Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal failure secondary to tumor infiltration of the kidneys is uncommon and largely described in patients with lymphoma or leukemia. We report a 64-year-old man previously diagnosed with limited stage small cell lung cancer who presented with acute renal failure (ARF). Renal imaging showed bilateral enlargement with features suggestive of an infiltrative process. A kidney biopsy established the diagnosis of metastatic small cell lung cancer with diffuse renal parenchymal infiltration. This case emphasizes the rare potential for cancers to metastasize to the kidneys, which can result in ARF. Early recognition of this cause of ARF is crucial, in particular, when the tumor is amenable to chemotherapy or irradiation.
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PMID:Acute renal failure secondary to small cell lung cancer with tumor infiltration of the kidneys. 1670

A 46-year-old previously healthy woman was diagnosed with acute lymphoblastic leukaemia. The induction phase was complicated by alpha-haemolytic streptococcal bacteremia which responded to antibacterial therapy. Subsequently, the patient developed pneumonie due to Chlamydiapneumoniae which responded to macrolides. Following this infection the patient developed recurrent fever and new pulmonary infiltrates were noted. Bronchoscopy was performed and treatment was administered with liposomal amphotericin B (L-AmB, AmBisome) for two days, but was complicated by acute renal failure. Aspergillus fumigatus was cultured from bronchoalveolar lavage fluid [corrected] L-AmB was discontinued and voriconazole and caspofungin were administered. Despite aggressive antifungal therapy the patient developed progressive invasive infection, with central nervous system involvement as well as lesions appearing in the kidneys and liver. The patient died one week following the diagnosis of aspergillosis.
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PMID:Disseminated invasive aspergillosis in a patient with acute leukaemia. 1691 60

Acute tubulointerstitial nephritis usually develops due to either acute infection of kidneys or delayed hypersensitivity reaction to medication and may rarely be associated with acute renal failure. The disease may very rarely be associated with hematologic/neoplastic diseases. Tubulointerstitial nephritis associated with leukemia is usually due to chemotherapeutic agents or viral infections of the severely immuno-compromised host mostly after bone marrow transplantation. We herein report 2 cases of acute tubulointerstitial nephritis associated with acute leukemia. To our knowledge, the cases are the first in literature in which acute tubulointerstitial nephritis was simultaneously diagnosed with acute leukemia without any chemotherapeutic insult or apparent viral infection. Despite the usual asymptomatic nature of the disease process, the cases are original in that acute tubulointerstitial nephritis associated with acute leukemia resulted in acute renal failure in both cases and hemodialysis was inevitable in one.
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PMID:Acute tubulointerstitial nephritis and acute leukemia: report of 2 cases. 1704 12

To prevent acute renal failure in children at risk for developing tumor lysis syndrome due to acute lymphoblastic leukemia or non-Hodgkin's lymphoma treated according to international BFM protocols, we investigated recombinant urate oxidase (rasburicase) in the first Central European openlabeled, prospective, multicenter phase IV trial. Rasburicase was administered intravenously, at 0.2 mg/kg for 5 consecutive days to 36 patients. Blood levels of uric acid, creatinine, phosphorus, calcium, lactate dehydrogenase and complete blood count were measured daily during rasburicase treatment and on days 6, 7 and 12. Initial uric acid level decreased significantly by 4 hours (from 343 micromol/L to 58 micromol/L, p<0.001), except for one steroid-resistant patient who required hemodialysis on day 14 after having introduced combined cytostatic treatment. Comparing the data of a subgroup of 12 patients receiving rasburicase with that of a historic cohort of 14 patients treated with allopurinol indicated the superiority of rasburicase over allopurinol in prophylaxis and treatment of hyperuricemia in children with leukemia and lymphoma.
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PMID:Prevention and treatment of hyperuricemia with rasburicase in children with leukemia and non-Hodgkin's lymphoma. 1738 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

Acute renal failure is a well-recognized complication of acute leukaemias. Howevcr, serious renal failure caused by leukaemic infiltration as a primary manifestation is unusual. Here we report two patients with acute lymphoblastic leukaemia presenting with acute renal failure due to leukaemic infiltration. The first patient died before the administration of specific therapy for leukaemia, whereas the second case recovered after chemotherapy. She was discharged without necessitating dialysis therapy.
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PMID:Acute lymphoblastic leukaemia presenting with acute renal failure: report of two cases. 1884 3

