response to corticosteroid. He was found to have Protein C deficiency, antigen: 44%, activity 31%, which was also present in his father and son. Digital subtraction angiography (DSA) revealed the obstruction of left internal iliac and deep femoral arteries at their origins. Renal and hepatic biopsy revealed minor glomerular abnormalities, and chronic active hepatitis. The presence of heterozygous Protein C deficiency, nephrotic syndrome and chronic active hepatitis seem to cause marked decrease in serum Protein C level and deep femoral artery thrombosis. He is now under successful control with warfarin (1.7 mg/day) and bucolome (300 mg/day). It was reported that Protein C might have a suppressive effect on hypercoagulability in nephrotic syndrome. Therefore, Protein C deficiency may not counteract the hypercoagulable state and promote thrombus formation in the case. The present report is the first of a case of Protein C deficiency associated with nephrotic syndrome and arterial thrombosis.
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PMID:[A case of heterozygous protein C deficiency associated with nephrotic syndrome and deep femoral artery thrombosis]. 206 19

A 61-year-old male patient had secondary polycythemia associated with idiopathic nephrotic syndrome. Renal biopsy revealed membranous nephropathy. Polycythemia did not change in spite of partial remission of proteinuria. Serum erythropoietin determined by an enzyme-linked immunosorbent assay was 7.2 mU/ml. His serum erythropoietin maintained at a constant level during polycythemia was higher than it was before the appearance of renal ischemia, so he was kept in a polycythemic state. Whether decreasing proteinuria can improve renal ischemia requires future study. We must observe the patient for the occurrence of thromboembolism. Renal ischemia possibly induced by nephrotic syndrome is likely to cause secondary polycythemia.
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PMID:Secondary polycythemia associated with membranous nephropathy. 218 32

This article describes a case of Goodpasture's syndrome controlled by double filtration plasmapheresis (DFPP) combined with steroid and immunosuppressant therapy. A 48-year-old male, clerk, complaining of fever, dry cough and macroscopic hematuria, was admitted to our hospital. Microscopic hematuria was first pointed out at age 40 on an annual check up. His laboratory data on admission revealed severe anemia, azothemia, macroscopic hematuria and proteinuria. His chest radiograph and CT revealed diffuse nodular densities in bilateral lung fields. Specimens obtained by transbronchial lung biopsy and open renal biopsy revealed linear deposition of IgG by direct immunofluorescent antibody methods. Circulating antiglomerular basement membrane antibody level determined with radioimmunoassay was 1.8% on admission, but one week later it elevated to 5.6% with progression of dyspnea, hypoxemia, and renal failure. Steroid pulse therapy and a total of 6 double filtration plasmaphereses were performed in the first month. Subsequently hypoxemia and dyspnea disappeared, and the chest radiograph of the 40th hospital day showed no abnormal shadows. Two months later recurrence of pulmonary hemorrhage was noticed. Immunosuppressant administration (Cyclophosphamide 100 mg/day) and a total of 10 DFPP procedures were performed with success. By DFPP, circulating anti-GBM antibody fell rapidly to within normal ranges, and anti-GBM antibody level elevated in removed plasma. We think DFPP is effective to remove circulating anti-GBM antibody in Goodpasture's syndrome.
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PMID:[Double filtration plasmapheresis in case of Goodpasture's syndrome]. 221 5

A boy, aged 14 1/2 years, presented with Burkitt leukemia. His renal status was normal before treatment. Chemotherapy (SFOP LMB 86 protocol) was begun Oct. 9, 1986. After the first 2 courses of chemotherapy, the patient had Gram negative sepsis treated with cefotaxime, netilmycine, Vancomycin and ornidazole. During sepsis, nephrotic syndrome developed (albumin 25 g/l, non selective proteinuria 15 g/24 h), with moderately high blood pressure, functional renal failure (creatinine 141 mumols/l, U/P urea = 20), polyuria and tubular damage. Kidney ultrasonography was normal. Needle biopsy showed minimal glomerular lesions, acute tubular lesions, and no deposits in immunofluorescence. The nephrotic syndrome disappeared within 3 weeks, with treatment of leukemia. He is at present in complete remission with a follow-up of 25 months.
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PMID:[Nephrotic syndrome and B leukemia]. 262 44

Idiopathic hypercalciuria (IH) in adults is recognized as a cause of urolithiasis. If IH is symptomatic, the symptoms are hematuria, renal colic, or obstructive uropathy with or without infection. In children, IH has been linked to the spectrum of urinary symptoms including hematuria, pyuria, dysuria, recurrent urinary infections, abdominal or suprapubic pain, proteinuria, and the frequency-urgency syndrome. Hematuria may appear prior to the appearance of stones, and thiazide therapy appears to prevent stone formation by decreasing urinary calcium excretion. This report describes an older adolescent with hematuria and flank pain. His urinary chemistry values were not consistently typical of IH, but a thiazide trial with withdrawal challenge was diagnostic. His case is remarkable because, though essentially an adult, his disease was typical of prepubertal disease. Adolescents with unexplained urinary symptoms should be evaluated for IH. The urinary calcium-creatinine ratio may not be elevated, and timed urinary calcium may be equivocal. In some cases a thiazide trial may be valuable and cost effective.
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PMID:Atypical idiopathic hypercalciuria in an adolescent. 318 67


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