Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ANCA positive sera, detected by the standard immunofluorescence method, derived from 37 patients with vasculitis were studied using formalin-acetone fixed chronic myelocytic leukemia cells (CML). All 37 sera were positive on CML cell smears. Furthermore formalin-actone fixation selectively impaired antinuclear antibody binding without reducing ANCA staining and thus facilitated differentiation of these autoantibodies which is often difficult with the standard immunofluorescence method. Two unequivocal and mutually exclusive ANCA binding patterns were identified using the CML smears: (1) type I with diffuse granular binding confined to the polymorphonuclear (PMN) cell lineage and preferentially staining immature cells; (2) type II with similar binding to the PMN cell lineage and, in addition, granular staining of the basophils. All type I antibodies were associated with a c-ANCA pattern suggesting that the major antigen recognized by these antibodies, recently identified as proteinase 3, is not detectable in basophils. The type II pattern was detected in both p-ANCA (84%) and c-ANCA (16%) positive sera. The type I sera remained positive on PMN cells from a myeloperoxidase (MPO) deficient subject and anti-MPO antibodies could not be detected in this group by ELISA. Conversely the type II pattern occurred in the presence of anti-MPO antibodies identified by immunofluorescence, ELISA and dot-blot with the exception of a single serum with antilactoferrin antibody. Type I binding only was observed in Wegener's granulomatosis (WG) but both patterns were found in microscopic polyarteritis (MPA) and rapidly progressive glomerulonephritis (RPGN).
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PMID:Determination of anti-neutrophil cytoplasm antibodies (ANCA) specificity by immunofluorescence on chronic myelocytic leukemia cells. 131 34

A 43-year-old man developed the nephrotic syndrome 26 months after allogeneic bone-marrow transplantation for chronic myeloid leukemia. This occurred during an exacerbation of graft-versus-host disease (GVHD) and both problems remitted after therapy with cyclosporine and prednisolone. Renal biopsy showed ultrastructural and immunofluorescence evidence of membranous nephropathy. Anti-nuclear antibodies (but not antiglomerular or anti-renal tubular epithelial antibodies) were detected in his serum. Experimental GVHD in mice has been associated with immune complex glomerulonephritis and the presence of IgG autoantibodies which has been attributed to abnormal T (donor)/B (recipient) cell co-operation. This association can be extrapolated to the human GVHD where autoantibody formation is better described than immune complex glomerulonephritis.
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PMID:Membranous nephropathy with graft-versus-host disease in a bone marrow transplant recipient. 156 14

An 81-year-old woman was admitted, complained general malaise, and edema on face and lower extremities. In the peripheral blood, leucocytosis (17,220/mm3), microcytic hypochromic anemia (RBC 348 x 10(4)/mm3, Hb 9.6 g/dl, Ht 29.2%), and thrombocytosis (130 x 10(4)/mm3) were present, and many myeloid cells containing of myeloblasts, promyelocytes and so on were observed. Bone marrow aspiration revealed increment of the myeloid series without hiatus leukemia . The Neutrophil Alkaline Phosphatase score and rate was low, and on bone marrow scintigram using indium chloride, liver and extremities were shown. On admission, proteinuria (21.5 g/dl) and hypoalbuminemia (2.5 g/day) were pointed out, and the renal biopsy specimen showed membraneous proliferative glomerulonephritis (MPGN), so we diagnosed this case that chronic myelogenous leukemia (CML) complicated with nephrotic syndrome. At first, she was treated with prednisolone, but proteinuria was not entirely improved, then busulfan was given, myeloid cells in peripheral blood were disappeared and proteinuria was gradually decreased. From this coarse, the causality between CML and nephrotic syndrome was verified.
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PMID:[A case of chronic myelogenous leukemia complicated with nephrotic syndrome]. 252 82

An adolescent with chronic myelogenous leukemia (CML) developed gross hematuria. Evaluation included renal biopsy revealing a proliferative glomerulonephritis with mesangial deposits of immunoglobulins A and G. An association between CML and immune-complex glomerulonephritis has not been previously reported and may represent a paraneoplastic phenomenon.
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PMID:Glomerulonephritis and chronic myelogenous leukemia. 297 36

