The clinical spectrum of pure bence jones proteinuria: A study of 66 patients

Pascali, E; Pezzoli, A

doi:10.1002/1097-0142(19881201)62:11<2408::aid-cncr2820621127>3.0.co;2-2

Cited by 18 publications

(6 citation statements)

References 28 publications

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“…Paraneoplastic syndromes characterized by urinary excretion of specific proteins are described in multiple myeloma or other lymphoid malignancies of humans (Pascali and Pezzoli, 1988), being Bence Jones proteinuria the paradigm of these paraneoplastic syndromes. Interestingly, Bence Jones proteins may crystallize in the renal tubules of patients with multiple myeloma (Evans, 1992).…”

Section: Discussionmentioning

confidence: 99%

Eosinophilic Crystals as a Distinctive Morphologic Feature of a Hyaline Droplet Nephropathy in a Mouse Model of Acute Myelogenous Leukaemia

Marchesi¹,

Monestiroli

Capillo

et al. 2003

Journal of Veterinary Medicine Series A

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Eosinophilic crystals have been described in the upper and lower respiratory tract, gall bladder, intrahepatic bile ducts and glandular stomach of different laboratory mice strains. They have been recently identified as chitinase-like (Ym1/Ym2) proteins. Here we describe the occurrence of eosinophilic crystals in the renal tubules of mice with experimentally induced acute myelogenous leukaemia. Fourteen FVB/N and 29 129Sv mice of both sexes, 8-10 weeks of age, were employed to establish a model of human acute myelogenous leukaemia. Nine mice that developed a widespread acute myelogenous leukaemia revealed the presence of eosinophilic crystals in renal tubules. The presence of eosinophilic crystals in the kidneys was constantly associated with a hyaline droplet nephropathy. Immunohistochemistry showed that the crystals and the hyaline droplets were composed of chitinase-like (Ym1/Ym2) proteins. Furthermore, immunoreactivity for Ym1/Ym2 proteins was also detected in the crystalline material stored in the cytoplasm of large macrophage-like cells or in extracellular localization within the leukaemic infiltrates. On the basis of our results we hypothesize that the detection of the Ym1/Ym2 proteins in the urine of mice might represent a feasible indicator of the burden and progression of the leukaemic condition in our murine model.

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Section: Discussionmentioning

confidence: 99%

Eosinophilic Crystals as a Distinctive Morphologic Feature of a Hyaline Droplet Nephropathy in a Mouse Model of Acute Myelogenous Leukaemia

Marchesi¹,

Monestiroli

Capillo

et al. 2003

Journal of Veterinary Medicine Series A

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“…For example, HCL may atypically present with cutaneous, visceral, bone, pleural, and meningeal involvement [22][23][24][25][26][27][28][29]. Polyclonal and monoclonal gammopathy have been reported in 3%-20% of patients and may be related to an associated plasma cell dyscrasia, lymphoma, or autoimmune disorder [30][31][32]. For reasons not yet elucidated, HCL may be associated with a variety of autoimmune disorders, most commonly vasculitis [25,[33][34][35][36][37][38][39].…”

Section: Clinical Manifestationmentioning

confidence: 99%

Hairy Cell Leukemia: An Elusive but Treatable Disease

Wanko

Castro

2006

The Oncologist

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Hairy cell leukemia (HCL) is a unique chronic lymphoproliferative disorder that can mimic or coexist with other clonal hematologic disorders and has been associated with autoimmune disorders. It should be entertained as an alternative diagnosis in patients with cytopenias being assigned the diagnosis of aplastic anemia, hypoplastic myelodysplastic syndrome, atypical chronic lymphocytic leukemia, B-prolymphocytic leukemia, or idiopathic myelofibrosis. Causative etiology or molecular defects remain unclear, although nonspecific chromosomal and molecular changes have been described. The typical presentation is that of a middle-aged man with an incidental finding of pancytopenia, splenomegaly, and inaspirable bone marrow. Treatment with a purine analogue, cladribine or pentostatin, results in extremely high, durable, overall, and complete response rates, although resistance and relapses do occur. A variant subtype exists and is frequently associated with a poor response. Because of its simplified dosing schedule, cladribine is commonly used as the initial therapy. Treatment of relapsed HCL is dictated by the duration of the preceding remission. Relapsed disease after a prolonged remission can often be successfully retreated with the same initial agent. Resistance in typical HCL is treated with the alternate purine analogue. New agents, such as rituximab and BL22, are actively being evaluated and show promising results in both HCL subtypes. This article uses two patients diagnosed with aplastic anemia and recently seen in consultation at our institution as a springboard to discuss the biology, pathogenesis, clinical presentation, diagnostic evaluation, and treatment options of HCL. The Oncologist 2006;11:780-789

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“…In ϳ20% of such patients, urine FLCs are the only monoclonal component detected (1)(2)(3)(4). FLCs produced in excess and secreted by a clonal population of plasma cells are excreted into urine in variable amounts as monomers, dimers, polymers, or low-molecular-weight fragments, frequently accompanied by significant quantities of polyclonal FLCs (1,2,(5)(6)(7).…”

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confidence: 99%