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)

Urine specimens from 164 patients sent to the laboratory for testing for Bence-Jones proteinuria were investigated using a new procedure. The protein in the untreated urine was subjected to isoelectric focussing in an agarose gel, transferred to a nitrocellulose membrane by blotting, and then stained by an immunoperoxidase technique for either immunoglobulin kappa or lambda chains. This technique was compared with a routine procedure for the detection of immunoglobulin light chains involving concentration by ultrafiltration, electrophoresis and then immunofixation. The new technique achieved a much increased rate of detection of Bence-Jones proteinuria. Among 51 patients known to have myeloma or macroglobulinaemia, Bence-Jones proteinuria was detected in 35 cases with the new procedure and in only 27 by the conventional method. In 28 patients with paraproteinaemia without other evidence of myeloma, macroglobulinaemia, leukaemia or lymphoma, 12 instances of Bence-Jones proteinuria were discovered with the new procedure, 10 of which were missed by the conventional method. The improved efficiency of detection is attributed to the high resolution of isoelectric focussing and the avoidance of protein loss from adsorption on to ultrafiltration membranes.
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PMID:Detection of Bence-Jones protein by isoelectric focussing of unconcentrated urine followed by nitrocellulose blotting and immunoperoxidase staining. 393 44

Further evidence implicating murine leukemia-like virus in the disorders of NZB mice was afforded by a study of antigens associated with murine leukemia virus (MuLV). MuLV group antigens were prevalent in extracts of spleen, kidney, and, to a lesser extent, thymus throughout a substantial portion of the life span of NZB mice as well as in extracts of lymphomas and sarcomas indigenous to the strain. G (Gross) soluble antigen, type-specific antigen, was first detected in plasma of untreated NZB mice at 3 months of age. G soluble antigen production increased thereafter in line with age, with 50% of reactions becoming positive at 5.3 months and 100% at 7 to 9 months. From months 3 to 9, the time-response curve for positive conversion of direct antiglobulin (Coombs) tests in untreated NZB mice corresponded closely to that for G soluble antigen production. Beyond the 9th month, G soluble antigen underwent elimination from the plasma of NZB mice, with positive reactions reduced to 50% at 13.3 months and to 0% at 18 months. G natural antibody was first detected in the serum of NZB mice at about 10 months of age and increased thereafter in line with age. The curves for G antibody production and G soluble antigen elimination bore a reciprocal relation to each other with crossover at 50% response occurring at 13.3 months. Significant proteinuria, a functional manifestation of membranous glomerulonephritis, became increasingly prevalent in female NZB mice as G soluble antigen was eliminated from plasma. Cumulative mortality of female NZB mice, mainly attributable to renal glomerular disease, increased in phase with G antibody production. MuLV group antigens were identified in the glomerular lesions by the immunofluorescence method. Positive conversion of direct antiglobulin tests was significantly delayed by vaccinating baby NZB mice with formaldehyde-inactivated cell-free filtrates of older NZB mouse spleens. The plasmas of vaccinated NZB mice with negative direct antiglobulin reactions at 4 to 7 months were likewise negative when tested for G soluble antigen. The 50% response time for G antibody production in the vaccinated NZB mice occurred at 7.3 months, that is, 6 months earlier than in untreated NZB mice. The collective findings implicate murine leukemia-like virus in the etiology of autoimmune hemolytic disease and membranous glomerulonephritis, as well as malignant lymphoma, of NZB mice and suggest that virus-specified cell-surface and soluble antigen is a factor in the immunopathogenesis of the renal disease and possibly also the autoimmune hemolytic disease.
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PMID:Further implication of murine leukemia-like virs in the disorders of NZB mice. 430 80

The pathogenesis of the spontaneous glomerulonephritis of NZB and (NZB x NZW) F(1) hybrid mice is related at least in part to the formation of natural antibody against antigens of the G (Gross) system, and apparently to the deposition in the glomeruli of immune complexes of G natural antibody with G soluble antigen (GSA), type-specific antigen specified by wild-type Gross leukemia virus. G natural antibody and GSA are detectable in the acid-buffer eluate of the kidneys of NZB mice during the course of the glomerulonephritis. (NZB x NZW) F(1) hybrid mice develop glomerulonephritis and produce GSA and free G natural antibody earlier in life than do NZB mice. The proteinuria manifestation of the gomerulonephritis of (NZB x NZW) F(1) hybrid mice becomes increasingly prevalent as GSA undergoes immune elimination from the circulation. Gross leukemia virus-specified antigens together with bound immunoglobulins are located in the glomerular lesions of (NZB x NZW) F(1) hybrid mice, both in the mesangium as observed in NZB mice and also in the wall of the peripheral capillary loops of the glomeruli.
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PMID:Wild-type Gross leukemia virus and the pathogenesis of the glomerulonephritis of New Zealand mice. 492 98

Serum levels, urinary excretion, and clearances of several proteins of different molecular weights were studied in 18 patients with mono- and myelomonocytic leukemia. Nine patients had normal renal function (group A) and nine had impaired renal function with azotemia (group B). The majority of patients in both groups had increased concentration of immunoglobulins, particularly IgG, IgA, and IgM; IgD level was normal. Serum transferrin and alpha(2)-macroglobulin were frequently reduced while the level of ceruloplasmin was often increased, especially in patients with azotemia. The activity of lysozyme in the serum was high in all patients, but was considerably higher in group B. Proteinuria was found in most patients but was more prominent in group B. Almost invariably albumin constituted less than 25% of the total protein excreted. Qualitative analysis of various urinary proteins by immunochemical techniques and clearance studies suggested the presence of glomerular as well as tubular dysfunction. Determination of urinary lysozyme frequently showed no direct correlation between the serum level of the enzyme and its concentration in the urine or its clearance by the kidney. In addition to glomerular filtration, impaired tubular reabsorption may account for the high level of lysozyme in the urine. It is postulated that the very high level of lysozyme in the glomerular filtrate and possibly hypergammaglobulinemia may play a role in the induction of tubular damage. Renal impairment has been correlated with histological changes in the kidneys. From a comparative study of various leukemias, it seems that the combined glomerular-tubular dysfunction is a manifestation unique to mono- and myelomonocytic leukemia.
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PMID:Serum and urinary proteins, lysozyme (muramidase), and renal dysfunction in mono- and myelomonocytic leukemia. 527 Sep 14

