Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A variety of tubular marker proteins, as compared to healthy controls, are excreted at an increased rate in the urine of patients with renal damage. Beside cytoplasmic glutathione-S-transferase and lysosomal beta-N-acetyl-glucosaminidase (beta-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, gamma-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein 'SGP-240' and adenosine-deaminase-binding protein. Urinary tissue proteins, e.g. brush border (BB) microvilli, are immunologically identical with those antigens prepared from cell membranes of the human kidney itself. BB antigens are shed into the urine of patients with glomerulonephritis, interstitial nephritis, systemic diseases, e.g. systemic lupus erythematosus (SLE), diabetes mellitus and multiple myeloma, arterial hypertension, infectious diseases (malaria, AIDS) and after operations, renal grafting and administration of X-ray contrast media, aminoglycosides or certain cytostatics (cis-platinum). Tissue proteinuria of tubular proteins is determined by enzyme-kinetic or quantitative immunological assays applying either poly- or monoclonal antikidney antibodies. Clinical, ultrastructural and histochemical studies support the idea that both 'soluble' and high-molecular-weight membrane particles (vacuolar blebs, greater than 10(6) dalton) as well as microfilamental components of the epithelial cytoskeleton contribute to tubular 'histuria' which appears as a sensitive parameter in monitoring tubular damage under clinical conditions at a very early phase.
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PMID:Urinary proteins of tubular origin: basic immunochemical and clinical aspects. 225 76

Urinary doubly refractile lipid bodies (DRLB) are a characteristic finding in patients with glomerular renal diseases causing heavy proteinuria. DRLB are felt to be an uncommon finding in glomerular diseases without heavy proteinuria, and a rare finding in nonglomerular renal diseases. In order to determine whether DRLB are found in nonglomerular renal diseases, we reviewed the medical records of all patients who had urinalyses performed in our laboratory from February 1975 to June 1983. Three hundred sixty one patients demonstrated less than or equal to +2 proteinuria, and at least two DRLB. Of these, 290 were identified as having a single renal diagnosis. One hundred forty eight patients (51%) had a variety of acute and chronic glomerular diseases, and 125 patients (43.2%) had nonglomerular renal diseases, including acute tubular necrosis (ATN), prerenal azotemia, chronic interstitial nephritis, polycystic kidney disease, acute interstitial nephritis, renal neoplasia, and acute myeloma kidney. Ten patients had transient proteinuria associated with acute illness, and seven patients had no renal disease at all. Only two patients with nonglomerular renal disease had more than five DRLB per 20 high power microscopic fields. The frequency of DRLB in patients with nonglomerular renal diseases was: chronic interstitial nephritis, 26%; polycystic kidney disease, 38%; prerenal azotemia, 20%; ATN, 15%; and acute interstitial nephritis, 33%. These data suggest that at lower levels of proteinuria, DRLB are found frequently in nonglomerular renal diseases, and that DRLB do not differentiate glomerular from nonglomerular renal diseases unless more than five DRLB are found on urinary sediment examination.
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PMID:Urinary doubly refractile lipid bodies in nonglomerular renal diseases. 335 69

Using polyacrylamide gel disc electrophoresis in presence of sodium dodecylsulfate (SDS) urinary proteins were studied in apparently healthy persons, in patients with chronic glomerulonephritis, chronic interstitial nephritis as well as in patients with myeloma, urine of which contained monoclonic light chains of immunoglobulins. SDS polyacrylamide gel disc electrophoresis is a suitable procedure for differential diagnosis of glomerular and tubulo-interstitial impairments of kidney. In some cases the procedure enables to ascertain not only the type but also severity of the kidney impairment as well as to study dynamics of the disease without a recourse to such invasive methods as kidney biopsy.
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PMID:[Biochemical diagnosis of glomerular and tubulo-interstitial impairments of kidney]. 679 82

