Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injection of isologous monoclonal antibodies (SR2, SR3) caused anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM nephritis) in WKY/NCrj rats. The antibodies were obtained from hybridoma cells derived from fusion of the spleen of a nephritic WKY/NCrj rat injected with rat solubilized renal basement membranes with adjuvant, and mouse SP2-myeloma cells. They belonged to the rat IgG2a subclass and bound to rat kidney in a linear pattern along the glomerular and tubular basement membranes. Histological changes in glomeruli were detected at day 1 after the injection; proteinuria with haematuria appeared on day 2; and proteinuria became severe and reached a plateau by day 5. These results demonstrate that anti-GBM nephritis can even be induced by an isologous monoclonal antibody and that the rat IgG2a subclass is at least nephritogenic. The experimental model of anti-GBM nephritis with isologous monoclonal antibodies makes it possible and easier to analyse further the mechanism of anti-GBM nephritis.
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PMID:Isologous monoclonal antibodies can induce anti-GBM glomerulonephritis in rats. 146 May 40

A 59-year-old woman with kappa light-chain myeloma had Fanconi's syndrome characterized by renal glycosuria, generalized aminoaciduria, bicarbonaturia and decrease of phosphorus and uric acid reabsorption. A bone marrow biopsy showed the presence of 27% of dystrophic plasma cells; the cytoplasm of these cells was intensely stained with anti-kappa light-chain monoclonal antibodies. By light microscopy, the renal biopsy revealed a tubulointerstitial nephritis without glomerular lesions and with intratubular casts. By immunofluorescence, no deposits were observed along the glomerular and tubular basement membranes, but a positivity with anti-kappa light chain was noticed in some tubular epithelia and casts. By electron microscopy, fibrils (35-nm diameter) were observed in the cytoplasm of proximal tubular cells. These fibrils were situated in vesicles (100- to 600-nm diameter) in the luminal side of tubular cells. In the basal pole of the cell, fibrils seemed to group in crystals (120- to 200-nm diameter). Only kappa light-chain protein was demonstrated in these fibrils and crystals by an immunoelectron microscopic technique. These data suggested the pathogenic role of the fibrils and crystals present in tubular epithelium in the tubular proximal syndrome.
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PMID:Fanconi's syndrome, kappa light-chain myeloma, non-amyloid fibrils and cytoplasmic crystals in renal tubular epithelium. 166 55

Autologous (Heymann) nephritis was induced by immunizing Sprague-Dawley rats with a crude membrane extract (Fx1A) prepared from renal cortical tubules. Urine protein excretion was monitored to determine the onset of nephritis and then the spleens of nephritic rats were fused with a non-secretor rat myeloma cell line. Supernatants from hybridoma cultures were first screened for production of anti-brush border membrane (BBM) antibody by immunodot blotting of highly purified rat BBM on nitrocellulose. Positive hybrids were then tested by indirect immunofluorescence for the presence of IgG, which binds to the brush border of rat renal proximal tubules. Those hybrids which were positive by both screening assays were subcloned twice. Two monoclonal antibodies (C5, D11) were studied in some detail. Both C5 and D11 immunoprecipitated a single polypeptide from BBM, labelled with 125I by the lactoperoxidase method. Radioautography of gradient 4-11% slab sodium dodecyl sulphate polyacrylamide gels revealed that the polypeptide against which C5 and D11 were directed co-migrated with the polypeptide immunoprecipitated by (i) IgG eluted from the renal cortex of nephritic rats, and by (ii) a mouse anti-rat monoclonal against gp 330 [a BBM constituent with proven pathogenicity [9]]. Supernatants which tested positive by immunodot blotting but negative by indirect immunofluorescence showed no detectable immunoprecipitate after reaction with BBM. Immunocytochemical staining by immunoperoxidase and immunogold methods localized C5 and D11 to the BBM of the renal proximal tubule and to the urine face of the glomerular epithelium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A rat hybridoma model of Heymann nephritis: production of a monoclonal anti GP330 from a nephritic rat. 227 21

