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)

Intralysosomal proteinase activity, due to cathepsins B and L, was measured in microdissected segments of rat nephron, using Z-Phen-Arg-7-amido-4-methylcoumarin as the substrate. Cathepsin B was determined with Z-Arg-Arg-7-amido-4-methylcoumarin. The enzymes cleave on the carboxy side of arginine and release free 7-amino-4-methylcoumarin, which is highly fluorescent and can be measured at very low concentrations in small volumes. Enzyme activities were measured in three individual microdissected segments of the proximal tubule and in six different segments of the distal tubule. Experiments were performed in normal non-proteinuric rats and in several rat models of glomerular proteinuria. The distributions of cathepsin activities along the nephron were similar. In all groups, the convoluted part of the proximal tubule had enzyme activities three times higher than in the remaining segments of the nephron. In the last millimeter of the pars convoluta and in the pars recta of the proximal tubule, enzyme activities were two to three times higher in proteinuric animals. These findings suggest that in proteinuric animals the increase in the protein load delivered to the proximal tubules selectively stimulated cathepsin B and L activities in the last millimeter of the pars convoluta and in the pars recta of the proximal tubule, presumably because of an increase in protein uptake, and that cathepsins B and L participate in lysosomal digestion of protein reabsorbed from the glomerular ultrafiltrate via endocytosis.
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PMID:Distribution of cathepsins B and L in the kidney and their role in tubular protein absorption. 149 60

Patients (pts) with rheumatoid arthritis (RA) may develop structural damage and functional deterioration of the kidney, where interstitial fibrosis and mesangioproliferative glomerulitis are seen most frequently. Compared to controls 80 pts with RA under various therapeutical regimes and 23 pts with SLE excreted immunoreactive membrane proteins of the proximal tubule at an increased rate. 30 out of 76 pts, but all with SLE, revealed a pathological pattern of proteinuria in SDS-PAGE.
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PMID:[Renal involvement in rheumatic (systemic) diseases: new diagnostic possibilities]. 191 74

Kidney disease is often cited as one of the adverse effects of chromium, yet chronic renal disease due to occupational or environmental exposure to chromium has not yet been reported. Occasional cases of acute tubular necrosis (ATN) following massive absorption of chromate have been described. Chromate-induced ATN has been extensively studied in experimental animals following parenteral administration of large doses of potassium chromate (hexavalent) (15 mg/kg body weight). The chromate is selectively accumulated in the convoluted proximal tubule where necrosis occurs. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by reports of low molecular weight (LMW) proteinuria in chromium workers. Excessive urinary excretion of beta 2-microglobulin, a specific proximal tubule brush border protein, and retinol-binding protein has been reported among chrome platers and welders. However, LMW proteinuria occurs after a variety of physiologic stresses, is usually reversible, and cannot by itself be considered evidence of chronic renal disease. Chromate-induced ATN and LMW proteinuria in chromium workers, nevertheless, raise the possibility that low-level, long-term exposure may produce persistent renal injury. The absence of evidence of chromate-induced exposure may produce persistent renal injury. The absence of evidence of chromate-induced chronic renal disease cannot be interpreted as evidence of the absence of such injury. Rather, it must be recognized that no prospective cohort or case-control study of the delayed renal effects of low-level, long-term exposure to chromium has been published.
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PMID:Chromium-induced kidney disease. 193 54

We report a patient who developed persistent nephrogenic diabetes insipidus associated with renal tubular acidosis, renal resistance to parathyroid hormone, aminoaciduria and proximal tubule pattern proteinuria in the presence of a reduced glomerular filtration rate (19-24 ml/min). A review of the previous reports of persistent nephrogenic diabetes insipidus revealed that in all patients the glomerular filtration rate had been less than 60 ml/min at presentation. Chronic renal failure may therefore predispose to the development of persistent nephrogenic diabetes insipidus in patients receiving lithium.
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PMID:Persistent nephrogenic diabetes insipidus, tubular proteinuria, aminoaciduria, and parathyroid hormone resistance following longterm lithium administration. 217 Sep 60

