Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some neutrophil cytoplasmic auto-antibodies produce perinuclear immuno staining of alcohol-fixed neutrophils called P-Anca pattern. These autoantibodies show chiefly reactivity with myeloperoxidase in Elisa but other specificities have been detected (elastase, cathepsin, lactoferrin). These P-Anca anti-MPO are more frequent with renal angiitis but P-Anca (anti-MPO negative) are associated with other diseases without renal failure (rheumatoid arthritis, Gougerot-Sjogren and ulceritis colitis).
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PMID:[Anti-polynuclear neutrophil cytoplasmic antibodies of the perinuclear type or p-ANCA]. 133 98

We report a case of microscopic polyarteritis nodosa associated with myeloperoxidase-antineutrophil cytoplasmic autoantibodies (MPO-ANCA). A 38 year-old female was admitted to our hospital, because of proteinuria, recurrent pyrexia, polyarthralgia, abdominal pain and purpura. She had a history of severe pulmonary hemorrhage and 4 kg weight loss for 8 months. On admission perinuclear ANCA without cytoplasmic ANCA was detected by indirect immunofluorescence assay and MPO-ANCA was detected by enzyme linked immunosorbent assay. But anti-nuclear antibodies, immune complexes and anti-glomerular basement membrane antibodies were not detected. Renal biopsy showed necrotizing crescentic glomerulonephritis without immune deposits. Skin biopsy revealed leukocytoclastic vasculitis. Diagnosis of microscopic polyarteritis nodosa was made by these clinical and histological evidence of vasculitis. As renal failure progressed after admission, corticosteroid and cyclophosphamide administration were started. Renal function and other symptoms improved paralleled with decreased MPO-ANCA titer to normal values. It is suggested that MPO-ANCA may be closely related to the pathogenesis of microscopic polyarteritis nodosa and it may be a good serological marker for diagnosis and disease activity of this disease.
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PMID:[A case of microscopic polyarteritis nodosa associated with myeloperoxidase-antineutrophil cytoplasmic autoantibodies (MPO-ANCA)]. 136 30

Selenium, aluminum, cadmium, and magnesium concentrations and glutathione-peroxidase activities in sera of 35 healthy individuals, 30 renal transplants, and 30 hemodialysis patients were measured. Serum selenium, aluminum, and cadmium concentrations in both groups of patients were higher than the controls (p less than 0.001), whereas the serum glutathione-peroxidase levels were lower (p less than 0.001). According to our results, it can be concluded that the patients receiving hemodialysis are subjected to more toxic elements than the transplantation patients. These findings imply that dietary selenium supplement may be suggested in renal failure for the detoxification of elements, such as cadmium and mercury. The essential trace element selenium takes part not only in the direct protection of endothelial cells against the accumulation of aggressive oxygen species, but also in the prevention of the toxic effects of cadmium or in the modulation of the active calcium transport.
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PMID:Serum selenium and glutathione-peroxidase activities and their interaction with toxic metals in dialysis and renal transplantation patients. 137 65

There have been many reports on renal lesions of alcoholic cirrhosis, but not on those of post-hepatitis cirrhosis (PHC) up to present. A clinical and pathological observation on PHC was carried out prospectively in 18 and retrospectively in 34 cases. Renal specimens were examined with light and electron microscopy and immunopathological methods (immunofluorescence and peroxidase anti-peroxidase). Clinically, recurrent gross hematuria was observed in 2 and wild urinary abnormality in 17 cases. One case developed renal failure and the remaining 32 cases had no clinical evidence of renal involvement. Light microscopy showed wild mesangial lesions in 44 cases and glomerular basement membrane (GBM) thickening with segmental splitting in 29 and diffuse splitting in 2 cases. Massive protein deposition was found in the GBM, mesangium (Ms) and tubular basement membrane as well as the epithelium and endothelium. Immunopathological examination showed massive deposition of various immunoglobulins and complements in GBM and Ms, with IgG dominant in 8, IgM dominant in 7, IgA dominant in 6 and "full house" in 11 cases. HBsAg was detectable in GBM and Ms in 5 cases (9.6%) and HBcAg in one. Focal interstitial fibrosis and lymphocytic infiltration were found in 15 (28.3%). Our data revealed that renal lesions of post-hepatitis cirrhosis are different from those of the so-called "cirrhotic glomerulonephritis" in certain aspects. They are characterized by definite GBM involvement and massive deposition of immunoglobulins and complements. Its pathogenesis may be more complicated than that of other types of liver cirrhosis.
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PMID:[Renal lesions of post-hepatitis cirrhosis]. 142 1