We studied renal histopathologic findings of 20 autopsy cases with multiple myeloma with particular attention to structural tubulovenous relationship. Urinary deposition in renal vein or lymphatics, which has been previously noted in pyelonephritis, obstructive uropathy, or vesicoureteral reflux was found in 14 cases. Four of 14 cases had unique tubulovenous communications designated as tubular prolase and tubular transformation of vein. Such communications were most frequently seen at the architectural weak point where the thin-walled interlobar vein and their tributaries adjoin the renal pyramid. Simultaneously, Tamm-Horsfall protein used as a marker for the location of urine was detected in renal vein. These changes had no significant correlation to morphologic severity of myeloma kidney or clinical manifestations of renal failure. Thus, tubulovenous communication producing backflow of urine into the circulation is frequently observed among myeloma kidney as well as other tubulointerstitial nephritis, but its clinical significance is unclear.
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PMID:Tubulovenous communication in myeloma kidney. Tubular prolapse and tubular transformation of renal vein. 271 73

Twenty-eight frozen renal biopsy specimens with a marked mononuclear cell interstitial infiltrate (MCI) were analyzed with monoclonal antibodies and a biotin-avidin peroxidase technique to define the surface phenotype distribution of the infiltrating cells. Twelve cases were diagnosed as tubulointerstitial nephritis of acute and chronic presentation, of unknown cause in 5 cases or secondary to multiple myeloma or drug reactions. Sixteen cases occurred in primary and secondary glomerulonephritis, 3 cases being associated with lymphoproliferative disorders. The results showed a remarkable heterogeneity of the MCI composition, even in cases with similar clinical and pathological findings. Namely, the T cells accounted for the majority of the infiltrating cells in most cases but a variable predominance of the T cell subsets Leu3 and Leu2 was observed. B cells and monocytes were also prominent in some cases. Such differences in the MCI composition may indicate the activation of different mechanisms of tissue damage, or a different phase of the renal disease. In the three cases of glomerulonephritis associated with lymphoproliferative disorders, the malignant origin of the MCI was demonstrated in one case, while in the remaining cases it was excluded.
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PMID:Immunophenotyping of mononuclear cell infiltrates associated with renal disease. 352 26

A large cohort of petroleum refinery workers with long duration of employment, long latency, and relatively young age at hire had its vital status updated through Dec. 31, 1980. The standardized mortality ratio (SMR) for all causes was 78. Each nonneoplastic cause had an SMR below 100, including SMRs of 63 for emphysema and for all diseases of the genitourinary system and of 73 for chronic nephritis. The SMR for all cancers was 87. SMRs for specific neoplasms included digestive system, 90; lung, 85; kidney, 68; brain, 89; leukemia, 101; multiple myeloma, 123; unspecified lymphoma, 112; polycythemia vera (four deaths), 455; myelofibrosis (three deaths), 201; and benign and unspecified brain neoplasms, 108. There were nine deaths from mesothelioma; all nine employees had more than 20 years of employment, with an SMR of 241.
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PMID:Update of a mortality study of workers in petroleum refineries. 373 21

The suppression of pathogenic antibodies to DNA in NZB/NZW f1 female mice was achieved by repeated inoculation of the mice with a monoclonal anti-idiotypic antibody (anti-Id). The anti-Id, an IgG1, kappa, was directed against a major cross-reactive idiotype (Id) on NZB/NZW IgG antibodies to DNA. One hundred micrograms of the anti-Id were inoculated i.p. every 2 wk, beginning at 6 wk of age (nondiseased mice--no circulating anti-DNA or proteinuria) or 20 wk of age (diseased mice--all with circulating anti-DNA, one-third with proteinuria). As controls, littermates received an IgG, kappa non-DNA-binding myeloma or no treatment. In the young mice, nephritis and anti-DNA antibodies appeared at the same time in all groups, and their circulating antibodies to DNA did not bear the target Id. In the older (20-wk-old) mice, survival was significantly prolonged because of delay in the onset of nephritis; the total quantities of antibodies to DNA were diminished, and the target Id, initially present on circulating IgG, was deleted. These benefits were transient; the suppression of antibodies was followed by the appearance of large quantities of anti-DNA that did not bear the major Id. Therefore, although administration of anti-Id was effective in reducing an undesirable antibody response after the target Id was present on circulating antibodies, the benefits were limited, probably by Id "switch" or by increased synthesis of pathogenic antibodies bearing a minor Id.
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PMID:Suppression of murine lupus nephritis by administration of an anti-idiotypic antibody to anti-DNA. 660 65

