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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple myeloma disrupts calcium homeostasis by a variety of mechanisms, including bone destruction and resorption. This causes hypercalcemia. When left untreated, hypercalcemia leads to nephrocalcinosis, impairment of kidney function, and eventually renal failure. Some degree of renal dysfunction is common in myeloma patients. Here, we report case studies showing the efficacy and renal safety of the single-nitrogen bisphosphonate, ibandronate, for the treatment of hypercalcemia and/or nephrocalcinosis in multiple myeloma patients hospitalized with acute renal failure. Patients (n = 7) received either one or two intravenous infusions of ibandronate (2-6 mg). Ibandronate was well tolerated in all patients and returned elevated blood calcium levels to normal. Renal function improved for all patients and normalized in 3/7 patients. We conclude that ibandronate is involved in rapidly improving or restoring acute renal function and calcium levels to within the normal range in this patient population. To clarify the exact value of ibandronate, further investigation is warranted in randomized prospective trials.
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PMID:Ibandronate for the treatment of hypercalcemia or nephrocalcinosis in patients with multiple myeloma and acute renal failure: Case reports. 1701 34

Acute interstitial nephritis and rheumatoid arthritis (RA) or RA-like polyarthritis are among the very rare paraneoplastic manifestations of multiple myeloma (MM). A 47-year-old man with acute renal failure due to interstitial nephritis was admitted to our university hospital and successfully treated with corticosteroid. He later developed a symmetric distal polyarthritis with morning stiffness mimicking RA. On follow-up, the patient had a rise in serum creatinine, hypercalcemia, anemia, and a monoclonal spike (Bence Jones protein) on the urine protein electrophoresis. Bone marrow biopsy demonstrated a diffuse neoplastic plasma cell infiltration. Diagnosis of MM was made and the patient received chemotherapy. After four-course chemotherapy, the patient's articular manifestations resolved, urine monoclonal spike disappeared, and serum creatinine returned to a near normal level. We hypothesize that in this case, immunologic hypersensitivity reactions to the light-chain molecules or other tumoral antigens deposited within the kidney or joint spaces, in the context of MM cytokine milieu may have resulted in this unusual presentation. Ultimately, clinicians and pathologists should consider MM in the differential diagnosis of the acute interstitial nephritis and RA-like polyarthritis.
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PMID:Multiple myeloma presented as acute interstitial nephritis and rheumatoid arthritis-like polyarthritis. 1702 47

Of patients with newly diagnosed multiple myeloma, approximately 10% have dialysis-dependent acute renal failure, with cast nephropathy, caused by monoclonal free light chains (FLC). Of these, 80 to 90% require long-term renal replacement therapy. Early treatment by plasma exchange reduces serum FLC concentrations, but randomized, controlled trials have shown no evidence of renal recovery. This outcome can be explained by the low efficiency of the procedure. A model of FLC production, distribution, and metabolism in patients with myeloma indicated that plasma exchange might remove only 25% of the total amount during a 3-wk period. For increasing FLC removal, extended hemodialysis with a protein-leaking dialyzer was used. In vitro studies indicated that the Gambro HCO 1100 dialyzer was the most efficient of seven tested. Model calculations suggested that it might remove 90% of FLC during 3 wk. This dialyzer then was evaluated in eight patients with myeloma and renal failure. Serum FLC reduced by 35 to 70% within 2 hr, but reduction rates slowed as extravascular re-equilibration occurred. FLC concentrations rebounded on successive days unless chemotherapy was effective. Five additional patients with acute renal failure that was caused by cast nephropathy then were treated aggressively, and three became dialysis independent. A total of 1.7 kg of FLC was removed from one patient during 6 wk. Extended hemodialysis with the Gambro HCO 1100 dialyzer allowed continuous, safe removal of FLC in large amounts. Proof of clinical value now will require larger studies.
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PMID:Efficient removal of immunoglobulin free light chains by hemodialysis for multiple myeloma: in vitro and in vivo studies. 1722 9