CD4+CD56+ haematodermic neoplasms (HDN) constitute a rare disease characterized by aggressive clinical behaviour and a poor prognosis. Tumour cells from HDN are leukaemic counterparts of plasmacytoid dendritic cells (pDCs). Despite increased knowledge of the ontogenetic origin of these tumours, the genetic causes and oncogenic signalling events involved in malignant transformation are still unknown. To delineate novel candidate regions and disease-related genes, we studied nine typical CD4+CD56+ HDN cases using genome-wide high-resolution array comparative genomic hybridization (CGH). Genomic imbalances, which were predominantly losses, were frequently detected. Gross genomic losses or gains involving an entire chromosome were observed in eight cases. The most frequent imbalances were deletions of chromosome 9, chromosome 13 and partial losses affecting 17p or 12p. Combinations of deletions of tumour suppressor genes (TSG), namely RB1, CDKN1B (p27), CDKN2A, (p16(ink4a), p14(arf)) or TP53 (p53), were observed in all cases. These results indicate that deletion events altering G1/S regulation are crucial for HDN oncogenesis. Furthermore, in addition to frequent sporadic gene losses, in one case we observed a 8q24 interstitial deletion that brought MYC closer to miR-30b/miR-30d, which may be related to their deregulation. Taken together, these results indicate that in addition to frequent G1/S checkpoint alterations, various genetic events could contribute to the chemoresistance of the tumour.
Leukemia 2009 Apr
PMID:Recurrent genomic aberrations combined with deletions of various tumour suppressor genes may deregulate the G1/S transition in CD4+CD56+ haematodermic neoplasms and contribute to the aggressiveness of the disease. 1915 33

Clofarabine, a nucleoside analogue for treatment of relapsed leukemia, is 50-60% excreted in urine. Clofarabine has not been studied in patients on hemodialysis. We measured levels in one patient in acute renal failure. Prior to dialysis, 43 hr after a 40 mg/m(2) infusion, plasma concentration was 139 ng/ml. One hour after beginning hemodialysis, a 20 mg/m(2) infusion began. Plasma concentrations were 84.2, 81.1, and 88.0 ng/ml while the dialysis and clofarabine infusion occurred simultaneously. Post-dialysis, while the clofarabine was still infusing, the level was 95.8 ng/ml. Hemodialysis does decrease clofarabine levels, but given its large volume distribution, hemodialysis may not be effective for clofarabine overdose.
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PMID:Effect of hemodialysis on the plasma levels of clofarabine. 2023 28

Acyclovir is an effective, frequently used antiviral agent. Adverse effects of this drug are well known and are especially seen with high doses and/or dehydration. In this article, we report a 6-year-old boy with leukemia with nonoliguric acute renal failure in normal hydration status after using acyclovir treatment. He had no preexisting renal impairment, and there were no additional symptoms. Dimercaptosuccinic acid radionucleid scyntigraphy and other laboratory findings revealed impairment of proximal tubule function, in addition to distal tubule. We emphasize that renal functions should be monitored carefully during treatment with acyclovir, and asymptomatic nephrotoxicity must be kept in mind.
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PMID:Acute renal failure with acyclovir treatment in a child with leukemia. 2030 48

Acute tumor lysis syndrome (ATLS) is a potentially lethal condition precipitated by the massive release of intracellular components such as nucleic acids, potassium, and phosphorus, following a rapid and widespread lysis of tumor cells. Herein, the authors describe the high incidence and characteristic histopathologic lesions of acute ATLS in p53-deficient mice used in 2 short-term carcinogenicity studies. ATLS was a frequent cause of early death in p53 (+/-) mice in these studies and was consistently associated with the presence of disseminated lymphoma and leukemia. Although a heavy tumor burden and leukemia were present in all affected mice, the absence of ATLS in other mice with equally severe lymphoma and leukemia indicates that these tumor burdens are necessary but insufficient to cause ATLS in mice. The hallmark histopathologic findings of ATLS in mice are the disseminated microemboli composed of nuclear and cytoplasmic debris derived from lysed tumor cells. The mechanical obstruction of capillary beds by these microemboli appeared to be the proximate cause of the early deaths of mice in these studies. Microemboli may contribute to the pathogenesis of acute renal failure and other clinical signs associated with ATLS in other species. Recognition of ATLS in laboratory animals is critical in studies intended to evaluate the efficacy and/or toxicity of anticancer treatments, where early deaths due to ATLS might otherwise be attributed to test article toxicity. Further studies on the role of microemboli in the pathogenesis of ATLS may elucidate pathogenetic mechanisms and lead to improved approaches to clinical management and treatment of this potentially lethal condition.
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PMID:Spontaneous acute tumor lysis syndrome as a cause of early deaths in short-term carcinogenicity studies using p53 +/- mice. 2043 82


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