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)

The proteinuria of fifteen patients treated with just aminoglycoside or aminoglycoside and either penicillin or cephalosporin was studied. The proteinuria was analysed by means of immunoelectrophoresis, acetate cellulose electrophoresis, thin-layer polyacrylamide gel electrophoresis and sodium dodecylsulphate acrylamide gel electrophoresis. We observed a urinary excretion of free immunoglobulin light chains and an increased urinary excretion of lysozyme in all cases. The increase in urinary excretion of beta-2-microglobulin and retinol-binding-protein appeared only in patients treated with aminoglycoside and cephalosporin. These disturbances disappeared a few days after the treatment was discontinued.
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PMID:Low molecular weight proteins as urinary markers of aminoglycoside nephrotoxicity in man. 9 49

Serum lipids and lipoproteins and urinary apolipoprotein A (Apo A) were determined in two groups of patients. One group consisted of 11 children (ages ranging from 4 to 14 years) with minimal change glomerular disease. The other group consisted of 13 patients, eight less than 19 years old five adults, with different types of chronic glomerulopathy. Elimination of urinary lysozyme was a feature of chronic glomerulopathies, and creatinine clearances were also significantly lower in this group. Patients with chronic glomerulopathies had significantly lower HDL cholesterol and Apo A concentrations in their sera. In contrast, urinary Apo A concentrations were significantly higher in patients with chronic glomerulopathies, who also showed significantly lower urinary protein selectivities. Lipoprotein electrophoresis of urines containing Apo A showed distinct high-density lipoprotein (HDL) fractions, suggesting that HDL is eliminated in the urine as a result of increased glomerular permeability. This is also supported by a correlation coefficient of 0.77 between the selectivity indices and the ratio of urinary Apo A to total proteinuria. The determination of urinary Apo A appears to give valuable diagnostic information in patients with glomerular disease. According to our results the absence of urinary Apo A is very suggestive of minimal change glomerular disease.
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PMID:Urinary high density lipoprotein in minimal change glomerular disease and chronic glomerulopathies. 22 12

The 24-hour urinary excretion of albumin, transferrin, haptoglobin, IgG, IgA, IgM, free lambda and kappa light chains from immunoglobulin, lysozyme, and beta2-microglobulin has been investigated in 22 patients with febrile diseases, using an automated immunoprecipitin reaction. The average excretion of the 10 proteins was significantly increased in the patients compared with a control group. In patients with body temperature is greater than or equal to 38.5 degrees C the tubular type of proteinuria was significantly increased compared with those with body temperature is less than 38.5 degrees C. Sequential studies in 10 patients showed that the tubular type of proteinuria occurred in all, whereas the glomerular type was demonstrated in 8. when the fever had subsided, the tubular proteinuria disappeared rapidly i in all patients, while the glomerular proteinuria disappeared in only 4 out of 8. It was shown that tubular proteinuria was caused by fever per se, and it is suggested that glomerular prteinuria might be due to an immue response to antigens, derived from the infectious agents, producing a transient or permanent glomerular injury.
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PMID:Urinary excretion of ten plasma proteins in patients with febrile diseases. 40 46

In order to assess to what extent glomerular or tubular function is involved in the renal handling of amylase and the lysozyme to creatine clearance ratios (CAm/CCr and CLys/CCr) were evaluated in 22 healthy volunteers and in 71 patients with different renal diseases. In normal controls, the mean CAm/CCr was 2.55 +/-1.54 SD, with an upper normal limit of 5.56. A normal ratio was found in patients with glomerulonephritis, with or without a nephrotic syndrome, and in patients with pyelonephritis. A significantly elevated ratio (P less than 0.001) was instead found in patients with uremia and in patients with uremia and in patients with either chronic or acute tubular damage. The CLus/CCr ratio was elevated in all the groups, except in patients with glomerulonephritis and minimal proteinuria. These results show that in humans, as in animals, the amylase filtered load undergoes partial tubular reabsorption. In renal diseases, an increase of the CAm/CCr is caused by either a marked reduction of functioning nephrons or a severe tubular damage, while the glomerular permeability does not seem to be involved. Some other mechanism is probably involved in the elevation of the CAm/CCr during acute pancreatitis.
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PMID:Amylase to creatine clearance ratio in renal diseases. 44 31

Using an automated immunoprecipitin reaction, the urinary excretion of albumin, transferrin, haptoglobin, IgM, IgG, IgA, free lambda and kappa light chains from immunoglobulin, lysozyme and beta2-microglobulin has been investigated in 40 long-term bilaterally nephrectomized renal transplant patients. The excretion of the proteins, except lysozyme, was significantly increased in 21 of the paitents with Albustix-negative urine. In patients with glomerulonephritis prior to the transplantation, the excretion of albumin, transferrin, and IgG was significantly increased compared with the other patients. The IgM excretion was significantly increased in patients who had received C and D matches compared with those with A and B matches. Patients with severe surgical complications in the postoperative period had a tubular proteinuria, and in patients surviving more than 60 months after transplantation the excretion of several proteins was significantly increased compared with patients surviving less than 60 months.
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PMID:The urinary excretion of ten plasma proteins in long-term renal transplant patients. 81 72