A patient with chronic myelogenous leukemia was initially seen with nephrotic syndrome. Minimal-change glomerulonephritis was verified by open renal biopsy, and the patient showed good response to treatment with a diuretic and prednisone. We believe this represents the first reported case of nephrotic syndrome in myelogenous leukemia.
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PMID:Chronic myelogenous leukemia with nephrotic syndrome. 657 79

We reported a 27-year-old man who developed nephrotic syndrome 12 months after a bone marrow transplantation from his HLA-identical sister for chronic myelocytic leukemia. Anti-nuclear antibodies had been serially investigated after the bone marrow transplantation. They were detected in his serum 5 months before the appearance of proteinuria, but he tested negative at the onset of nephrotic syndrome. Histological analysis of the renal biopsy revealed subepithelial and subendothelial immune deposits in the glomerular basement membrane with increased mesangial matrix and cells. These findings suggested immune complex glomerulonephritis due to chronic graft-versus-host disease (GVHD) after bone marrow transplantation. In murine experimental chronic GVHD, anti-nuclear antibodies, which generate immune complexes that deposit or form in the kidney have been detected.
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PMID:[A case of nephrotic syndrome after bone marrow transplantation]. 919 64

Advanced glycation end products (AGE) contribute to diabetic tissue injury by two major mechanisms, i.e., the alteration of extracellular matrix architecture through nonenzymatic glycation, with formation of protein crosslinks, and the modulation of cellular functions through interactions with specific cell surface receptors, the best characterized of which is the receptor for AGE (RAGE). Recent evidence suggests that the AGE-RAGE interaction may also be promoted by inflammatory processes and oxidative cellular injury. To characterize the distributions of AGE and RAGE in diabetic kidneys and to determine their specificity for diabetic nephropathy, an immunohistochemical analysis of renal biopsies from patients with diabetic nephropathy (n = 26), hypertensive nephrosclerosis (n = 7), idiopathic focal segmental glomerulosclerosis (n = 11), focal sclerosis secondary to obesity (n = 7), and lupus nephritis (n = 11) and from normal control subjects (n = 2) was performed, using affinity-purified antibodies raised to RAGE and two subclasses of AGE, i.e., N(epsilon)-(carboxymethyl)-lysine (CML) and pentosidine (PENT). AGE were detected equally in diffuse and nodular diabetic nephropathy. CML was the major AGE detected in diabetic mesangium (96%), glomerular basement membranes (GBM) (42%), tubular basement membranes (85%), and vessel walls (96%). In diabetic nephropathy, PENT was preferentially located in interstitial collagen (90%) and was less consistently observed in vessel walls (54%), mesangium (77%), GBM (4%), and tubular basement membranes (31%). RAGE was expressed on normal podocytes and was upregulated in diabetic nephropathy. The restriction of RAGE mRNA expression to glomeruli was confirmed by reverse transcription-PCR analysis of microdissected renal tissue compartments. The extent of mesangial and GBM immunoreactivity for CML, but not PENT, was correlated with the severity of diabetic glomerulosclerosis, as assessed pathologically. CML and PENT were also identified in areas of glomerulosclerosis and arteriosclerosis in idiopathic and secondary focal segmental glomerulosclerosis, hypertensive nephrosclerosis, and lupus nephritis. In active lupus nephritis, CML and PENT were detected in the proliferative glomerular tufts and crescents. In conclusion, CML is a major AGE in renal basement membranes in diabetic nephropathy, and its accumulation involves upregulation of RAGE on podocytes. AGE are also accumulated in acute inflammatory glomerulonephritis secondary to systemic lupus erythematosus, possibly via enzymatic oxidation of glomerular matrix proteins.
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PMID:Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease. 1096 90

