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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nephrotic syndrome complicating malignancy in the absence of renal vein thrombosis, amyloid or neoplastic infiltration of the kidney is an unusual occurrence. A case of diffuse, well differentiated, lymphocytic lymphoma and lipoid nephrosis documented by light microscopy, electron microscopy and immunofluorescent studies is reported. A review of the literature revealed 76 case reports in which the nephrotic syndrome was associated with neoplasia. The most frequently associated neoplasms are Hodgkin's disease, various carcinomas, nonHodgkin's lymphoma and leukemia in descending order. The most frequent renal lesion in patients with the nephrotic syndrome associated with various carcinomas is membranous glomerulonephritis (81 per cent) as opposed to patients with lymphomas or leukemias who have predominantly lipoid nephrosis (60 per cent). The evidence is reviewed suggesting that the lesions in membranous nephropathy are immunologically mediated by tumor or viral antigen-antibody complexes and in lipoid nephrosis perhaps by a defect in t-lymphocyte function.
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PMID:The nephrotic syndrome associated with neoplasia: an unusual paraneoplastic syndrome. Report of a case and review of the literature. 18 Aug 1

A review is presented of the association between a glomerular disease and a malignancy. The incidence of Hodgkin's disease in patients with glomerulopathy is very low, but the incidence of a solid tumour in a patient with glomerulopathy varies between 3 and 13%, mean 7%, and may be as high as 22% in patients over 60 years of age with a membranous nephropathy. A solid tumour was found most frequently in patients with membranous nephropathy. On the other hand, minimal change nephropathy is often associated with Hodgkin's disease and membrano-proliferative glomerulopathy with chronic lymphatic leukaemia. In Hodgkin's disease-associated glomerulopathy, a defect in the function of T lymphocytes is probably important, but the precise pathogenesis has not yet been elucidated. The other glomerulopathies may be mediated by immune complexes, containing tumour-derived antigens and their antibodies, either formed in situ or deposited as complexes from the circulation.
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PMID:Glomerulopathy as a paraneoplastic phenomenon. 267 59

The first case of imported visceral leishmaniasis in the dog in Denmark, and probably in Scandinavia, is described. The dog, a 5-year-old female wire-haired bird dog, became ill about 21 months after it had returned from a year's stay in Spain (Malaga). The clinical signs were fever, lameness, enlargement of the popliteal lymph nodes and weight loss. A tentative clinical diagnosis of leukaemia was discarded after the microscopic recognition of Leishmania organisms in a biopsy from a popliteal lymph node (Fig. 1). The diagnosis was confirmed by the demonstration of the kinetoplast in the organisms by electron microscopy (Fig. 3 a-b). The organisms measured about 2 micron in diameter indicating that the species in question was Leishmania donovani infantum, which is indigenous to Spain and other Mediterranian countries. The dog was killed, and Leishmania were found in sections of mesenteric and popliteal lymph nodes, spleen, liver, lung and kidneys. The most interesting histologic features were interstitial nephritis, dominated by numerous plasma cells and membranous glomerulonephritis (Fig. 2). It is suggested that the glomerulonephritis is immune complex-mediated as it is in human visceral leishmaniasis. The risk of bringing dogs in and out of the Mediterranean region is stressed, and veterinarians are advised to have leishmaniasis in mind when they are confronted with dogs taken ill with non-specific symptoms after a stay in that part of the world, even if as much as two years have elapsed between the return and the onset of clinical signs.
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PMID:Imported canine visceral leishmaniasis in Denmark. 399 51

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 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

Human T-cell leukaemia virus type-1 (HTLV-1) is known to cause adult T-cell leukaemia. The prevalence of anti-HTLV-1 antibody in haemodialysis patients has been reported to be higher than that in the general population. The anti-HTLV-1 antibody-positive rate in patients with primary glomerulonephritis in the Nagasaki district, an endemic area of HTLV-1, was evaluated. The antibody-positive rates in patients with primary glomerulonephritis (9.9%) and in haemodialysis patients (18.4%) were significantly higher than the rate in general blood donors (6.6%). Of 142 patients with primary glomerulonephritis, 14 (9.9%) were positive for the antibody; histological evaluation of these patients showed minor glomerular abnormality in one, mesangial proliferative glomerulonephritis in eight (IgA nephropathy in six and non-IgA nephropathy in two), membranous nephropathy in three, and crescentic glomerulonephritis in two. Evaluation of 10 antibody-positive patients by immunofluorescent microscopy showed immunocomplex-type nephritis in nine, suggesting the involvement of HTLV-1-associated antigen in the development and progression of glomerulonephritis.
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PMID:Evaluation of anti-HTLV-1 antibody in primary glomerulonephritis. 777 59

