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)

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

Antibodies to glomerular basement membrane (GBM) of the rat could be fractionated according to their avidity by elution from trypsin-digested GBM (bound to Sepharose) with increasing concentrations of KSCN. The percentage of kidney-fixing antibody in each fraction and the degree of proteinuria induced as determined 24 h after injection increased with the avidity of the antibody fraction when equal doses were administered.
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PMID:Effect of antibody avidity on the induction of renal injury in anti-glomerular basement membrane nephritis. 74 13

Antigens of porcine lung were prepared by homogenization and ultrasonic treatment of lung tissue. The antigens were digested by collagenase and trypsin and chromatographed on Sephadex G 200. After immunization of rabbits with certain fractions of the chromatographed material, antibodies could be obtained in rabbits which fixed in vitro and in vivo in the glomerular mesangium of rats, hogs and the human, but not in the basement membrane of glomeruli of these species. Following intravenous injection into rats, the antibodies could be observed in the mesangial area without an apparent loss of antigenicity for 55 days. While 5 days after the application of 20 mg of the anti-mesangial IgG-preparation, there were no glomerular changes histologically demonstrable, after 55 days small amounts of rat-IgG could be demonstrated histochemically within the mesangium. Deposits of rat-complement (C3) could not be demonstrated with certainty. Severe morphological lesions were absent. Rats injected with the same doses of antibody and simultaneously immunized with rabbit-IgG showed a substantially greater deposit of autologous rat-IgG and rat-complement within the mesangial area after 55 days. By histological examination focal and segmental scleroses of the mesangium were determined. A significant pathological proteinuria did not occur. The present model constitutes a new possibility for studying the function of the glomerular mesangium.
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PMID:Antibodies reacting with the glomerular mesangium. Isolation and immunopathology. 80 22

To investigate plasma renin and prorenin levels in non-insulin-dependent diabetes mellitus (NIDDM) and their relation with autonomic nervous function and renal impairment, we measured plasma renin and prorenin levels in 39 NIDDM patients. The patients included 21 males and 18 females, aged 56.3 +/- 6.2. Thirty-four normal age-matched subjects served as controls. Autonomic nervous function was evaluated in 23 patients by the performance of cardiovascular reflex tests. The plasma renin concentration was measured by angiotensin I generation after the addition of an exogenous substrate. Plasma prorenin was activated by trypsin. The results showed that the plasma renin concentration was similar between NIDDM patients and normal subjects, while plasma prorenin was higher in NIDDM patients. No correlation existed between the plasma renin or prorenin levels and autonomic nervous function. The patients with abnormally high levels of prorenin also had a similarly high plasma renin level but not a high creatinine clearance (Ccr) or daily proteinuria. The plasma renin level was correlated inversely with daily proteinuria but not with Ccr. These results suggest that the high plasma prorenin levels in some diabetic patients cannot be explained by renal impairment, poor prorenin conversion or autonomic dysfunction. The hyporeninemia in some patients may be related to microvascular involvement of the kidney.
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PMID:Plasma prorenin and renin levels in non-insulin-dependent diabetes mellitus. 136 16

In our previous studies, we found increased levels of urinary trypsin inhibitory activity in gentamicin-induced nephrotoxicity in rats. Following administration of the Bowman-Birk trypsin and chymotrypsin inhibitor (BBI), no proteinuria was detected in gentamicin-treated rats, and a decrease in creatinine clearance was noted in only 50% of the injected rats. In the present study, we examined the antimicrobial activity of gentamicin against Escherichia coli in the presence of BBI in gentamicin-induced nephrotoxicity in rats. We found that 50% of rats with E. coli-positive blood cultures died of septicemia. All the rats injected with E. coli plus gentamicin or E. coli plus gentamicin plus BBI survived, the latter showing no proteinuria or deterioration in creatinine clearance. In conclusion, BBI, which is an effective inhibitor of gentamicin-induced nephrotoxicity, does not affect the antimicrobial activity of gentamicin sulfate.
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PMID:Antimicrobial gentamicin activity in the presence of exogenous protease inhibitor (Bowman-Birk inhibitor) in gentamicin-induced nephrotoxicity in rats. 152 44