Thirty-six patients received allogeneic (34) or syngeneic (two) bone marrow transplants as treatment for severe aplastic anaemia or acute leukaemia. Nineteen of the allogeneic recipients received methotrexate (MTX) and 15 received cyclosporin A (CyA) as the predominant immunosuppressive agent to minimize graft-versus-host disease (GVHD) post transplant. In the first 100 d post transplant renal dysfunction was much less frequent in the MTX recipients than in the CyA recipients who exhibited three distinct syndromes of nephrotoxicity: most commonly. CyA recipients developed asymptomatic azotaemia, proteinuria, urinary casts, impaired urinary concentrating ability and hypertension. Secondly, two CyA recipients developed acute reversible renal failure precipitated by systemic bacterial infection which required dialysis and in which the kidney was the sole target organ; thirdly, two recipients of HLA-genotypically non-identical grafts developed a rapidly progressive fatal syndrome with multiple organ involvement including lung, brain and kidney which clinically and histologically resembled thrombotic thrombocytopenic purpura.
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PMID:Cyclosporin A associated nephrotoxicity in the first 100 days after allogeneic bone marrow transplantation: three distinct syndromes. 634 55

The nephrotic syndrome is uncommon in patients with chronic lymphocytic leukemia. When present, the most frequently documented cause is membranous nephropathy, although several other glomerular lesions have also been described. This report describes a patient with chronic lymphocytic leukemia of an unusual surface marker phenotype recently suggested to be associated with an increased incidence of proteinuria. Renal biopsy specimens demonstrated membranous glomerulonephritis. Immunofluorescence staining demonstrated glomerular deposition of IgG and C3, but not the human T-lymphocyte antigen, T65, which had been found on circulating leukemia cells.
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PMID:Membranous nephropathy associated with an unusual phenotype of chronic lymphocytic leukemia. 664 Apr 96

A patient with acute myelomonocytic leukemia was found to have IgG paraprotein on serum electrophoresis Bence Jones K proteinuria and increased plasma cells (30%) on marrow examination. The simultaneous occurrence of the two diseases was well documented by cytochemical immunological and electron-microscopic findings. Bone marrow chromosome investigations showed an abnormal karyotype: hypodiploidy was prevalent and marker chromosomes were present. A possible relationship between acute leukemia and multiple myeloma is discussed.
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PMID:Multiple myeloma and acute myelomonocytic leukemia: simultaneous occurrence without previous chemotherapy. 678 Nov 97

A case of chronic lymphocytic leukemia complicated by the nephrotic syndrome (due to membranoproliferative glomerulonephritis) is reported. There was complete remission of the proteinuria on two occasions in response to treatment of the leukemia. Possible etiological mechanisms are discussed and review of the literature is presented.
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PMID:Recurrent proteinuria in chronic lymphocytic leukemia. 727 96

A phase I trial of diglycoaldehyde (Inox) in children with leukemia established that the maximum tolerated dose of a 5-day schedule was 1.5 g/m2/day. A phase II study was undertaken by the Children's Cancer Study Group to evaluate the efficacy of this dose. Forty-seven children with acute leukemia refractory to conventional forms of therapy were entered in the study: 29 patients with acute lymphocyte leukemia/acute undifferentiated leukemia and 18 with acute nonlymphocytic leukemia. Inox was administered at a dose of 1.5 g/m2 as a 4-6 hour iv infusion daily for 5 days every 14 days. Toxic effects included myelosuppression, proteinuria, nausea, vomiting, diarrhea, local tissue reactions, hypocalcemia, transitory serum amylase elevation, and transitory hypotension. There was one life-threatening episode of drug-related renal toxicity. Of the 27 patients who received a minimum of two courses, partial remissions were observed in two patients with acute nonlymphocytic leukemia. Inox was inactive against advanced acute lymphocytic leukemia.
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PMID:Phase II evaluation of diglycoaldehyde (Inox) in children with acute leukemia: a children's cancer study group report. 742 52

We report a case of smoldering adult T-cell leukemia (ATL) with B-cell lymphoma and early gastric cancer. A 64-year-old man was admitted to our hospital because of proteinuria and hypergammaglobulinemia. Systemic lymphadenopathy, "flower cells" in peripheral white blood cells, and hypergammaglobulinemia with monoclonal gammopathy (IgA, lambda type) were found. As Southern blot analysis revealed monoclonal integration of human T-lymphotrophic virus type I proviral DNA in peripheral blood mononuclear cells, he was diagnosed as having smoldering ATL. The tissue specimen of an inguinal lymph node showed proliferation of abnormal lymphocytes which were stained with anti-lambda antibody, indicating B-cell lymphoma. A polypoid lesion in the stomach was histologically diagnosed as early gastric cancer.
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PMID:Smoldering adult T-cell leukemia with B-cell lymphoma and early gastric cancer. 772 76


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