We report a case of idiopathic crescentic glomerulonephritis with pulmonary hemorrhage associated with anti-myeloperoxidase antibodies (anti-MPO ab). A 74 year-old female was admitted to our hospital because of rapidly progressive glomerulonephritic syndrome and dyspnea with bloody sputum. On admission anti-MPO ab, one of anti-neutrophil cytoplasmic antibodies, were detected but anti-GBM antibodies and immune complexes were not detected. Renal biopsy showed crescentic glomerulonephritis and lung biopsy showed massive alveolar hemorrhage. Both tissue had pauci-immune deposit by immunofluorescence microscopy. Hemodialysis and steroid administration were started. Pulmonary hemorrhage was improved remarkably, but renal failure progressed rapidly to end stage kidney, then hemodialysis was continued. Although subsequent 3 years uneventful maintenance hemodialysis had been performed, she admitted to our hospital again because of progressive dyspnea with hemoptysis after upper respiratory tract infection. On admission anti-MPO ab were detected again and steroid administration was started. Pulmonary hemorrhage was improved with decreased anti-MPO ab titer. While tapering the dosis of steroid, anti-MPO ab again increased and pulmonary hemorrhage recurred. Although pulse methylprednisolone therapy and plasma exchange were performed, respiratory failure progressed rapidly and she died of sepsis. Postmortem examination showed no evidence of systemic vasculitis. In this case, titer of anti-MPO ab was associated with not only idiopathic crescentic glomerulonephritis but also with pulmonary hemorrhage. We tried to detect enzymatically active MPO in serum. Titer of serum MPO was also associated with disease activity and anti-MPO ab. It is suggested that both anti-MPO ab and serum MPO are closely related to the pathogenesis of idiopathic crescentic glomerulonephritis and pulmonary hemorrhage.
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PMID:[A case of anti-myeloperoxidase antibodies-associated idiopathic crescentic glomerulonephritis with pulmonary hemorrhage]. 166 75

We investigated the effect of excess complement factor D on the immune complex solubilization activity (ICSA) of serum. First, we estimated the concentration of factor D, ICSA and the hemolytic activity via the classical complement pathway (CH50) in the sera of 16 healthy individuals and 36 patients on hemodialysis for end-stage renal failure. The serum concentration of factor D in these patients (mean +/- SD: 12.12 +/- 2.38 micrograms/ml) was significantly higher (p less than 0.001) than that in the healthy subjects (1.02 +/- 0.11 micrograms/ml). In this study, peroxidase and antiperoxidase rabbit IgG were used as immune precipitates for ICSA. The ICSA in patients (45.8 +/- 7.4 normal human serum %, NHS%) was significantly lower (p less than 0.001) than that in the healthy subjects (100.2 +/- 12.5 NHS%). There was no difference in CH50 between the sera of the patients (31.8 +/- 2.5) and that of the healthy group (32.4 +/- 2.6). Second, we determined that increasing amounts of purified factor D added to fresh serum resulted in a decrease in ICSA. This occurred in the serum of a healthy individual as well as in that of a patient. CH50 did not change regardless of the concentration of factor D used. There was an increase in C3 conversion in the sera to which purified factor D had been added, as observed by crossed immunoelectrophoresis. It is suggested that ICSA had deteriorated due to the excess of factor D, which had activated the alternative pathway of complement.
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PMID:Deterioration of immune complex solubilization activity of serum by increased concentration of factor D. 175 30

Three hybridoma cell lines secreting monoclonal IgG antibodies specific for human tumor necrosis factor-binding protein I (TNF-BP I), the extracellular domain of the 60 kDa TNF receptor, were developed by fusion of spleen cells from mice immunized with TNF-BP I purified from urine. The antibodies recognize three different epitopes on TNF-BP I. Two of the antibodies were used to develop a two-site ('sandwich') enzyme immunoassay with horseradish peroxidase as the marker enzyme. The assay was able to measure TNF-BP I in serum, urine and cell culture supernatants with a sensitivity of about 200 ng/l and a precision better than 10%. TNF-BP I was detected in the serum of healthy individuals at a mean concentration of 2.1 +/- 1.0 micrograms/l (mean +/- standard deviation; range, 0.52-5.4 microgram/l, n = 42); no significant difference was seen in patients with chronic polyarthritis (2.3 +/- 0.79 micrograms/l; n = 15). Serum TNF-BP I was significantly elevated in patients with burns (6.5 +/- 1.7 micrograms/l; n = 10) and markedly increased in patients with renal failure (49 +/- 17 micrograms/l; n = 6). TNF-BP I was also detectable in urine from normal individuals (2.2 +/- 1.2 micrograms/l; range 0.78-4.3 micrograms/l; n = 16). Culture supernatants of several human tumor cell lines also contained TNF-BP I. The assay will be a useful tool to detect activation of the TNF receptor by the physiological ligands, TNF-alpha and TNF-beta, as well as transmodulation by other mediators in various pathological conditions.
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PMID:A monoclonal antibody-based enzyme immunoassay for quantitation of human tumor necrosis factor binding protein I, a soluble fragment of the 60 kDa TNF receptor, in biological fluids. 191 33

