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 nephrotic syndrome, characterized by nonselective proteinuria, hypoproteinemia, hypoalbuminemia, and ascites, was observed in a 10-month-old male cat. Profound glomerular changes and renal tubular changes appear to have been induced by iatrogenic chronic exposure to metallic mercury originally contained in a rectal thermometer. Large concentrations of mercury were present in the kidneys, liver, spleen, and urine. Evaluation of glomeruli by immunofluorescent microscopy revealed interrupted granular deposition of immuno-globulin G and the third component of complement in glomerular capillary walls and the mesangium. Electron microscopic evaluation of glomeruli revealed diffuse alterations in glomerular basement membranes and visceral epithelial cells. Small electron dense deposits were observed in capillary walls, but they were not characteristic of immune complexes. The mechanism(s) responsible for the mercury induced glomerulonephropathy in this patient could not be determined on the basis of available data.
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PMID:Membranous glomerulonephropathy and nephrotic syndrome associated with iatrogenic metallic mercury poisoning in a cat. 725 62

To facilitate the study of mechanisms and patterns of proteinuria, radioimmunoassays for human lysozyme (LZM) and albumin (alb) were established to permit quantitation of physiologic amounts of these proteins in urine. Commercially available LZM and alb preparations were radiolabeled with I125, and single antibody, competitive protein binding assays were developed. Separation of free and antibody-bound radioprotein was achieved with 20 per cent polyethylene glycol. LZM and alb 24-hr excretion rates for 12 normal subjects were 7 to 64 microgram and 2.3 to 16.1 mg, respectively. Of 6 renal disease patients with undetectable urine LZM by bioassay, 5 were shown to have elevated LZM concentrations by radioimmunoassay. The ease of establishing and performing these assays and their reproducibility suggest that they may have clinical and investigative value.
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PMID:Lysozyme and albumin radioimmunoassays. New techniques for the study of proteinuria. 737 42

We studied the role of proteinase inhibitors (Pls) alpha 1-antitrypsin and alpha 1-antichymotrypsin in relation to lysozyme (LZM), and membrane attack complex (C5b-9) in renal tubular damage by immunohistochemical techniques. Fifty-five cases, including 45 patients with glomerular diseases, and 10 controls were studied. The patients were divided into two groups; one with tubulo-interstitial lesions (TILs; 30 cases), and the other without (15 cases). Significant antiproteinase response was observed in the proximal tubules in both disease groups, indicating that they were subjected to proteolytic attack. This response correlated with proteinuria and occurred in tubules which showed protein reabsorption as demonstrated by the presence of LZM staining in consecutive serial sections. Increased deposition of membrane attack complex (C5b-9) was observed in the disease group with TILs, indicating direct damage to cell membranes. C5b-9 may also generate oxygen species, potent inhibitors of Pls, which allow the proteases to cause tubular damage.
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PMID:Renal tubular antiproteinase (alpha-1-antitrypsin and alpha-1-antichymotrypsin) response in tubulo-interstitial damage. 750 11

The presence of monocytes/macrophages (MPs) in renal glomeruli was investigated in 86 dogs with different types of glomerulopathies. The identification of MPs in tissue sections was based on cytological criteria and the immunohistochemical demonstration of lysozyme. The highest numbers of MPs in glomeruli were observed in focal and diffuse mesangial proliferative glomerulonephritis (MesPGN), diffuse endocapillary proliferative glomerulonephritis (DEPGN), and diffuse mesangiocapillary glomerulonephritis (DMCGN). In cases of minor glomerular abnormalities (MGA), focal and segmental hyalinosis and sclerosis (FGS), diffuse membranous glomerulonephritis (DMemGN), and diffuse sclerosing glomerulonephritis (DSGN) the presence of glomerular MPs was low. Particularly in MesPGN, the number of MPs was correlated with glomerular hypercellularity and, additionally in DMCGN, with the degree of proteinuria. The results of this study suggest that MPs may be involved in functional and morphological alterations in different types of canine glomerulopathies.
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PMID:Participation of monocytes and macrophages in canine glomerular disease. 765 16

Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS PAGE) of urinary proteins was performed in 56 children with nephrotic syndrome during relapse, of whom 31 had their urines tested within 2 months of the onset of disease. The urines of all 32 steroid-sensitive [presumed minimal change nephrotic syndrome (MCNS)] patients revealed albumin and transferrin bands only; whereas 19 steroid-resistant children with focal glomerular sclerosis showed additional excretion of IgG and low molecular weight proteins (lysozyme, beta 2-microglobulin). This mixed pattern of proteinuria was also detected in 5 other steroid-resistant patients, 3 of whom were Africans with MCNS on biopsy and 2 who were Indians and not biopsied. Findings in patients studied within 2 months of presentation were identical to those investigated later in the course of the disease. SDS PAGE analysis of urine, which appears to distinguish steroid-responsive from steroid-resistant patients may provide a valuable adjunct to the management of childhood nephrotic syndrome.
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PMID:Sodium dodecyl sulphate polyacrylamide gel electrophoresis of urinary proteins in steroid-responsive and steroid-resistant nephrotic syndrome in children. 769 97

Early morning urine specimens were obtained from two groups of non-insulin dependent diabetic patients and a group (43 subjects) of normal controls. The diabetic patients were divided into two subgroups according to the degree of diabetic control as judged by their glycosylated haemoglobin (HbA1) levels (well-controlled, 47 subjects; poorly controlled, 51 subjects). The concentration of the low-molecular-weight enzyme (lysozyme) was determined in each urine specimen and related to the concentration of creatinine (lysozyme/creatinine). The mean urinary lysozyme concentration was higher in each of the two diabetic groups as compared with the control group. However, it was not significantly different between the two diabetic groups. These result suggest that there is no association between the degree of glycaemic control and tubular proteinuria.
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PMID:Low-molecular-weight (tubular) proteinuria is not related to glycaemic control in non-insulin dependent diabetes mellitus. 787 44