A 15-year-old boy developed nephrotic syndrome and acute renal failure 4 years after allogenic bone marrow transplantation (BMT) for lymphoid crisis of chronic myelocytic leukemia. On admission, he presented with clinical features of chronic GVHD including transient exacerbation of cholestatic liver injury. Renal biopsy showed diffuse proliferative glomerulonephritis with cellular crescents. The patient was treated with methylprednisolone pulse therapy (1 g/day, for 3 days) followed by oral prednisolone. Renal function gradually improved but nephrotic state was persistent. A second renal biopsy showed improvement of acute tubular necrosis and endocapillary proliferation and transformation of crescents into a fibrous form. After tapering of oral prednisolone, cyclophosphamide was started, which resulted in a gradual improvement of proteinuria. Several cases of nephrotic syndrome occurring after BMT have already been reported, but most cases had membranous nephropathy. In our case, renal biopsy revealed diffuse proliferative glomerulonephritis with findings of active cellular immunity, and aggressive treatment resulted in attenuation of these findings. Moreover, chronic GVHD-related liver injury was noted at the time of this episode. Our findings suggest that chronic GVHD may be complicated with diffuse proliferative glomerulonephritis through unknown cellular immune mechanism.
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PMID:Diffuse proliferative glomerulonephritis after bone marrow transplantation. 1235 94

Graft-versus-host disease (GVHD) is one of the most frequent complications that occur after hematopoietic stem cell transplantation (HSCT). Recently, renal involvement, including membranous nephropathy, focal segmental glomerulosclerosis, and minimal change disease, has been described as a manifestation of chronic GVHD. This case report describes a patient who developed antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis after HSCT. Following preparation with chemotherapy, a 29-year-old man with chronic myeloid leukemia underwent allogenic peripheral blood stem cell (PBSC) transplantation, after which first acute and then chronic GVHD developed. Treatment with prednisone resulted in improvement in the patient's GVHD. After the termination of steroid therapy and about 10 months after PBSC transplantation, nephritic syndrome appeared and the patient's serum creatinine value increased to 1.7 mg/dL. Laboratory evaluation revealed perinuclear antineutrophilic cytoplasmic antibody (p-ANCA) in the serum. Histological examination of renal biopsy tissue showed focal segmental proliferative glomerulonephritis with glomerulosclerosis in 20% of available glomeruli, large cellular crescents in 6% of glomeruli, and no staining of immunoglobulins or complement along the capillary walls. Electron microscopy revealed no immune deposits. After treatment with prednisone 60 mg/d, diltiazem 120 mg/d, and enalapril 10 mg/d, the proteinuria gradually decreased, and p-ANCA was undetectable. These findings suggest that in this patient the ANCA-associated glomerulonephritis was associated with renal involvement that occurred during the course of chronic GVHD.
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PMID:Antineutrophil cytoplasmic antibody-associated glomerulonephritis in chronic graft-versus-host disease after allogenic hematopoietic stem cell transplantation. 1621 51

Emergency plasma exchange therapy is life saving in many cases. Therefore, clinicians must be aware of the indications at which any delay in initiating therapy may prove to be fatal. Different hematological (Moschkowitz-, hyperviscosity- and catastrophic antiphospholipid syndrome; massive haemolysis [e.g Wilson's disease]), neurological (myasthenic), endocrine (thyrotoxicosis) and nephrological (rapidly progressive glomerulonephritis) crisis situations and for prevention of them; certain poisonings, fulminant liver failure, severe pancreatitis due to chylomicronaemia, meningococcus sepsis and iatrogenic or suicidal drug-overdose. In this latter, it is of fundamental importance that the protein binding of the drug should be high (>80%), whereas the volume of its distribution should be relatively low (<0,2 l/kg body weight) and the endogenous clearance of it should be less, than 500 ml/min. Urgent leukocytapheresis should be performed above 50.000 blasts/microl, in acute or chronic myeloid leukemia if symptoms of leukostasis are present (if blasts are above 100.000/microl, cytoreduction is mandatory even without symptoms). Similarly, urgent thrombocytapheresis should be administered above platelet numbers 1000 G/l, when there is concomitant thrombophilia or clinical symptoms of thrombostasis are present.
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PMID:[Indications of urgent plasma exchange and cytapheresis therapies--a review based on literature data and personal experience]. 1706 1


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