We have reviewed our experience in the management of myeloma patients who present with features of severe renal impairment, to examine the role of intensive treatment of the renal failure, and to assess the role of renal biopsy. Between March 1983 and August 1991, 16 patients, who were subsequently diagnosed as having myeloma, presented to the Department of Renal Medicine for investigation of renal failure; nine with symptoms of uraemia and seven with pneumonia, bone pain, emphysema, or ischaemic heart disease. Renal biopsy was performed on 14 patients. Eleven patients had myeloma cast nephropathy, two of whom had concurrent hypertensive nephropathy, two patients had light chain deposition disease, and one patient had interstitial nephritis. Renal function improved in six patients with aggressive rehydration, but three of them subsequently required dialysis. In all 11 patients required dialysis, two short-term and nine long-term. Seven patients were given conventional melphalan and prednisolone and nine patients received VAMP as induction cytotoxic chemotherapy. Five of the VAMP sub-group received interferon alpha 2b as maintenance therapy. The median renal survival was five months (range 0-36 months) and median overall survival was 20 months (range 1-54 months). We conclude that intensive treatment, including dialysis, in myeloma patients with renal failure may result in survival durations approaching those of unselected myeloma patients, and a significant proportion will enjoy a reasonable quality of life.
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PMID:Intensive treatment of renal failure in patients with myeloma. 773 18

Many renal diseases involving the tubular epithelium appear to preferentially affect certain nephron segments. While major portions of the nephron, such as proximal and distal convoluted tubules and collecting ducts, can be identified in the normal kidney, the distinction of diseased nephron segments can be difficult in tissue sections. Thus, to identify which nephron segments are involved in pathologic changes is usually impossible by routine histologic examination alone. Recently antibody and lectin probes that react with specific nephron segment-specific epitopes and carbohydrates, respectively, have become available. Some of these antibodies and lectins can be used on formalin-fixed, paraffin-embedded, archival tissues. Because renal tubules appear to retain their nephron segment-specific epitopes and glycoprotein moieties under most pathologic conditions, these nephron segment-specific tubular epithelial markers provide a method to study renal diseases involving the tubular system also in archival material. Such nephron segment-specific tubular epithelial markers are: the lectins, Tetragonolobus purpuras and Phaseolus vulgaris erythroagglutinin (proximal tubular markers); antibodies to low-molecular-weight cytokeratin (AE1/AE3); epithelial membrane antigen and the lectin Arachis hypogaea (distal nephron [distal convoluted tubule and collecting duct] markers); and antibodies to Tamm-Horsfall protein (labeling the thick ascending limb of Henle). We review the application of these and other renal tubular epithelial markers in the normal kidney and in various renal diseases including cystic disease of the kidney, interstitial nephritis, tubular atrophy, acute tubular necrosis, myeloma cast nephropathy, and renal tumors.
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PMID:Immunohistochemical and lectin dissection of the human nephron in health and disease. 825 Jun 94

Idiopathic CD4+ T cell lymphocytopenia was unexpectedly detected in a 33-year-old, otherwise healthy young woman with no HIV or other viral infection, autoimmune, or neoplastic disease or increased susceptibility to infection. CD4+ T cell levels were 60-140/microl over a 3.5-year period. Following an uneventful pregnancy, the patient developed anemia and interstitial nephritis associated with a plasma cell dyscrasia with a monoclonal IgA gammopathy and a shifting immunoglobulin pattern that included IgG and IgA monoclonal proteins and increased urinary light chains. Osteolytic lesions were never detected and bone marrow aspirations revealed up to 10% atypical plasma cells. Various therapies often used in treating multiple myeloma only temporarily controlled the increasing renal damage. IL-2 therapy of 600,000 to 1 million units subcutaneously daily resulted in increased CD4+ T cells to normal levels, a decrease in the gammopathy, a return of renal function, energy, and weight gain, and apparently normal health status sustained for 2 years. The findings are compatible with a potentially fatal but nonmalignant immunoregulatory disorder that can be controlled by IL-2 administration.
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PMID:Idiopathic CD4+ T cell lymphocytopenia evolving to monoclonal immunoglobulins and progressive renal damage responsive to IL-2 therapy. 1131 2

