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)

A clinicopathological study of 206 Indian children with nephrotic syndrome showed a primary renal cause in 195 (96%), of which 77% were boys. In 126 children (96 boys, 30 girls) onset of the disorder occurred before the age of 5 years. Renal biopsy showed minimal lesions in 150 patients (77%); in 85 of these biopsy was done 3 months to 16 years after onset of the nephrotic syndrome. Significant renal histological abnormalities in 45 cases were labelled as mesangiocapillary 8, mesangioproliferative 4, proliferative with extensive crescents 2, membranous 3, focal segmental glomerulosclerosis 9, focal global glomerulosclerosis 2, advanced nonspecific 8, and mild proliferative 9. Nephritic manifestations were mainly associated with significant renal lesions, which were more frequently encountered when the onset of disease was after the age of 5 years. Clearance of proteinuria with corticosteroid therapy was practically confined to patients with minimal or mild renal histological changes. Our findings suggest that the pattern of idiopathic nephrotic syndrome in Indian children is similar to that reported from Western countries.
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PMID:Nephrotic syndrome in indian children. 0 Sep 73

The kidney is one of the target organs involved as a consequence of the systemic complications seen in drug abusers. This may manifest itself in one of the following forms: acute hepatitis with modest proteinuria (less than 2 Gm. per day); bacterial endocarditis with hematuria, azotemia, and a focal or diffuse glomerulonephritis; the nephrotic syndrome with focal mesangial sclerosis and diffuse interstitial nephritis often pursuing a fulminant course terminating in uremia; acute renal failure secondary to rhabdomyolysis and myoglobinuria; polyarteritis nodosa with renal involvement; and obstructive uropathy secondary to fungus ball in the urinary tract.
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PMID:Renal complications of drug addiction. 1 1

Although the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-alpha-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 +/- 2.9 mumol TAMe hydrolyzed/ml plasma/hr (mean +/- SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallifrein inhibitor activity in 11 normal children was 0.94 +/- 0.04 units. During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 +/- 7.24 mumol/ml/hr; and kallikrein inhibitor, 0.35 +/- 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 +/- 3.2 mumol/ml/hr; and kallikrein inhitor, 0.78 +/- 0.03 mumol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 +/- 4.8 mumol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 +/- 0.03 units. A subset of 9 patients had marked depression of plasma prekallikrein to levels less than 20 mumol/ml/hr and essentially undetectable inhibitor activity. Serum alpha-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 +/- 29 mg/100 ml; during corticosteroid-maintaining remission, 615 +/- 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 +/- 20 mg/100 ml. The proportional reduction of plasma prekallikrein and kallikrein inhibitor suggested that an enzyme-inhibitor complex formed in vivo, perhaps at a local site of activation in proximity to the glomerular basement membrane. These data suggest that the plasma kinin-generating system may be the host effector mechanism subserving the increased glomerular capillary permeability in the minimal lesion nephrotic syndrome of childhood.
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PMID:A study of the plasma kinin-generating system in children with the minimal lesion, idiopathic nephrotic syndrome. 5 8

Samples of renal tissue from 373 patients were examined for the presence of immunoglobulin E (IgE) by immunofluorescent techniques. Only trace to ++ amounts ( on a scale of ++++) were found in 20 patients: 4/9 with post-streptococcal acute glomerulonephritis (GN), 5/30 with GN associated with systemic lupus erythematosus, 3/20 with membranous GN, 1/4 with Goodpasture's syndrome, 2/18 with recurrent microhematuria and focal GN, 1/5 with hemolytic anemia and uremia, 3/73 with renal homografts, and 1/5 with dermatomyositis. No IgE was found in 18 patients with lipoid nephrosis, 8 of whom were being treated with prednisone, nor in 5 patients with focal glomerular sclerosis and the nephrotic syndrome. Serum IgE was measured in 9 of the 20 patients with glomerular deposits of this globulin. With one exception, levels of IgE were within the range generally considered to be normal. However, they were greater than the mean of this range in all but two and near the highest limits of normal in most. Neither the amounts of serum IgE nor the degree of proteinuria could be related to the intensity of stain for IgE in the glomeruli of these patients.
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PMID:Immunoglobulin E in renal disease. 5 86

Sensitivity to cow's whole milk investigated in six patients with the idiopathic nephrotic and an elemental diet was given. After proteinuria had decreased to less than or equal to 500 mg/24 hours on consecutive days patients were challenged with cow's milk. This resulted in the return of significant proteinuria, oedema, and decreased urine volume together with a decrease in serum-IgG concentrations in four patients. Acute alteration of plasma C3 complement component accompanied milk challenge in all 6 patients. There were no consistent alterations in other immunoglobulin concentrations. Intradermal skin testing with cow's milk extract was positive in all patients. These results suggest that in some individuals clinical and biochemical manifestations of the nephrotic syndrome of childhood may be related to hypersensitivity of food products.
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PMID:Severe steroid-responsive nephrosis associated with hypersensitivity. 6 10