We report on a patient with an almost 20-year history of B chronic lymphocytic leukemia (B-CLL). During the last 2 years, the patient developed nephrotic syndrome (NS) due to membranous glomerulonephritis (MN), refractory to standard therapeutic regimens. Neither NS nor B-CLL responded objectively to systemic administration of two different combinations of corticosteroids and alkylating agents (chlorambucil, cyclophosphamide). Third-line therapy with cyclosporin A resulted in reduction of proteinuria and improvement of leukemia. Withdrawal of the drug led to an increase in leukocyte count.
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PMID:Effect of cyclosporin A in a patient with refractory nephrotic syndrome associated with B chronic lymphocytic leukemia. 885 99

Nephrotic syndrome occurs rarely after bone marrow transplantation. We describe three patients with myeloid malignancy who developed nephrotic syndrome from 5, 22 and 25 months after allogeneic stem cell transplantation (SCT), confirmed by electron microscopy as membranous glomerulonephritis in two and minimal change glomerulonephritis in one. Proteinuria was initially severe in all and clinically distinct from prior graft-vs.-host disease in two patients. While all responded initially to prednisolone and cyclosporine therapy, two recipients with high-risk leukemia developed late solid organ and bone marrow relapse of their disease, which ultimately proved fatal. The third patient remains alive and disease-free with minimal proteinuria off immunosuppressive therapy. Hence, the onset of de novo high-grade proteinuria after allogeneic SCT should prompt renal histological confirmation, and a trial of immunosuppressive therapy after other causes of nephritic syndrome have been excluded.
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PMID:Nephrotic syndrome after stem cell transplantation. 1565 48

Kidney disease frequently complicates malignancy and its treatment. Although many solid and hematologic cancers may involve the renal parenchyma, clinical sequelae are usually not prominent. Published reports cite membranous nephropathy as the most common malignancy-associated glomerulopathy, occurring with many carcinomas and occasionally with leukemia and lymphoma followed by minimal change disease. Rarely membranoproliferative glomerulonephritis (MPGN) has been reported in patients with malignancy. The mechanism by which malignancy induces disease remains unproved, but may involve deposition of tumor antigen in the subepithelial space with in situ immune complex formation and subsequent complement activation. Treatment of the underlying malignancy may lead to resolution of nephrotic syndrome, lending indirect support to this theory. We report a rare autopsy case of a patient with metastatic carcinoma (with unknown primary) associated with MPGN. The association between MPGN and metastatic carcinoma with unknown primary is uncommon and has not been previously reported in the literature.
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PMID:Membranoproliferative glomerulonephritis in a carcinoma with unknown primary: an autopsy study. 1860 90

A 56-year-old man presented with peripheral monocytosis and massive nephrotic syndrome. He was diagnosed as having chronic myelomonocytic leukemia and membranous glomerulonephritis. He received prednisone, chlorambucil and hydroxyurea, but the nephrotic syndrome persisted. Seven months after diagnosis, he was started on cyclosporin A; 1 month later he developed acute renal failure due to radiolucent bilateral renoureteral stones. His kidney function recovered after placing ureteral catheters and urine alkalization. Afterward, he was given mycophenolate mofetil, and proteinuria decreased to subnephrotic levels (1 g/24 hours). This case highlights 2 severe renal complications in this type of leukemia. To the best of our knowledge, there are only 2 previous cases of glomerulonephritis, histologically proven, associated with chronic myelomonocytic leukemia. On the other hand, reversible acute renal failure due to radiolucent bilateral renoureteral stones has never been reported. Also, as far as we know, mycophenolate mofetil was successfully used here for the first time for treating glomerulonephritis-related chronic myelomonocytic leukemia.
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PMID:Severe renal complications in chronic myelomonocytic leukemia. 1865 53


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