We previously reported that lysozyme electrostatically inhibits the fibronectin-mediated DNA binding to the glomerular basement membrane (GBM) and reduces in situ DNA-anti-DNA complex formation in the GBM in NZB/W F1 mice [1]. In this study, we further noticed significant increases in urinary excretion of anti-DNA antibodies and immune complexes (IC) in lysozyme-treated NZB/W F1 mice. Their clearance ratios of IgG anti-DNA antibody to whole IgG were markedly high compared with those of saline-treated animals. A large number of IgG and C3 positive granules were observed in the tubular cells of NZB/W F1 mice treated with lysozyme. On the contrary, nil or only small amounts of anti-DNA antibodies were detected in the urine of NZB/W F1 mice without lysozyme administration despite a large amount of proteinuria, suggesting entrapment of the antibodies in lupus glomeruli. Lysozyme neither inhibited the binding of anti-DNA antibodies to DNA or heparan sulphate nor did it displace anti-DNA antibodies and IC from the kidney homogenates of lupus mice. It thus appears that the inhibition of DNA binding to the GBM due to lysozyme reduced the entrapment of anti-DNA antibodies in the GBM, resulting in urinary excretion of the antibodies.
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PMID:Specific increases in urinary excretion of anti-DNA antibodies in lupus mice induced by lysozyme administration: further evidence for DNA-anti-DNA immune complexes in the pathogenesis of nephritis. 841 71

1. Metabolic acidosis invariably accompanies chronic renal failure, and short periods of metabolic acidosis cause renal growth and proteinuria in normal rats. Rates of ammoniagenesis are increased in chronic renal failure, and it has been suggested that this contributes to disease progression. This study assessed (i) whether prolonged acidosis causes chronic renal injury in the normal kidney and (ii) whether abrogation of acidosis slows disease progression in the remnant kidney. 2. Metabolic acidosis was induced in normal rats by dietary hydrochloric acid. Urinary excretion of total protein, lysozyme and albumin increased, peaking at week 8 but returning to baseline by week 14. At killing after 14 weeks, kidney weights, glomerular filtration rates and serum creatinine were the same in both groups, but kidney/body weight and kidney/heart weight ratios were greater in the acidotic group. All kidneys were normal by light microscopy. 3. Rats subjected to five-sixths nephrectomy were given sufficient dietary bicarbonate to abolish uraemic acidosis, and their outcome was compared with that of non-alkalinized remnants (controls). Proteinuria, glomerular filtration rates, blood pressure, histological injury and time to the development of terminal uraemia were no better in bicarbonate-supplemented animals than in controls. 4. These data demonstrate that metabolic acidosis neither causes nor exacerbates chronic renal injury. We conclude that the treatment of uraemic acidosis is unlikely to influence disease progression in patients with chronic renal failure.
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PMID:Metabolic acidosis does not contribute to chronic renal injury in the rat. 854 84

We have encountered a 49-year-old female with persistent proteinuria and hematuria. Blood pressure, renal function, physical findings and chest X-p showed no abnormality, but blood tests disclosed mild thrombocytopenia, elevated serum ACE activity, serum lysozyme activity and serum IgA concentration. Abdominal echography and CT revealed multiple nodules in her spleen. In order to make a definite diagnosis and exclude the possibilities of malignant lymphoma or metastatic malignant tumor, splenectomy, and open renal biopsy were performed at the same time. On histological examinations, light microscopic appearance of the spleen was characterized by non-caseating granulomas compatible with sarcoidosis. Renal biopsy specimen showed diffuse proliferative glomerulonephritis with positive staining of IgA predominantly located in the mesangial area, compatible with IgA nephropathy. The present case may provide suggestive evidence for a link between sarcoidosis and IgA nephropathy in the pathogenesis. IgA nephropathy complicated by sarcoidosis is rare, and thus is of particular interest because common immunological abnormalities might be considered in the disease process of both diseases. We feel that despite a low index of suspicion, physicians must be alert to the possibility of IgA nephritis associated with sarcoidosis. The literature is reviewed regarding the relationship between IgA nephropathy and sarcoidosis.
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PMID:[Sarcoidosis representing multiple splenic nodules in a patient with IgA nephropathy]. 885 36

A 39-year-old Japanese woman had been receiving propylthiouracil for 5 years for hyperthyroidism when she developed myalgia, scleritis, proteinuria, fever, and inflammation of the nose. Examination of a renal biopsy specimen showed focal segmental necrotizing glomerulonephritis. Indirect immunofluorescent staining showed a highly positive perinuclear pattern of anti-neutrophil cytoplasmic antibody (ANCA) in her serum. Enzyme-linked immunosorbent assay (ELISA) of the ANCA showed positivity for anti-proteinase 3, anti-myeloperoxidase, anti-leukocyte elastase, and anti-lactoferrin, but anti-cathepsin G and anti-lysozyme were negative. Because ELISA showed the titer of anti-leukocyte elastase antibody to be markedly elevated, we challenged this data by performing dot blot analysis. The patient's serum reacted with the native form, but not with denatured leukocyte elastase. Propylthiouracil-induced vasculitis was suspected. Symptoms abated within 2 weeks and all values of ANCA were reduced after the drug was withdrawn. Vasculitis is a rare side-effect of propylthiouracil therapy. Recently it was reported in association with ANCA. We present the findings of this patient and compare them with those described in 19 published cases of propylthiouracil-induced vasculitis associated with ANCA.
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PMID:Case of propylthiouracil-induced vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA); review of literature. 918 Dec 82


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