A young female with Fisher-Evans' syndrome and a previous melanoma developed acute renal failure with generalized lymphoadenopathy and fever. The appearance of renal lesions is common in the course of several hematological disorders, but is unusual in Fisher-Evans' syndrome. Fisher-Evans' syndrome, defined as Coombs' positive hemolytic anemia and immune thrombocytopenia, is more frequently associated with the other autoimmune diseases, but not with renal involvement. In our case report, having excluded amyloidosis, myeloma, interstitial nephritis and sepsis, the rapid involvement of renal function with enlarged renal size seemed to suggest renal lymphoma. However, the lack of a monoclonal T-lymphocyte population in the renal tissue and peripheral blood, along with a clinical course characterized by a rapid reversibility of acute renal failure made this diagnosis rather an unlikely one. Polyclonal lymphocyte infiltration in a patient with a persistent autoimmune disease made us suspect a hyperimmune reaction. This syndrome is a non-neoplastic proliferation of B-cells involving an exaggeration of lymphocyte transformation. However, the clinical course is progressive and fatal, and can trigger a lymphoproliferative systemic disease. In our patient, two elements led us to suspect it was not a typical hyperimmune syndrome: first, polyclonal lymphocytes had massively infiltrated the kidney and, secondly, the clinical outcome was extremely favorable. Therefore, we were faced with an "atypical" and "singular" hyperimmune reaction with renal involvement, polyclonal proliferation of T-lymphocytes that had exhausted itself over time. Infective or toxic agents or drugs such as cyprofloxacin could have triggered the phenomenon, in the presence of a favorable condition such as Fisher-Evans' syndrome.
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PMID:Acute renal failure in a young woman with Fisher-Evans' syndrome. 1559 44

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

A retrospective analysis of 1592 renal biopsies received from various hospitals all over Kerala over a period of two years was done. Of the 1544 native kidney biopsies majority of cases (300; 18.84%) were focal segmental glomerulosclerosis. Next infrequency was IgA nephropathy (227; 14.26%). The other diagnoses included post infectious glomerulonephritis (GN) (150; 9.42%), lupus nephritis (131; 8.23%), membranous glomerulonephritis (118; 7.41%), minimal change disease (94; 5.94%), interstitial nephritis 87(5.46%), membranoproliferative glomerulonephritis (MPGN) and severe glomerulosclerosis (74; 4.64% each), IgM nephropathy (72; 4.52%), acute tubular necrosis and diabetic glomerulopathy (24; 1.5% each), ANCA-related GN (21;1.32%), amyloidosis (13; 0.82%), Henoch Schonlien purpura (12; 0.75%) atd thrombotic microangiopathy (10; 0.63%). Afew others like myeloma cast nephropathy, cholesterol embolism, Clq nephropathy, oxalosis, mixed connective tissue disorder (MCTD, Wegner's granulomatosis etc. also were seen occasionally. 48 cases were allograft biopsies (3.02%).
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PMID:Non-neoplastic renal diseases in Kerala, India--analysis of 1592 cases, a two year retrospective study. 1788 50

Neolymphangiogenesis has recently been demonstrated in transplanted kidneys as well as in chronic interstitial nephritis and IgA nephropathy. However, its significance in kidney disease remains to be defined and a systematic study of renal lymphangiogenesis is warranted. We investigated patients with multiple myeloma (MM) presenting in the great majority with acute renal insufficiency. Controls were allograft kidney donors and patients with renal insufficiency due to acute renal failure (ARF). Lymph vessel length density (LVD) was quantified immunohistochemically by means of antipodoplanin staining followed by computer-assisted stereology. The mean LVD in kidneys of patients with MM (23.19 mm(-2)) was higher when compared with allograft donors (7.42 mm(-2), P = 0.0003) and patients with ARF (6.78 mm(-2), P = 0.0002). The higher LVD was significantly associated with interstitial inflammation, and the newly formed lymph vessels were accompanied by diffuse and nodular interstitial infiltrates composed mainly of CD20(+) B cells and CD27(+) plasma cells. The infiltrates in patients with MM also displayed a higher expression of the B-cell chemoattractant CXCL13. These results demonstrate for the first time that lymphangiogenesis is a prominent feature in MM kidneys and that it is associated with a significant accumulation of macrophages, CD20(+) and CD27(+) B lymphocytes. Further studies should clarify whether these changes represent a beneficial or detrimental factor in the progression of the myeloma-related kidney damage.
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PMID:Lymphangiogenesis is upregulated in kidneys of patients with multiple myeloma. 2064 79


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