Urinary excretion of lysozyme was investigated in a group of 66 patients with various renal diseases, nephrolitiasis and urinary tract infections. The results obtained demonstrate that the amount of the enzyme excreted is related to the entity of tubular damage whereas is not with glomerular damage. No correlation was found between lysozyme excretion neither to the degree of proteinuria neither to the amount of leukocytes and bacteria in the urine. In patients with urinary infections urinary lysozyme increases only when there is a tubular injury of some entity. In 90 pediatric patients with urinary infection and pyelonephritis lysozyme in the urine was found only in two cases. Therefore urinary lysozyme determination cannot be considered for the detection of early tubular injury and is not a helpful diagnostic tool in urinary tract infections.
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PMID:[Behaviour of urinary excretion of lysozyme in renal diseases and in urinary tract infections (author's transl)]. 102 90

This is a study of the changes, both in serum and urine, of a wide enzymatic pattern whose origin is well known to be the renal parenchyma (LDH, LAP, AP and lysozyme), in the course of two experimental prototype lesions induced in rats. Simultaneously a similar enzymatic study was carried out in a group of patients with nephropathies. The experimental lesions were a toxic tubular dysfunction using a mercury salt and an immune glomerulonephritis of two types: by foreign proteins (human albumin) and by rabbit nephrotoxic serum. In all these cases, there has been a convincing evidence, both direct (histological and inmunofluorescent) and indirect (marked proteinuria), of the induced lesions which were similar to the experimental models reported in the literature. The isolated enzymatic changes we observed in serum made us conceed less value to this pattern in comparison to the urinary one which proved to be more important in our study. It was possible to define the following urinary enzymatic patterns for each of the experimental groups: a) The acute toxic tubular dysfunction has a marked rise in the activity of LDH and LAP, and less so in the activity of AP and lysozyme. The retarded tubular lesion has a moderate rise in LAP. b) The glomerular lesion has a moderate and exclusive rise in the activity of LDH and LAP. Likewise the clear similarity between each experimental group and its clinical equivalent was demonstrated as refers to the urinary enzymatic pattern.
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PMID:[Renal enzymology: experimental patterns and clinical symptoms]. 123 86

Low molecular weight proteins are of interest in children because their increased urinary excretion is a sign of renal tubular disease and their increased plasma concentration is inversely related to glomerular filtration rate. These proteins include beta 2-microglobulin (B2M), retinol-binding protein (RBP), alpha 1-microglobulin (A1M) and lysozyme. B2M is unstable in acid urine, in contrast to RBP and A1M which are more stable. Any increase in the urinary excretion of B2M or RBP is highly specific for tubular disease, whereas increased excretion of A1M may be seen with glomerular proteinuria. Areas of clinical application include tubular and glomerular diseases, detection of drug toxicity, reflux nephropathy, birth asphyxia and insulin-dependent diabetes mellitus. Methods of sample collection and analysis of these proteins are discussed.
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PMID:Low molecular weight proteins in children with renal disease. 128 25

To elucidate the relationship between localization of beta 2-microglobulin (beta 2-MG) and renal lesions or dysfunction, 119 patients with various renal diseases and various degrees of renal injuries were examined: patients with beta 2-MG deposition (group 1, n = 69), and patients without renal beta 2-MG deposition (group 2, n = 50). beta 2-MG was found mainly in the tubular epithelium and tubular casts. No significant difference in the degree of proteinuria and hematuria were found between the two groups. Group 1 had a significant decrease in glomerular filtration rate (GFR; p less than 0.01): the average values of GFR in group 1 and 2 were 61.1 +/- 35.7 and 95.4 +/- 34.5 ml/min. Group 1 had a significant decrease in the phenolsulfonphthalein excretion test (p less than 0.01) and the maximum urine specific gravity in Fishberg's concentration test (p less than 0.02). Group 1 had a significant high incidence of glomerular sclerotic lesions (p less than 0.001), arteriolar elastosis (p less than 0.01), tubulo-interstitial changes (p less than 0.001) and renal deposition of lysozyme (p less than 0.001). The present study demonstrates that the immunohistological study of renal beta 2-MG deposition is a reliable method to identify renal dysfunction and renal injuries, especially the presence of tubulo-interstitial changes, in various renal diseases.
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PMID:Immunohistological localization of beta-2-microglobulin in renal tissue as an indicator of renal dysfunction. 155 3

We report herein data on 6 male patients with progressive tubulopathy. These patients belonged to two families: the propositus, his father, a paternal first cousin, two paternal uncles, and a maternal uncle. A 7-year-old proband had mild proteinuria (1 g/day), consisting of beta 2-microglobulin, alpha 1-microglobulin and lysozyme, and aminoaciduria. Glycosuria and acidosis were absent. A 38-year-old father had mild proteinuria (2 g/day), including low-molecular-weight protein. Hypokalemia, hypophosphatemia, glucosuria, phosphaturia, aminoaciduria, and reduced urinary concentrating ability were also present. The other 4 affected family members also had low-molecular-weight proteinuria, detected by screening for beta 2-microglobulin. In addition, there were several abnormalities; aminoaciduria in all 6, phosphaturia in 4 of 6, hypercalciuria in all 6 and glycosuria in 2 of 6 patients. Tubular dysfunction was more severe in the older subjects, hence, the disease seems to progress with age. Familial low-molecular-weight proteinuria is apparently a progressive disease linked to a X-linked or to an autosomal dominant inheritance.
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PMID:Familial progressive renal tubulopathy. 158 58


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