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)

The effect of acute and chronic renal failure on cell proliferation in rapidly dividing tissues has been examined in man and animal models. The evidence reviewed supports the hypothesis that renal failure results in a general inhibition of cell proliferation. Cell population kinetic studies of gastrointestinal and skin epithelia in experimental acute renal failure show a prolongation of the cell generation cycle. Less detailed investigations of other proliferative cell systems indicate an inhibitory effect on proliferation within the generative compartment of the erythroid series, lymphoid tissue, seminiferous epithelia and wound granulation tissue. This inhibition appears partly responsible for anaemia and impaired wound healing and may contribute to the abnormal immune responses, gastrointestinal tract lesions and male sterility found in renal failure.
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PMID:Inhibition of cell proliferation in renal failure and its significance to the uraemic syndrome: a review. 122 2

Forty-nine children with recurrent acute lymphoblastic leukemia (ALL) were entered into a randomized Phase II trial evaluating 2'-deoxycoformycin (dCF) alone or in combination with adenine arabinoside (ara-A). 2'-Deoxycoformycin is an inhibitor of adenosine deaminase (ADA), an enzyme found in relatively high amounts in malignant lymphoid cells. Ara-A inhibits DNA polymerase and DNA synthesis. Because its efficacy in vivo as an anticancer agent is limited by its rapid inactivation by ADA, ara-A was combined with dCF to produce cytoreductive levels of ara-A. Twenty-four patients were assigned to receive dCF alone and 25 to receive the combination. No patient responded to dCF alone, and one patient developed a complete remission after treatment with the combination. The toxicity of dCF alone was minimal, except for one patient who became obtunded on day 5 following the first cycle of therapy. In contrast, five patients developed severe toxicity with the combination, including renal failure (three patients), hepatic failure (three patients), and neurologic toxicity (two patients). These results indicate that, at the doses and schedule used in this study, the combination of dCF and ara-A has significant toxicity and minimal activity against recurrent ALL in children.
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PMID:Lack of significant activity of 2'-deoxycoformycin alone or in combination with adenine arabinoside in relapsed childhood acute lymphoblastic leukemia. A randomized phase II trial from the Childrens Cancer Study Group. 144 10

This report deals with an unusual case of primary macroglobulinemia with hypercalcemia, chronic renal failure and systemic amyloidosis. In May 1990, a 63-year-old male was transferred to our hospital because of hypercalcemia (13.5 mg/dl) and renal failure. Clinical examinations showed anemia, macroglossia, lymph node swellings and hepatomegaly. Laboratory findings included Bence-Jones (kappa type) proteinuria (0.8 g/day), a monoclonal gammopathy of the IgM-kappa type (2.8 g/dl), a proliferation of lymphoid cells in the peripheral blood (5%) and the bone marrow (59.6%), and lymphomatous involvement of an inguinal lymph node. Serum creatinine concentration was 8.5 mg/dl. The serum levels of parathormone and vitamin D3 metabolites were normal. The roentgenogram of bones showed a compression fracture of the lumbar spine and systemic osteoporosis. The treatment included eel calcitonin, prednisolone and the CHOP regimen, followed by hemodialysis and plasmapheresis. The serum level of IgM increased to 4.6 g/dl. The patient died three months later and postmortem examination demonstrated marked systemic amyloidosis.
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PMID:[Primary macroglobulinemia with hypercalcemia, renal failure and systemic amyloidosis]. 146 88

A patient with chronic T-cell leukemia characterized by a suppressor phenotype is reported. A 71-year-old woman presented with symptoms and signs of hypercalcemia. Peripheral blood specimen showed abnormal lymphoid cells with an oval to cleaved nucleus, rather condensed chromatin, occasional prominent nucleolus, and basophilic cytoplasms with vacuoles which seems to be a T-cell counterpart of B-cell chronic lymphocytic leukemia with mixed cell types. The phenotype of these cells was CD4-, CD8+, CD5+, CD6+ with poor expression of CD3, CD7, and CD25. Southern blot analysis of T-cell receptor beta-chain gene revealed one allele rearranged band. The serum antibodies were positive against human T-cell leukemia virus, type I-associated antigens, but monoclonal integration of proviral DNA was not detected in the leukemic cells suggesting that she was just a carrier of this virus. Interestingly, serum PTH-related peptide (PRP) was elevated. The combination therapy with vincristine and prednisolone for leukemia decreased not only the number of leukemic cells but also the serum PRP levels. The clinical course was aggressive. She only responded transiently to treatments, and died of renal failure due to uncontrollable hypercalcemia six weeks after admission.
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PMID:A patient of CD4-/CD8+ chronic T-cell leukemia associated with hypercalcemia. 182 9

A patient with chronic myelogenous leukemia (CML) in lymphoid blast crisis developed acute tumor lysis syndrome following administration of high-dose busulfan, cyclophosphamide and cytarabine (Ara-C) in preparation for allogeneic bone marrow transplantation. Preconditioning cytoreduction, close monitoring and rapid institution of therapeutic measures were required to avoid renal failure and a fatal outcome. Acute tumor lysis syndrome has not been reported in marrow transplant patients receiving conventional preparative regimens as treatment for CML in blast crisis, and it is likely that its occurrence in this patient was precipitated by high-dose Ara-C.
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PMID:Acute tumor lysis syndrome in a patient with chronic myelogenous leukemia in blast crisis: role of high-dose Ara-C. 208 2