Plasma cell leukemia is a rare form of malignant plasma cell dyscrasia. It can occur as a primary form without prior evidence of multiple myeloma or as a secondary form which is a terminal event in multiple myeloma. A case of primary plasma cell leukemia presenting as acute renal failure is reported here.
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PMID:Plasma cell leukemia presenting as acute renal failure: a case report. 1747 70

A 63-year-old woman was diagnosed as having multiple myeloma (MM), IgG-kappa type, stage IIIA, in October 2003. She achieved partial response after receiving three courses of VAD therapy and one course of high dose dexamethasone therapy (HDD); maintenance therapy consisted of melphalan and prednisolone. In November 2004, the patient developed spinal canal stenosis that required surgery. At the end of December 2004, the patient developed renal dysfunction that progressed to anuria. A CT scan showed multiple retroperitoneal masses that impinged on and obstructed both ureters and caused bilateral hydronephroses. Renal function improved after a right percutaneous nephrostomy and chemotherapy consisting of HDD, cyclophosphamide, vincristine, and doxorubicin. Nevertheless, the patient died due to MM in February 2005. On autopsy, multiple retroperitoneal and pelvic plasmacytomas with 13q- and t(4;14) (p16;q32) were found. Our patient is a rare case that, in the terminal stage of MM, developed aggressive phase multiple myeloma with extramedullary plasmacytomas that caused acute renal failure due to compression on both ureters.
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PMID:[Aggressive phase multiple myeloma with post-renal acute renal failure due to multiple extramedullary plasmacytomas]. 1769 6

A 59-year-old-woman received related non-myeloablative allogeneic peripheral blood stem cell transplantation (PBSCT) subsequent to autologous PBSCT in our hospital five years after she was diagnosed as oligo-secretory myeloma. She was admitted to our hospital because of vomiting and grayish diarrhea 4 months after non-myeloablative allogeneic PBSCT (mini-alloPBSCT). Although her initial symptoms improved after admission, she gradually showed thrombocytopenia, anemia, and oliguria during the 2 weeks after admission. Our diagnosis was thrombotic thrombocytopenic purpura (TTP) and acute renal failure (ARF) secondary to mini-alloPBSCT. After cessation of cyclosporine administration, we began to treat her with plasma exchange (PE) and hemodialysis. During the three and a half months after we started PE, the TTP gradually improved. Although PE had been reported to be ineffective for TTP post bone marrow transplantation, we could finally discontinue PE. In contrast, since her anuria continued, she was managed with hemodialysis. One month after PE was started, her activity of von Willebrand factor-cleaving protease was 41% (normal range, >50%) and the ultrasonographic investigation of both kidneys was normal. She could be discharged after four and a half months hospitalization and lived well as an outpatient for a further two months. She died shortly after readmission from multiple organ failure without the relapse of TTP. The patient's clinical course would suggest that TTP post mini-alloPBSCT could be treated with PE in some cases, despite the development of dialysis-requiring severe ARF being a poor prognostic factor.
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PMID:A case report of thrombotic thrombocytopenic purpura and severe acute renal failure post non-myeloablative allogeneic peripheral blood stem cell transplantation treated with plasma exchange and hemodialysis. 1784 2

Renal involvement is common in multiple myeloma. Although several types of renal disease are observed, most of them are considered to be specifically related to monoclonal immunoglobulin light chains. Myeloma cast nephropathy is the most frequent and sometimes associated with acute renal failure. AL amyloidosis and monoclonal immunoglobulin deposit disease are often presented as a nephrotic syndrome. In this review, we describe the pathogenesis and diagnosis of these three renal diseases. We also focus on the treatment of renal disease in multiple myeloma, in the view points of the chemotherapy to reduce M-protein and the prevention to reduce the risks of promoting renal injury.
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PMID:[Renal disease in multiple myeloma]. 1806 65