The serum and urine levels of alpha-2-macroglobulin (alpha2-MG) was determined in 33 children with glomerular diseases and in 26 healthy control children. Healthy children showed a minimum level of 275 mg% and maximum level of 337 mg%, with a mean concentration of 301 mg% and a standard deviation of 13 mg%. No alpha2-MG was detected in the urine. Steroid-treated patients with idiopathic nephrotic syndrome displayed elevated inhibitor levels of up to 490 mg%. This might be a direct result of steroid therapy or a consequence of reactively-increased protein synthesis in response to the renal protein loss. In all these patients the urine was found to be alpha2-MG-negative, irrespective of the presence or absence of proteinuria. In the miscellaneous group of glomerulopathies without the nephrotic syndrome, serum levels of alpha2-MG were shown to be normal. The urinary concentrations of alpha2-MG were related to the activity of the disease. alpha2-MG determination in serum and urine seems to be a tool for differential diagnosis and prognosis in some cases of glomerular disease.
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PMID:[Alpha-2-macroglobulin in children with glomerular diseases (author's transl)]. 6 38

Main components of kinin system, the arginine-esterase activity and proteinase inhibitors were estimated in blood serum of patients with nephrotic syndrome of various etiology (glomerulonephritis, amyloidosis, systemic lupus erythematous) and also in patients with latent nephritis and in healthy donors. Content of all the kinin system components (kallikreinogen, kininogen and kininase 1) proved to be increased in all the forms of nephropathy studied. Free kallikrein was found in blood serum of patients with nephrotic syndrome as distinct from healthy persons and patients with latent nephritis. The arginine-esterase activity, which shows the level of trypsin-like proteinases, was altered dissimilarly, depending on the nephrotic syndrome etiology: it was maximally increased in nephrotic syndrome of amyloid genesis and decreased in patient with systemic lupus erythematosus. High content of kallikrein and kininase I with simultaneous decrease in kininogen was typical for patients with severe form of nephrotic syndrome. Impairment of kidney in nephrotic syndrome was also characterized by an increase in alpha1-antitrypsin and in the total antitryptic activity, which reached the maximal value in nephrotic syndrome of the I degree and decreased at the II degree of the disease. In nephrotic syndrome content of alpha2-macroglobulin was maximally increased at the II degree of nephrotic syndrome and decreased in severe form of the disease. The primary alteration in content of proteinase inhibitors and high level of kinin system components were assumed to determine the conditions for activation of kinin system in blood serum and to impair the nephrotic syndrome pathogenesis, which was complicated by systemic manifestations. High content of kinin system components was apparently determined by the increased synthesis in liver tissue in response to inflammation and massive proteinuria; kininase I and alpha2-macrolgobulin, as proteins with high molecular weight, were likely to be selectively retained in blood circulation when the capillary penetration was increased.
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PMID:[State of the kinin system and level of serum proteinase inhibitors in latent nephritis and the nephrotic syndrome of different etiology]. 7 Jan 11

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

The development of severe proteinuria or nephrotic syndrome as an adverse reaction to gold therapy in rheumatoid arthritis is well known. Morphologic examination reveals membranous glomerulonephritis in almost all cases. Since the beginning of 1978 there has been a striking increase in the number of such cases seen at this institute. 5 patients aged from 17 to 65 years who had been treated with sodium aurothiomalate for rheumatoid arthritis developed severe proteinuria. In all cases only minimal glomerular changes were observable by light microscopy. Electron microscopy demonstrated multiple electrondense, subepithelial deposits which were confirmed by fluorescence microscopy. In all cases characteristic lysosomes ("aurosomes") were demonstrated in the cytoplasm, mainly of the epithelial glomerular cells. This unusual accumulation of almost identical cases coincides with the introduction of a new gold preparation, Na-aurothiomalate (Tauredon), containing 46% metallic gold.
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PMID:[Conspicuous accumulation of membranous glomerulonephritis following gold therapy in chronic polyarthritis--a side effect of a new preparation?]. 10 66

Total serum and urinary thyroxine (T4), triiodothyronine (T3), and thyroxine-binding globulin (TBG) as well as serum free T4, thyroid-stimulating hormone (TSH), and T3 resin uptake (T3RU) were measured in seven patients with the nephrotic syndrome. The nephrotic syndrome was defined by proteinuria exceeding 3 g/24 h. All patients were clinically euthyroid. Most values for total serum T4, free T4, T3, T3RU, TBG, and TSH were within normal limits. However, the mean serum T3 and TBG values were significantly lower in patients compared with the control group. The values (mean +/- 2 SD) for urinary T4 were 24.3 +/- 20.3 in the patient group and 1.5 +/- 0.7 microgram/24 h in the control group. Urinary T3 values for patients and the control group were 2100 +/- 856 and 848 +/- 253 ng/24 h respectively. Urinary TBG was 2.1 +/- 1.8 mg/24 h in the patients and undetectable in the control group. There was no correlation between daily urinary T3 and T4 and urinary TBG. There was a weak correlation between daily urinary protein excretion and urinary T4 (r = 0.5).
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PMID:Thyroid function studies in the nephrotic syndrome. 10 51


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