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)

Haematuria in children is either of glomerular or nonglomerular origin. In the latter case intravenous urography should always be performed. A renal biopsy is indicated if unexplained haematuria persists for at least one year or if an unfavorable prognosis is indicated by the appearance of hypertension, significant proteinuria or persistently low levels of serum complement (C3). The importance of screening the families of haematuric patients is emphasized. More than half of our cases with persistent or intermittent haematuria undergoing renal biopsy showed no or only minimal glomerular changes. In other children with a similar clinical picture more severe histological lesions were detected. In any case the kidney tissue obtained by biopsy should be examined by immunofluorescence and by electron microscopy. One of the most frequent causes for persistent or intermittent haematuria during childhood is Berger's disease (IgA/IgG nephropathy).
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PMID:[Haematuria in children. I. Differential diagnosis of haematuria in childhood (author's transl)]. 63 89

One case of lecithin cholesterol acyltransferase (LCAT) deficiency is discovered by renal biopsy. Through the study of a French family, native to Brittany, one sister is found to be carrier of the trait. This finding suggests that the gene defect hitherto reported from Scandinavia is not restricted to this region. The patient shows typical signs of the disease, corneal opacities, anemia with a hemolytic component and lack of plasma LCAT activity. She has proteinuria, HTA, hematuria, no renal insufficiency. Signs previously unreported were noted: sensorineural hearing loss and platelet environment disorder. Histological abnormalities of two types are found: foam cells and subendothelial deposits, of which the tinctorial characteristics indicate a lipid composition. The lack of glomerular fluorescent staining observed is not in favor of an immune complex nephropathy. The study of this case suggests the determining role of lipid abnormalities in the genesis of anemia and of the vascular depositions in the induction of renal failure encountered in several cases of LCAT deficiency.
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PMID:Hereditary lecithin cholesterol acyltransferase deficiency. Report of a new family with two afflicted sisters. 63 18

Some of the first clues suggestive of renal disease are hematuria and proteinuria, and when present in a child, deserve careful consideration. The clinical experience and diagnostic evaluations at a new renal unit are examined to familiarize the practicing urologists with the diagnostic approach which will generate the correct diagnosis. The indications and results of kidney biopsy in children are also presented.
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PMID:Hematuria and proteinuria in pediatric patient. Diagnostic approach. 63 24

The clinical course of diabetic nephropathy was evaluated in 150 patients and the effect of hemodialysis in 68 of them. Proteinuria was the first sign of renal disease. Once renal dysfunction becomes evident, there is a rapid deterioration leading to dialysis within 3.0 +/- 0.2 years. Hypertension and circulatory congestion are common complications. The hypertension is probably volume dependent. Retinopathy was not invariably present at the onset of renal insufficiency but appeared with progression of renal failure. The course during hemodialysis was complicated by continued progression of diabetic vascular disease manifested by vascular access difficulties, worsening of retinopathy and blindness, and cardio- and cerebrovascular deaths. Mortality was higher than in nondiabetic dialysis patients.
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PMID:Diabetic nephropathy: clinical course and effect of hemodialysis. 64 44

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

The frequency of the association between extramembranous glomerulopathy and a visceral tumour suggests the responsibility of various antigen-antibody systems related to malignancy, at the origin of the nephropathy. In a number of special cases, the role of these systems has been more precisely demonstrated. The cases reported here emphasise the need to seek a visceral tumour when the onset of extramembranous glomerulitis occurs after the age of 40 years, in particular since the onset of proteinuria may precede the first clinical signs of the tumour by several months. The presence of polynuclear cells in the glomerular capillary loops, associated with extramembranous deposits, is an additional element of orientation in the direction of neoplastic aetiology.
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PMID:[Extramembranous glomerulitis associated with visceral tumours. Clinical and histological study based upon 10 cases and a review of the literature (author's transl)]. 66 20

This study analyzes the role of genetic and/or viral factors as etiologic agents in systemic lupus erythematosus in NZB/NZW F1 hybrid mouse, first by a backcross within the NZ strains. A separate study involved an outcross, production of an F2 generation, and then backcross to both NZ parents. The results were assayed by histologic evaluation of renal disease. Assay techniques for anti-DNA and proteinuria showed no evidence for segregation and were not useful. Histology of the kidney showed distinct segregation patterns consistent with the interpretation of the etiology as co-dominant genetic factors. While the virus[es] was not considered etiologic, mechanisms for relating activity to the pathogenesis were discussed.
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PMID:NZB/WF1 hybrid autoimmune disease: a genetic analysis. 67 29

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

A retrospective study is presented of the effect of propranolol on fetal outcome in pregnancies complicated by maternal hypertension. In nine pregnancies in which propranolol was given to markedly hypertensive women (diastolic blood pressure over 105 mm Hg) the fetal outcome was worse than in 15 patients using other hypotensive agents. The probability of fetal or neonatal death was related to the amount of proteinuria and the presence of parenchymal renal disease but was also significantly higher when the mother had been treated with propranolol. Experimental evidence suggests that beta-adrenergic blockade is harmful to the hypoxic fetus, for these reasons the use of propranolol in hypertensive pregnancies complicated by placental insufficiency may be contraindicated unless there is no satisfactory alternative.
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PMID:The possible adverse effect of propranolol on the fetus in pregnancies complicated by severe hypertension. 69 49

The initial clinical and histologic renal findings and the subsequent course of 90 patients with SLE were evaluated in a study of the natural history of lupus nephropathy. Initial renal biopsy revealed focal glomerulonephritis in 32 patients, diffuse glomerulonephritis in 47, membranous nephropathy in seven and minimal changes in four. Forty-one patients were rebiopsied three months to five years later; ten of 15 patients with focal glomerulonephritis showed progression to diffuse glomerulonephritis or membranous nephropathy, whereas changes in morphologic pattern were less common in the other types of lupus nephropathy. There was no difference between the patients with the focal lesion who progressed and those who did not in age, sex distribution, duration of SLE prior to biopsy, renal function, and serological studies; however, the patients with progression initially had more proteinuria, higher histologic activity on light microscopy, and more intensive glomerular electron-dense deposition. Focal lupus glomerulonephritis progresses frequently to diffuse glomerular involvement. Certain clinical and morphologic findings at initial evaluation may help to predict future progression in the course of lupus nephropathy.
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PMID:Changing histopathology patterns in lupus nephropathy. 69 93


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