Sixteen years earlier a 42-year-old woman with an IgA kappa plasma cell neoplasm presented with bleeding disorder. Her prolonged course was complicated by subsequent development of rheumatoid arthritis, vascular purpura, and an acute membranoproliferative glomerulonephritis (MPGN). The paraprotein and its (Fab')2 fragment showed affinity for a test myeloma IgG2 (lambda ) paraprotein. The patient's serum and the IgA-IgG complex separated by gel filtration did not exhibit cryoprecipitation. The complex also did not dissociate by ultracentrifugation. Electron microscopic and immunofluorescent studies of a renal biopsy sample taken during the episode of nephritis showed subendothelial deposits and a lacy fluorescent pattern strongly positive for IgA and IgG. The same immunoglobulins were eluted from the kidney at postmortem. A low concentration of monoclonal IgA kappa (antibody) and excess unbound polyclonal IgG (antigen) were demonstrated in the patient's serum at the time of MPGN, apparently analogous to the conditions necessary for the induction of experimental immune complex nephritis.
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PMID:Pathogenic role of a monoclonal IgA (kappa ) anti-IgG paraprotein associated with hemorrhagic diathesis, rheumatoid arthritis, vascular purpura, and acute membranoproliferative glomerulonephritis. 680 64

Circulating antibody to Tamm-Horstall protein (THP) was measured using a radioimmunoassay in forty-five patients on maintenance hemodialysis and compared to levels of antibody titers measured in sera from ten healthy controls. The etiology of the end-stage kidney disease in the patient population was polycystic kidney disease in thirteen, glomerulonephritis in fourteen, diabetic nephropathy in nine, interstial nephritis and chronic pyelonephritis in three each, multiple myeloma in two, and urinary tract obstruction in one. Four patients had significantly elevated titers of antibody to THP but shared no other unifying characteristics. The results also indicate that none of the groups studied had mean antibody titers significantly different from controls. Furthermore, no general trend was apparent between levels of antibody to THP and number of months on dialysis. Observations made during the study revealed that heparinized samples of blood had lower titers of antibody to THP than did non-heparinized samples from the same patient. This finding was repeated when other anti-coagulants, i.e., ethylenediaminetetraacetate (EDTA) and sodium citrate, were used. Titers returned toward normal when CaCl2 was added back to samples anticoagulated with EDTA and sodium citrate. This suggests that clotting factors, probably fibrinogen, interfered with the measurement of antibody titers. Therefore, only serum should be used in further investigations of THP antibody using this assay.
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PMID:Tamm-Horsfall protein antibody in patients with end-stage kidney disease. 739 72

A man, aged 34, was treated in 1954 for duodenal ulcer by antroduodenectomy followed by X-irradiation to the stomach in a dose of 2,000 rads. Over two decades, he developed several conditions attributable to the previous irradiation, including the physical appearances of premature ageing, shrinkage of the left kidney due to irradiation nephritis, immune deficiency, multiple myeloma of IgA type, and lastly, carcinoma of the stomach. The kidneys, especially the left, the bone marrow and stomach would have been in the field of X-irradiation. These effects of local X-irradiation are discussed in relation to the known effects of total body irradiation in causing decreased longevity in animals and inducing cancer in man.
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PMID:Multiple myeloma and gastric carcinoma. Possible late effects of limited abdominal X-irradiation. 745 10


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