Hypercalcemia arises in the advanced stage of myeloma due to marked increase in osteoclastic bone resorption by local factors in the bone marrow, and is among the most serious complications in myeloma. It can progress rapidly and provoke acute renal failure and coma, which may become life-threatening. Early detection by serum calcium levels and treatment of hypercalcemia is important, although its clinical symptoms are difficult to distinguish from those in other underlying complications. Bisphosphonates, potent inhibitors of bone resorption, are recommended as the most effective therapy and have been approved for treatment of hypercalcemia in myeloma.
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PMID:[Hypercalcemia in myeloma]. 1806 68

Amyloidosis is a systemic disorder characterized by the extracellular tissue deposition of insoluble, toxic aggregates in bundles of beta-sheet fibrillar proteins. These deposits are typically identified on the bases of their apple-green birrefringence under a polarized light microscope after staining with Congo red, and by the presence of rigid, nonbranching fibrils 8 to 10 nm in diameter on electron microscopy. The type of amyloid fibril unit can be further defined by immunohistology or by immunoelectron microscopy. It has been described at least 25 different human protein precursors of amyloid fibrils, which will describe its corresponding amyloid disease. The most common types of amyloidosis are AL (primary) and AA (secondary) types; the former, is the most frequent and is due to deposition of proteins derived from immunoglobulin light chain fragments, occurring alone or in association with multiple myeloma. The later (AA), is caused by deposition of fibrils composed of fragments of the acute phase reactant serum amyloid A (SAA) and complicates chronic diseases with ongoing or recurring inflammation, namely; rheumatoid arthritis (RA), juvenile chronic polyarthritis, ankylosing spondylitis, familial periodic fever syndromes (Familial Mediterranean Fever), chronic infections and furthermore, some neoplasms (mainly renal cell carcinoma and Hodgkin's disease). Despite its less frequent association, some benign neoplasms can subsequently complicate to AA amyloidosis, therefore, an early diagnose and successful treatment may lead indeed, to regression of the amyloid disease. Herein, we present two cases of AA amyloidosis, both of them caused by 2 different benign neoplasms: 1. A 34 year-old woman, after chronic oral contraceptive use, developed an hepatic adenoma (fig. 1) which finally lead to AA amyloidosis with primary kidney presentation (pure nephrotic syndrome) (table 1). Post-surgical complications yield to acute renal failure from which unfortunately could not be recovered. After being on hemodialysis therapy during 10 months she received a first renal allograft without any complication. 2. A 20 year old woman, was diagnosed of AA amyloidosis after a renal biopsy (fig. 2) because of nephrotic syndrome (table 1). Further investigation lead to the finding of a hialyne-vascular type Castleman's disease located in the retroperitoneum (fig. 2). Despite surgical resection and medical treatment (colchicine) she developed progressive renal failure requiring initialization of hemodialysis therapy. After 6 years being on hemodialysis, she received a first renal allograft which is currently functioning after one year of follow- up. Although other chronic inflammatory diseases complicate more frequently to AA amyloidosis, benign tumors have to be taken into account as a potential ethiological cause for secondary amyloidosis.
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PMID:[Systemic AA amyloidosis induced by benign neoplasms]. 1833 38

Primary non-Hodgkin's lymphoma of bone (PLB) is rare, and generally presents as a single extensive and destructive bone lesion. Histopathologically, most cases present as diffuse large B-cell lymphoma, and T-cell lymphoma is rare. By contrast, multiple myeloma is a disease defined as the neoplastic proliferation of a single clone of plasma cells producing a monoclonal immunoglobulin. We report a case of multiple myeloma that developed during treatment of PLB in a type of T-cell. A 48-yr-old man was diagnosed as T-cell PLB, stage IE, 18 months ago. The patient received the chemoradiotherapy and salvage chemotherapy for PLB. However, the lymphoma progressed with generalized bone pain, and laboratory findings showed bicytopenia and acute renal failure. On bone marrow biopsy, the patient was diagnosed as having multiple myeloma newly developed with primary T-cell lymphoma of bone. In spite of chemotherapy, the patient died of renal failure.
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PMID:Newly developed multiple myeloma in a patient with primary T-cell lymphoma of bone. 1858 98


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