Tissue antigens in normal and pathologic urine samples: A review

Rosenmann, E.; Boss, J. H.

doi:10.1038/ki.1979.136

Cited by 13 publications

(9 citation statements)

References 60 publications

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“…after (transitory) ischemia, arterial hyperten sion, exposure to toxins including heavy metals, radiocontrast agents, aminoglycosides, c/s-platinum cytostasis [4,[6][7][8][9][10][11][12][13][14].…”

Section: Pathophysiological Background Of Tubular Histuriamentioning

confidence: 99%

“…Recent studies have focused not only on the integ rity of the BB hydrolases, but also on the expression of BB 'microdomains' and the arrangement of BB cytoskeletal components, such as spectrin, myosin, villin, fimbrin, fodrin, the camodulin complex, calpactin [21]. All these BB constituents may also appear in the urine and represent potential diagnostic markers of proximal tubu lar injury [6,8,[22][23][24][25][26]. However, BB tissue proteinuria appears to be associated with the capability of tubular cells to recover from (temporary) injury.…”

Section: Pathophysiological Background Of Tubular Histuriamentioning

confidence: 99%

“…The biologically significant tissue components found in urine specimens under normal and pathological conditions originate from the kidney itself [4][5][6], For example, basement membrane material from glomeruli, a variety of tubular marker enzymes and other proteins including Tamm-Horsfall uromucoid of the distal neph ron contribute to kidney-tissue-specific proteinuria (ta ble 1) [1][2][3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Scherberich¹

1990

Am J Nephrol

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A variety of tubular marker proteins, as compared to healthy controls, are excreted at an increased rate in the urine of patients with renal damage. Beside cytoplasmic glutathione-S-transferase and lysosomal β-N-acetyl-glucosaminidase (β-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, γ-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein ‘SGP-240’ and adenosine-deaminase-binding protein. Urinary tissue proteins, e.g. brush border (BB) microvilli, are immunologically identical with those antigens prepared from cell membranes of the human kidney itself. BB antigens are shed into the urine of patients with glomerulonephritis, interstitial nephritis, systemic diseases, e.g. systemic lupus erythematosus (SLE), diabetes mellitus and multiple myeloma, arterial hypertension, infectious diseases (malaria, AIDS) and after operations, renal grafting and administration of X-ray contrast media, aminoglycosides or certain cytostatics (cz’s-platinum). Tissue proteinuria of tubular proteins is determined by enzyme-kinetic or quantitative immunological assays applying either poly- or monoclonal antikidney antibodies. Clinical, ultrastructural and histochemical studies support the idea that both ‘soluble’ and high-molecular-weight membrane particles (vacuolar blebs, > 10⁶ dalton) as well as microfilamental components of the epithelial cytoskeleton contribute to tubular ‘histuria’ which appears as a sensitive parameter in monitoring tubular damage under clinical conditions at a very early phase.

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Section: Pathophysiological Background Of Tubular Histuriamentioning

confidence: 99%

Section: Pathophysiological Background Of Tubular Histuriamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Scherberich¹

1990

Am J Nephrol

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“…Their increase has been associated with cellular damage caused by pathologic processes [8][9][10]15,28,29]. Increased excre tion of renal tissue constituents can be interpreted as a result of cellular breakdown, necrosis or increased cell turnover.…”

Section: Discussionmentioning

confidence: 99%

“…Demonstra tion of kidney-derived urinary membrane proteins, speci fic for distinct parts of the human nephron, could be a reliable and highly sensitive indicator of tubular damage [7][8][9][10][11][12][13][14], It is assumed that under pathologic conditions surface proteins a n d /o r breakdown products from high molecular structures originating from the luminal mem brane of tubular epithelial cells (TECs) are released di rectly into the urine [15,16]. Demonstration of this pri mary damage process by sensitive immunological, nonin vasive methods should precede conventional clinically recognizable secondary effects.…”

Section: Introductionmentioning

confidence: 99%

Urinary Detected Renal Antigens in the Early Diagnosis of Kidney Graft Rejection

Müller

Engler-Blum²,

Gassner³

1991

Nephron

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The determination of renal antigens in the urine with an immunoassay, based on monoclonal antibodies (moabs), is a noninvasive test system for the analysis and monitoring of renal injury. New moabs allowing an immunohistologic dissection of the human nephron were generated by a direct intrasplenic immunization of mice with pathologic urine samples. A sandwich enzyme immunoassay was developed to quantitate renal cell membrane antigens in the urine. While antigen excretion in healthy individuals is low, preliminary data of a clinical investigation suggest the usefulness of these assay systems in diagnosis of tubular injury in human kidney transplant recipients. The immunoassay can provide very early hints of renal graft rejection prior to the appearance of clinical symptoms or the detection by routine clinical laboratory investigations.

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Early detection of the nephrotoxic effects of industrial chemicals: State of the art and future prospects

Lauwerys

Bernard

1987

American J Industrial Med

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This paper discusses several tests that may permit the early detection of renal changes induced by long-term exposure to nephrotoxic industrial chemicals and may possibly serve as advance warning of pending renal damage. Some tests mainly attempt to assess the integrity of the glomerulus: high molecular weight proteinuria, glomerular basement membrane (GBM) antigens in blood and in urine, circulating anti-GBM antibodies, glomerular filtration rate after an acute oral load of proteins, and estimation of membrane negative charges (ie, glomerular polyanion). Others mainly attempt to identify functional and/or morphological changes at the tubular level: low molecular weight proteinuria, aminoaciduria, glucosuria, hyperphosphaturia, hypercalciuria, enzymuria, tubular antigen excretion, kallikrein, and prostaglandin excretion. Some of these tests are already routinely used, although controversy may still persist with regard to their clinical significance. Recently, new tests have been developed that may open new perspectives for assessing the significance of the early renal changes induced by chemicals.

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Tissue antigens in normal and pathologic urine samples: A review

Cited by 13 publications

References 60 publications

Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Urinary Detected Renal Antigens in the Early Diagnosis of Kidney Graft Rejection

Early detection of the nephrotoxic effects of industrial chemicals: State of the art and future prospects

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