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)

Single proteins and tubular enzymes have been proposed as markers to detect and differentiate prerenal, glomerular, tubular and postrenal forms of proteinuria and hematuria. By quantitation of total protein, albumin, alpha 1-microglobulin, IgG, alpha 2-macroglobulin and N-acetyl-beta,D-glucosaminidase (beta-NAG) activity it has become possible to clearly separate these forms by analysis of a single sample of second morning urine. When this program was applied to screening of hospital patients, albumin, total protein and NAG proved to be sufficient to exclude clinically relevant disturbances. alpha 1-Microglobulin was useful to separate primary glomerulopathies from tubulo-interstitial diseases. Glomerular and postrenal hematuria could be clearly separated by their different excretion rates of alpha 2-macroglobulin, if urine albumin concentration exceeds 100 mg/l. The results imply that wider application of these techniques can help to detect renal abnormalities at an earlier stage and differentiate their various forms by less invasive techniques.
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PMID:Markers for the diagnosis and monitoring of renal tubular lesions. 129 6

Extracorporeal shock wave lithotripsy (ESWL) causes proteinuria. In our study we investigated the protein fractions and the electrolyte composition of the urine in patients who had been treated with ESWL. The aim was to obtain information on the degree and the localisation of the glomerular, tubular or vascular destruction caused by ESWL in humans. A total of 34 patients with stones had been treated with ESWL. As parameters we used: urine output, creatinine clearance, total protein, albumin, immunoglobulin G, N-acetyl-beta-D-glucosaminidase (beta-NAG), alpha-1-microglobulin, the fractional excretion of Na+ and apolipoprotein-A-1. After ESWL treatment proteinuria and albuminuria are found. Our parameters show no deterioration of the glomerula or the tubulus. The increase in apolipoprotein-A-1, a postglomerular parameter, however, is interpreted as a manifestation of vascular destruction after ESWL; this is normally temporary, leaving no permanent damage.
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PMID:[Localization and extent of tissue damage caused by extracorporeal lithotripsy (ESWL)]. 171 30

Monoclonal antibodies (Mabs) were produced by immunizing mice with human kidney microsomal antigen. Mab-B1 recognized brushborder (B1-Ag) in proximal tubules. Using Mab-B1, B1-Ag was assayed in the urine and serum of renal disease patients by sandwich ELISA. The subjects included normal control (Nor), minimal change nephrotic syndrome (MCNS), IgA nephropathy (IgA), membranous nephropathy (MN), membranoproliferative glomerulonephritis (MPGN), and chronic renal failure (CRF) (s-Cr greater than 2 mg/dl). Urinary B1-Ag demonstrated significant increases in the IgA (p less than 0.001), MN (p less than 0.001), MPGN (p less than 0.001) and CRF (p less than 0.01) groups as compared to the Nor group. There was no significant increase in the MCNS group. In the CRF group, B1-Ag in urine showed a significant increase in the progressive CRF group with delta s-Cr greater than 1.0 mg/dl/month as compared to the stationary CRF group with delta s-Cr less than 1.0 mg/dl/month. No correlation was observed between urinary B1-Ag and proteinuria, hematuria, s-Cr, s-BMG and u-NAG. The above findings suggested that the assay of urinary B1-Ag was useful as a new parameter in detecting the site and degree of proximal tubular damage.
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PMID:[Study on the assay of proximal tubular antigen in urine and serum with an anti-human renal monoclonal antibody]. 177 Jun 27

The hyperexcretion of urinary enzymes with systemic Lupus Erythematosus (SLE) was assayed. 31 patients with confirmed SLE (30 women, and 1 man, age 16-33 years) were studied. Patients were divided into two groups according to the degree of kidney damage: 21 patients with proteinuria, and 10 patients without proteinuria. 12 patients of the first group had nephrotic syndrome (NS). 30 practically healthy subjects served as a control group. In patients with Lupus-nephritis (LN) the increase of activities of urinary GGT, AP, BGRS, NAG, and CHE was observed, the increase was especially clearly shown in LN-patients with NS. The increase of activity of urinary GGT and NAG was shown in the group of SLE patients who did not have clinical and laboratory signs of LN, which can be used as early index for the damage of tubular epithelium.
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PMID:The significance of the assays of urinary enzymes activity in patients with systemic lupus erythematosus. 198 35