Daily intraperitoneal (i.p.) injection of genatmicin at a dose of 70 mg/kg for 11 days produced nephrotoxicity in female Sprague-Dawley rats as evidenced by increased excretion of urinary protein and trypsin inhibitory activity as well as rise in renal individual class and total phospholipid. The observed proteinuria was associated with a significant twofold fall in creatinine clearance and histopathological changes, including the presence of hyaline casts and flattened epithelial cells within the lumen of proximal convoluted tubules. Although pyridoxal-5-phosphate (50 mg/kg) administered i.p. did not significantly alter creatinine clearance, histopathology, proteinuria, and urinary trypsin inhibitory activity, an increase in individual class and total phospholipid was noted in kidney. In rats simultaneously administered gentamicin and pyridoxal-5-phosphate, the observed fall in renal gentamicin content was associated with a return of individual class and total phospholipid to control values. However, the decline in creatinine clearance, enhanced proteinuria, and increase in urinary trypsin inhibitory activity in the simultaneous-treated group was similar or greater than that seen in the gentamicin-only injected rats. Morphological examination of simultaneous-treated rats revealed extensive alterations in proximal tubules including numerous mitotic figures, large vesicular nucleii, and prominent nucleoli in epithelial cells as well as hyaline casts within the lumen. Our data combined with results of previous studies suggest that sex and type of rat strain are important factors in aminoglycoside-induced nephrotoxicity. It is evident that a specific concentration of pyridoxal-5-phosphate may be necessary to provide protection against all manifestations of aminoglycoside-induced renal damage.
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PMID:Effect of interaction between gentamicin and pyridoxal-5-phosphate on functional and metabolic parameters in kidneys of female Sprague-Dawley rats. 163 20

A Hispanic girl with Lowe oculocerebrorenal syndrome (OCRL), an X-linked recessive condition characterized by cataracts, glaucoma, mental retardation, and proteinuria, is reported. A balanced X;20 chromosomal translocation with the X chromosome breakpoint at q26.1 was found with high-resolution trypsin-Giemsa banding. Somatic cell hybridization was used to separate the X chromosome derivative and the chromosome 20 derivative in order to position, with respect to the translocation breakpoint, several DNA loci that are linked to the Lowe syndrome locus (Xq24-q26). DXS10 and DXS53 were found to be distal to the breakpoint, whereas DXS37 and DXS42 were located proximal to it. These studies suggest that the OCRL locus lies in the region between these probes. The translocation chromosome originated from an unaffected male without a visible translocation, indicating that the most likely cause of OCRL in this patient is the de novo translocation that disrupted the OCRL locus.
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PMID:Lowe oculocerebrorenal syndrome in a female with a balanced X;20 translocation: mapping of the X chromosome breakpoint. 189 26

A 10-year-old mentally retarded girl was sent to our hospital due to generalized edema, vomiting and poor appetite for several days. Serum albumin level was low, but no proteinuria was detected. Her stool was bulky and foul. Stool examination for parasite with formalin-ether concentration method revealed negative result. Trypsin activity test of stool revealed low trypsin activity as compared with normal specimen. Daily fecal fat exceeded upper normal limit. The diagnosis of giardiasis was confirmed by duodenal juice examination. Intestinal histology revealed mild shortening of the villi with increased mononuclear cell infiltration in the lamina propria. The daily stool amount decreased markedly after treatment with metronidazole 250 mg three times a day for 7 days. The edema subsided during the treatment. Serum albumin bevel returned to normal after the treatment. Giardiasis with malabsorption syndrome has often been overlooked in Taiwan. It is advised that in case of malabsorption syndrome giardiasis should be included in the list of differential diagnosis.
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PMID:[Giardiasis with malabsorption syndrome: report of one case]. 227 67

IgG levels and tryptic inhibition were investigated in sequentially collected mare's colostrum and milk, foal serum and urine. The colostral trypsin-inhibitor was "transfused" to the newborn foal by the colostral intestinal route in parallel with IgG. However, the trypsin-inhibitor as a small molecular weight inhibitor became excreted into urine peaking at about 20 hours. The physiological proteinuria in foals during the first 2 days is mostly due to immunoglobulin fragments and colostral-derived trypsin-inhibitor. Analysis of urine for IgG light chains or trypsin inhibitor will therefore reveal ingestion of colostrum.
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PMID:Sequential changes of IgG and antitrypsin in different compartments during the colostral-intestinal transfusion of immunity to the newborn foal. 278 97

We measured plasma alpha 1-proteinase inhibitor (alpha 1-PI) levels in patients with idiopathic nephrotic syndrome (INS), chance proteinuria and/or hematuria, and normal controls to examine the roles of proteinase inhibitors in the pathogenesis of renal diseases. Plasma alpha 1-PI concentrations were significantly decreased in patients with INS at relapses and remissions of INS. The alpha 1-PI activities, anti-trypsin and anti-elastase activities, were also decreased in relapses of INS. However, the values revealed no statistically significant difference in remissions of INS. Significant correlations between the PI activities and alpha 2-macroglobulin levels were revealed, which suggested a possible contribution of alpha 2-macroglobulin to the plasma PI activities in INS. From these results we conclude that the decrease in plasma alpha 1-PI activities may be responsible for the reduction of glomerular negative charge, possibly caused by some unknown proteinase(s), and the resultant development of proteinuria.
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PMID:[Decreased plasma alpha 1-proteinase inhibitor activity in idiopathic nephrotic syndrome]. 278 67


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