Antineutrophil cytoplasmic autoantibodies (ANCA) are specific for constituents of neutrophil primary granules and monocyte lysosomes. There are different types of ANCA with different specificities. By indirect immunofluorescence microscopy using alcohol-fixed neutrophils as substrate, two major categories of ANCA can be recognized, one with cytoplasmic staining (C-ANCA) and the other with artifactual perinuclear staining (P-ANCA). Some C-ANCA have specificity for proteinase 3 (PR3-ANCA) and some P-ANCA have specificity for myeloperoxidase (MPO-ANCA), but there are additional C-ANCA and P-ANCA specificities. ANCA are found in the blood of patients with necrotizing systemic vasculitis, such as Wegener's granulomatosis and polyarteritis nodosa, and patients with idiopathic crescentic glomerulonephritis. The glomerular lesion in patients with systemic and renal-limited ANCA-associated diseases is the same, ie, a pauci-immune necrotizing and crescentic glomerulonephritis. No matter where the vascular lesions of ANCA-associated disease are (eg, kidney, lung, gut, muscle, skin), they are characterized by necrotizing inflammation and a paucity of immune deposits. The distribution of disease correlates to a degree with the ANCA specificity, although there is substantial overlap. For example, patients with Wegener's granulomatosis most often have C-ANCA and patients with renal-limited disease most often have P-ANCA. In patients with P-ANCA-associated glomerulonephritis, approximately 90% of the P-ANCA have specificity for MPO. The clinical manifestations of ANCA-associated diseases often begin following a flu-like illness. The onset is most often in the winter and least often in the summer. The renal disease usually presents as rapidly progressive renal failure with nephritis. One of the most life-threatening components of the systemic involvement is pulmonary hemorrhage caused by a necrotizing alveolar capillaritis. Intravenous cyclophosphamide plus steroids is as effective as oral cyclophosphamide plus steroids for controlling ANCA-associated diseases. Using life-table analysis, the 2-year patient and renal survival rate in both patients with renal-limited and systemic disease is greater than 70%. There is evidence that in addition to being a useful serologic marker, ANCA are directly involved in the pathogenesis of the vascular injury in patients with ANCA-associated diseases. Although ANCA antigens are normally in the cytoplasm of neutrophils and monocytes, priming of these cells, as occurs following exposure to certain cytokines, results in the release of small amounts of ANCA antigens at the cell surface. In vitro, ANCA-IgG causes cytokine-primed neutrophils to undergo a respiratory burst and degranulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antineutrophil cytoplasmic autoantibodies and associated diseases: a review. 197 31

Peroxidase activity was assessed cytochemically in macrophages from peritoneal dialysate of 50 patients with terminal renal failure treated by intermittent peritoneal dialysis. In 22 patients cells were harvested for the second time after development of peritonitis as the complication of the treatment. The obtained results were compared with those of the control group consisting of 30 patients with normal renal function. Patients treated with peritoneal dialysis showed both in complication-free period and during the course of peritonitis significantly higher peroxidase activity in macrophages as revealed by the semiquantitative score test. In the course of peritonitis, peroxidase activity in macrophages was significantly lower than in complication-free period. Electron-microscopic cytochemistry demonstrated that in macrophages obtained from both control and dialyzed patients the peroxidase activity was located exclusively in cytoplasmic granules, suggesting a similarity of the studied cells and exudative macrophages.
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PMID:Peroxidase activity in peritoneal macrophages of patients with terminal renal failure treated by intermittent peritoneal dialysis. 215 83

Peroxidase activity was assessed cytochemically in the peritoneal dialysate neutrophils of 50 patients with terminal renal failure treated by intermittent peritoneal dialysis. In 22 patients cells were harvested for the second time after they developed peritonitis as a complication of the treatment. The results obtained were compared with those in the control group consisting of 30 patients with normal renal function. The patients treated by peritoneal dialysis showed both in the complication-free period and in the course of peritonitis significantly higher peroxidase activity in the neutrophils, as revealed by the semiquantitative score test. In the course of peritonitis, the neutrophils peroxidase activity was significantly lower than in the complication-free period.
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PMID:Peroxidase activity in peritoneal neutrophils of patients with terminal renal failure treated by intermittent peritoneal dialysis. 217 39


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