A chelator, dichloromethane diphosphonate (Cl2MDP), used to treat for malignancy-induced hypercalcemia, has nephrotoxic potential. An acute animal model developed to examine the mechanism was used to further characterize the renal effects. NAG enzymuria appears to be an early premonitor of injury. Ultrastructurally, an increase in size and number of protein-containing phagolysosomal reabsorption droplets in proximal convoluted tubules associated with proteinuria precedes advent of tubular cell necrosis indicating these organelles to be a potential target site for Cl2MDP in the kidney. In vitro studies using rabbit cortical tubules and rat brush border membrane vesicle preparations suggest that the renal toxicity is not due to perturbation of phosphate transport or oxidative metabolism. An operational hypothesis emerges indicating that Cl2MDP may be protein bound affecting carrier protein charge facilitating glomerular leakage with tubular accumulation via protein transport. Cl2MDP may induce critical cation perturbation at the subcellular level as the mechanism of cell death.
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PMID:Characterization of the early ultrastructural and biochemical events occurring in dichloromethane diphosphonate nephrotoxicity. 215 Dec 1

Nephrotoxicity from exposure to therapeutic agents and chemicals in the environment and workplace results in a broad spectrum of clinical renal disease that may mimic disorders from other causes. Nephrotoxic agents may, in fact, be responsible for some fraction of renal disease of undetermined etiology. Specific diagnosis and treatment by removal from exposure to the toxic agent is more likely in the early phase of the disorder. Measurement and characterization of proteinuria provides the most sensitive and reliable method of early detection. Increased urinary excretion of serum proteins with molecular weight in excess of 50,000, such as albumin and transferrin, is an early indicator of glomerular injury. Low-molecular-weight proteinuria (beta 2-microglobulin or retinol-binding protein) and enzymuria, particularly excretion of NAG, are sensitive indicators of renal tubular cell injury. Tests that reflect hypersensitivity reactions are often indicative of immunologically mediated nephrotoxicity but are not specific for the kidney. Cancers of the kidney and urinary bladder appear to be increasing and are most common among the socially active and affluent. Susceptibility of the urinary tract to toxicity and carcinogenicity reflect contact of excreted toxins with the epithelial cells of nephrons and urinary bladder.
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PMID:Environmentally related diseases of the urinary tract. 218 Dec 10

Using a monoclonal antibody (Mab-G3) recognizing glomerular basement membrane (GBM), we assayed GBM antigen (G3-Ag) in the urine and serum of renal disease patients by sandwich ELISA. The subjects included normal control (NOR), minimal change nephrotic syndrome (MCNS), IgA nephropathy (IgA), membranous nephropathy (MN), membranoproliferative glomerulonephritis (MPGN) and chronic renal failure (CRF). The urine and serum was used as the material. With urinary G3-Ag, there were no statistically significant differences among the NOR, MCNS, IgA, MN, MPGN and CRF groups. Although no correlation was observed with proteinuria, hematuria, serum creatinine, serum beta 2 microglobulin and urinary NAG, urinary G3-Ag showed a significant (p less than 0.05) increase in excretion in the group of progressive CRF patients with s-Cr more than 1.0 mg/dl/month as compared to the stationary CRF group with s-Cr less than 1.0 mg/dl/month. Serum G3-Ag showed lower values in almost all cases, and there were no significant differences among the renal disease groups. The above findings led us to believe that the assay of urinary G3-Ag was useful in determining the degree of GBM disorder. It was also presumed that assay of renal antigens in urine and serum with the respective anti-human renal monoclonal antibodies could be a new tool in diagnosing renal diseases.
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PMID:[Assay of GBM antigen in urine and serum with an anti-human renal monoclonal antibody]. 237 9