Patients with chronic renal failure who were undergoing dialysis were recently shown to have a low prevalence of duodenal Helicobacter (Campylobacter) pylori colonisation in spite of a high incidence of gastric metaplasia. The prevalence of the organism in the gastric antrum of 50 similar patients was estimated and compared with that in a control group comprising 120 consecutive patients with no renal failure who were being investigated for a variety of symptoms and signs related to the upper alimentary tract. Seventeen of the patients with renal disease had upper gastrointestinal symptoms. The prevalence of antral H pylori was significantly less in patients with renal disease (12, 24%) than in the control group (51, 42%), but was associated with a similar active chronic inflammatory reaction with prominent lymphoid follicles. The prevalence of the bacteria in patients with renal disease was similar to that reported in normal volunteers, and was the same whether the patients had upper gastrointestinal symptoms or not. This low prevalence may be related to the wide variety of medication, including antibiotics, which these patients are prescribed during the course of their illness.
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PMID:Antral Helicobacter pylori in patients with chronic renal failure. 237 Mar 8

In order to maintain adequate circulating numbers of blood cells, the bone marrow must produce billions of cells each day and must be able to rapidly increase production by 10-20-fold in response to infection and hemorrhage. The existence of circulating factors that regulate this process has been suspected for over 100 years. Recently, the genes encoding these growth factors were cloned and their functions are now identified. Interleukin-3 (IL-3) acts on the most primitive hematopoietic stem cell, driving this self-renewing cell to produce progeny of all hematopoietic lineages. Granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulates the granulocyte-macrophage progenitor cell, as well as cells committed to the erythroid lineage, to differentiate. G-CSF and M-CSF stimulate the most differentiated myeloid progenitors to produce granulocytes and monocytes/macrophages, respectively. Erythropoietin stimulates the differentiation of late erythroid progenitors. In the lymphoid progenitor lineage, IL-2 stimulates T cell differentiation; IL-4 and IL-6 stimulate differentiation of B cells. The colony-stimulating factors also enhance function and cause activation of the mature cells whose production they induce. In clinical trials, these hormones have successfully ameliorated anemia in renal failure, chronic disease, and in prematurity. They have improved pancytopenias in aplastic anemia, myelodysplastic syndromes, and congenital cytopenias, and they have hastened recovery from chemotherapy and bone marrow transplantation.
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PMID:Hematopoietic hormones: from cloning to clinic. 267 59

We report a case of Castleman's disease of multifocal plasma-cell type revealed by a severe general weakness, associated to a nephrotic syndrome with renal failure. The characteristic aspects of lymphoid hyperplasia with hyalinization of follicles and interfollicular vascular proliferation were observed in mesenteric lymph nodes, the spleen was involved by an infarcted localisation of Castleman's disease. The glomerular lesions were consistent with a proliferative mesangial glomerulonephritis. The removal of the spleen and of the mesenteric nodes involved by the disease, associated with a steroid course was curative. The nephrotic syndrome appears to be etiologically related to the presence of the Castleman's tumor. The removal of the tumor relieves the proteinuria and the renal failure as in other cases reported in the literature.
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PMID:[Castleman's disease and glomerular nephropathy (apropos of 1 case]. 269 15

The authors studied 35 marrow biopsies from 32 patients with rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, polymyositis, and psoriatic arthritis. Reasons for biopsy included cytopenia, fever of unknown origin, and malignancy. Cellularity was abnormal in 71%. Plasma cells were increased in 60% and associated with lymphoid aggregates. Immunoperoxidase stains showed polyclonal perivascular plasma cells and increased T-cells forming lymphoid aggregates. Two patients had granulomas without documented infection. Anemic patients had findings consistent with anemia of chronic disease, erythroid aplasia, hemolysis, and iron deficiency. Iron stores were variable. Platelet and granulocyte precursors were variably altered and did not predictably correlate with the presence, absence, or cause of thrombocytopenia and neutropenia. Myelodysplastic syndromes were present in two patients with rheumatoid arthritis. Osteomalacia and osteoporosis were seen, resulting from renal failure and steroids. Marrow findings are unpredictable and reflect the diverse causes of cytopenias in patients with connective tissue disorders.
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PMID:Bone marrow findings in connective tissue disease. 281 17

Eleven patients with rheumatoid arthritis that had been refractory to conventional drug therapy were treated with total lymphoid irradiation (TLI). Followup continued for 6 months in 9 patients, 12 months in 6 patients, and 24 months in 3 patients. At 6 and 12 months post-TLI, a significant improvement in clinical disease activity was demonstrated. Side effects noted during TLI included fatigue, nausea, diarrhea, and vomiting. One patient died of cardiorespiratory arrest, 2 patients died of kidney failure secondary to generalized amyloidosis, and 1 patient died of septic shock secondary to a multilocular septic arthritis. One patient experienced 2 episodes of septic arthritis; 2 patients manifested delayed wound healing. Immunologic assessments showed consistent lymphopenia in all patients. T lymphocyte subsets decreased after TLI, and showed a transient increase at 6 months post-TLI. The suppressed mitogen responsiveness, which was noted 2 months after irradiation, was found to increase almost to the pre-TLI levels at 12 months. The observed increase in morbidity and mortality after TLI is evidence that discourages the use of this therapeutic technique, at least in its present form.
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PMID:Total lymphoid irradiation in patients with refractory rheumatoid arthritis. 293 45


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