In 68 type I diabetics without permanent proteinuria, mean age 28 +/- 9 years, where diabetes was detected at the age of 14 +/- 7 years and persists for 14 +/- 8 years the urinary excretion of albumin and beta-2-microglobulin was assessed. The results were evaluated in relation to the persistence of diabetes, the blood pressure reading, family-history of diabetes and type of insulin therapy. In addition to microalbuminuria in 29% of the subjects which is a manifestation of glomerular damage, the authors detected in 58% elevated beta-2-microglobulin excretion indicating early changes of the proximal tubule. There was a relationship between microalbuminuria and "relative hypertension" which enhances albumin excretion and increases the risk of diabetic nephropathy. The relationship between microalbuminuria and a positive family-history of diabetes supports the hypothesis of a genetic background for the possible development of nephropathy. There was also a relationship with the duration of diabetes and the favourable effect of prolonged intensive insulin treatment. The clinical impact of beta-2-microglobulinuria in the diagnosis of the incipient stage of diabetic nephropathy must be tested in future investigations.
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PMID:[Early diagnosis of nephropathy in type I diabetics]. 224 68

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 beta-N-acetyl-glucosaminidase (beta-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, gamma-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 (cis-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, greater than 10(6) 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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PMID:Urinary proteins of tubular origin: basic immunochemical and clinical aspects. 225 76

As a contribution to the noninvasive diagnosis of kidney damage, polyclonal antisera specifically directed against brush border surface glycoproteins of the proximal tubule of the human kidney were used in radioimmunoblotting studies for the assessment of kidney-tissue proteinuria. Urine specimens from healthy controls, from patients (n = 41) with various forms of renal involvement and from those suffering from symptomatic HIV-infection (AIDS) but having normal kidney function, were investigated for the excretion of kidney-derived membrane proteins. After SDS-polyacrylamide gel electrophoresis of urine samples and electroblotting of protein bands on nitrocellulose sheets, followed by incubation with the antibody and subsequently with 125I-labelled protein A, 3 major tubular glycoproteins (Mr 240 000, 160 000, 120 000) were revealed by autoradiography. The results indicate and increased shedding of epithelial membrane glycoproteins in the urine of patients with kidney lesions, and they also demonstrate the suitability of radioimmunoblotting for the determination of such tissue-antigens ("brush border-histuria").
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PMID:Tubule-derived membrane glycoproteins in the urine of patients (including those with AIDS) as analysed by radioimmunoblotting. 231 34

Two patients admitted after ingestion of 80% acetic acid are described. Only the first patient developed haemolysis, slight intravascular coagulation and oliguric kidney insufficiency. They were treated with a nasogastric tube and total parenteral feeding. During the first week after admission urinary excretion of beta 2-microglobulin, alanine-aminopeptidase and N-acetyl-glucosaminidase was significantly increased. The patients remained haemodynamically stable and did not develop fever. The above-mentioned elevated excretions returned to normal levels. Both patients showed similar patterns of tubular proteinuria. The observations in the second patient suggest a direct toxic effect of acetic acid on the proximal tubule of the kidney.
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PMID:[Kidney tubule dysfunction caused by acetic acid]. 256 37

Since the first description of tubular proteinuria in 1958, much progress has been made with regard to diagnostic means for detecting small changes in the function of the proximal tubule. Small increases in the excretion of low-molecular-weight proteins can now be determined with great accuracy. Determination of total protein is an economic way of screening large populations but does not give specific information on the type of damage. Determinations of glucose, phosphate and amino acids are relatively insensitive methods, since their excretion is also dependent on diet and nutritional status. Determination of high-molecular-weight enzymes released from damaged tubular cells may be of use for studies of acute as well as chronic effects of nephrotoxic agents, but more data are needed.
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PMID:Markers of tubular dysfunction. 265 26

Severity and duration of renal injury produced by low levels of uranyl fluoride (UO2F2) were examined in the rat. Rats received multiple ip injections of UO2F2 (cumulative dose: 0.66 or 1.32 mg U/kg body wt). Renal injury was characterized histologically by cellular and tubular necrosis of pars recta of proximal tubule (S2 and S3), with less severe cellular injury to thick ascending limb of loop of Henle and collecting tubule. Injury was evident when renal uranium levels were between 0.7 and 1.4 micrograms U/g wet kidney and was most severe when renal uranium burden was between 3.4 and 5.6 micrograms U/g. Repair of injury was rapid, with complete restoration within 35 days after exposure. Associated with injury were abnormalities in renal function, including impaired tubular reabsorption, proteinuria, and enzymuria, which appeared temporally related, to variable degrees, to progression of renal injury. Thus, reversible renal injury occurs in the rat at levels of uranium in kidney below the present Nuclear Regulatory Commission standard of 3 micrograms U/g kidney for renal injury in humans.
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PMID:Reversible uranyl fluoride nephrotoxicity in the Long Evans rat. 276 62


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