As the semiautomated electrophoretic analysis of proteinuria still needs technical experience, interest was focused on easy-to-perform methods of urinary protein measurement. SRID-tests for albumin, transferrin, IgG, alpha-1-microglobulin and a spectrophotometrical test for beta-NAG were carried out in 50 normal controls and compared to PCI/ECI-values of patients suffering from rheumatoid arthritis (n = 52) and various types of chronic glomerulonephritis (n = 41). Elevated levels of alpha-1-M and beta-NAG in chronic glomerulonephritis were interpreted as indicative for tubulointerstitial involvement in the chronic inflammatory process. PCI/ECI elevation in individual RA-samples may be caused by functional impairment of tubular protein handling due to chronic ingestion of non-steroid analgesics. The serum assays for transferrin (TF) and IgG based on SRID technique turned out to be too insensitive for the application on unconcentrated urine of normal control persons. In renal patients, however, TF-PCI values above 30 mg/g crea and IgG-PCI values above 50 mg/g crea have to be interpreted as pathologic indicating damage of the glomerular basement membrane. To elucidate TF- and IgG-values in urines with low protein content, highly sensitive nephelometric methods should be used. Concentration of urinary proteins using membrane filters may lead to protein losses, resulting in miscalculation of PC-indices.
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PMID:Application of urinary indicator proteins in the non-invasive assessment of glomerulo-tubular lesions in patients with chronic glomerulonephritis and rheumatoid arthritis. 247 10

Urinary enzyme excretion and proteinuria were studied in 316 children with different underlying diseases. Activities on N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase decreased progressively with age in the urine of 66 healthy prematures, newborns, infants or children. In 51 children with nephrotic syndrome, tubulopathies or chronic renal failure, excretion of NAG and AAP rose 3 to 30 fold. Contrary to molecular weight dependent protein analysis, determination of enzymuria did not allow to differentiate between glomerular and tubular disorders. After renal transplantation, 31 out of 52 children had a pathological enzymuria. NAG and AAP were more frequently elevated during treatment with cyclosporine A (21/29), than with azathioprine (10/23). The influence of nephrotoxic drugs upon enzymuria was documented in 14 children with cystic fibrosis or septicaemia treated with tobramycin. Activities of NAG and AAP rose transiently, whereas proteinuria remained almost unchanged. Only three out of 45 children receiving nonsteroidal antiinflammatory drug therapy for juvenile rheumatoid arthritis or spondylarthritis showed a pathological increase in enzymuria. Mean urinary NAG and AAP excretion in 154 children with insulin dependent diabetes mellitus were not different from controls and were unrelated to either duration of disease or HbA1 concentration. The determinations of urinary enzymes as non-invasive tests of renal integrity in medicine and toxicology provide a very sensitive indicator of renal damage. The assays of NAG and AAP have proven to be most valuable; however, due to a lack of specificity for the type and origin of renal dysfunction, these urinary enzyme assays are most useful when carried out in conjunction with electrophoretic analyses of proteinuria.
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PMID:[Enzymuria and kidney diseases in childhood]. 288 Nov 98

Renal function tests were performed in 101 unselected patients who had been on lithium for two weeks to 12 years. None had a recorded episode of lithium intoxication. The glomerular filtration rate (GFR), was not correlated with the cumulative dose of lithium or the duration of use of other psychotropic drugs. Nine patients had creatinine clearances lower than predicted; in six of these, no cause was identified and the small reductions in GFR may have been related to lithium use. Urinary concentrating ability (Umax) declined with age, and total dose of lithium received. Although the concurrent use of neuroleptics did not significantly reduce the Umax, the total duration of treatment with these drugs showed a negative correlation. The results suggest that prolonged use of neuroleptics, particularly in patients treated with lithium, may be responsible for an irreversible reduction in urine concentrating ability. Microalbuminuria was present in 40 per cent of the patients, although the rate of albumin excretion was not correlated with duration of use of psychotropic drugs. beta 2 microglobulin excretion was only raised in nine of these patients, suggesting that increased glomerular permeability rather than impaired proximal tubular protein reabsorption was responsible for the proteinuria. The urinary excretion of beta 2 microglobulin and N-acetyl-beta-glucosaminidase were slightly increased in small numbers of patients, indicating little evidence for proximal tubular damage. Increased NAG excretion did not correlate with reduced distal tubular function. However, there was a tendency to higher urinary beta 2 microglobulin excretion in patients with a reduced Umax.
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PMID:Renal function during lithium treatment. 648 19


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