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 66-year-old man with kappa-light chain multiple myeloma had adult Fanconi syndrome. Renal tubular transport abnormalities consisted of renal tubular acidosis, renal glycosuria, aminoaciduria, phosphaturia and renal hypouricemia. After therapy for multiple myeloma, urinary Bence Jones protein became undetectable, and all these renal tubular abnormalities except urate wasting were corrected. Histological examination revealed electron-dense tubular and rod-like deposits in proximal tubular epithelium. This clinical observation suggests that the renal tubular transport defects were secondary to the myeloma process, possibly due to Bence Jones proteinuria.
Nephron 1990
PMID:Adult Fanconi syndrome secondary to kappa-light chain myeloma: improvement of tubular functions after treatment for myeloma. 211 47

A 57-year-old man with end-stage renal failure secondary to myeloma kidney developed haemorrhagic complications due to endogenous glycosaminoglycan anticoagulant production. Glycosaminoglycan levels and anticoagulant effect were reduced by plasma exchange and this contributed to control of the haemorrhagic manifestations.
Nephron 1990
PMID:Plasma exchange as a treatment for endogenous glycosaminoglycan anticoagulant induced haemorrhage in a patient with myeloma kidney. 212 68

It has been assumed, but not documented, that hypercalcemia induces an appreciable reduction in the serum anion gap (AG) because it represents an increase in the level of unmeasured cations. To test this question, we retrospectively compared the data of 59 hypercalcemic patients with malignancy [group 1, serum Ca 13.3 +/- SE 0.3 mg/dl] with those of 108 patients whose hypercalcemia was of parathyroid origin (group 2, serum Ca 12.1 +/- 0.1 mg/dl), and those of 51 control subjects (group 3, serum Ca 9.5 +/- 0.1 mg/dl). The AG of group 2 subjects (8.7 +/- 0.3 mEq/l) was significantly lower than that of the other two groups (p less than 0.001 for both) despite their higher serum albumin and lower serum Ca in comparison to group 1. The AGs of group 1 (11.1 +/- 0.4 mEq/l) and group 3 (11.1 +/- 0.3 mEq/l) were identical. There was no statistically significant correlation between the AG and serum Ca in the hypercalcemic patients. The major finding that the association of hypercalcemia with reduced AG is seen in hyperparathyroidism, but not in malignancy-related hypercalcemia, is not explained by differences in serum albumin, renal function, or acid-base status. Overlap of values between groups limits the diagnostic usefulness of the AG in an individual patient. Nevertheless, in the absence of multiple myeloma, the finding of an AG of 5 mEq/l or less in a hypercalcemic patient may be a helpful clue suggesting that malignancy is not the etiology.
Nephron 1990
PMID:Effect of hypercalcemia on the anion gap. 236 30

A 72-year-old woman presented with rapidly progressive renal failure and multiple myeloma. The patient died 6 months later of severe hepatic insufficiency. The light-microscopic, immunological and ultrastructural findings showed widespread kappa-light-chain deposits including the kidneys, liver, spleen, heart, lungs, tongue, ovary, pancreas and bone marrow associated with massive AL amyloid deposits in the same organs and in the thyroid gland. The concurrent presence of two different deposits is very unusual and the possible mechanisms for such an association are discussed.
Nephron 1989
PMID:Massive systemic amyloidosis associated with light-chain deposition disease. 250 Jun 13

Seven years after a cadaver kidney transplantation a 33-year-old man presented with a monoclonal gammopathy secondarily complicated by AL amyloidosis mainly expressed as a sicca syndrome, gammopathy that ultimately developed into multiple myeloma. The mechanisms responsible for the occurrence of monoclonal gammopathy in renal transplant recipients are discussed.
Nephron 1989
PMID:Multiple myeloma and AL amyloidosis in a renal transplant recipient. 260 5

Advanced renal failure, nephrotic-range proteinuria due to proliferative glomerulonephritis and multiple myeloma with circulating IgG2 lambda and free lambda light-chain paraproteins occurred in a 31-year-old male. Commonly established causes of renal failure in multiple myeloma were excluded. Immunofluorescence revealed heavy granular glomerular deposition of C3. Serum C3 was decreased, and C3c was increased. C3 nephritic-factor (C3 NeF)-like activity was demonstrated in the serum. Plasmapheresis and chemotherapy resulted in a decrease in paraprotein concentration up to 90%, a decrease in C3 NeF-like activity to negligible, normal serum complement levels and a marked improvement in both renal function and proteinuria. With reference to the literature, the possibility of a syndrome of paraproteinemia, C3 NeF-like activity and glomerulonephritis is forwarded.
Nephron 1989
PMID:Hypocomplementemic proliferative glomerulonephritis with C3 nephritic-factor-like activity in multiple myeloma. 266 48

Amyloid bone lesions were found in 2 chronic hemodialysis patients presenting with pathologic hip fractures. These amyloid deposits were noted as lytic defects on plain skeletal radiographs. No evidence for disseminated amyloidosis was discovered on physical examination, skin biopsy, or bone marrow biopsy. Myeloma, other plasma cell dyscrasia, and preceding chronic inflammatory states were not found in either patient. The amyloid deposits had staining characteristics suggestive of secondary amyloid based on the potassium permanganate reaction. Isolated amyloid bone deposits should be included in the differential diagnosis of lytic bone lesions or pathologic fractures in chronic dialysis patients.
Nephron 1986
PMID:Pathologic fractures associated with idiopathic amyloidosis of bone in chronic hemodialysis patients. 370 63

Widespread, progressive skin necrosis developed in a 42-year-old male with a 5-year history of osteosclerotic myeloma. Biopsy of the necrotic lesions demonstrated a leucocytoclastic vasculitis with extensive vascular calcification. Radiological investigations demonstrated widespread arterial calcification. Clinical improvement of the established skin lesions followed the institution of a forced calciuresis and parathyroid hormone suppression by induced hypermagnesaemia and phosphate depletion. No further cutaneous necrosis developed. Subsequent treatment with oral immunosuppressive therapy and the diphosphonate, EHDP, has been associated with a complete 18-month remission. The relationship of this apparently unique pathological process to the osteosclerotic myeloma is discussed, together with the rationale for the therapeutic regime instituted.
Nephron 1985
PMID:Osteosclerotic myeloma complicated by diffuse arteritis, vascular calcification and extensive cutaneous necrosis. 392 May 44

A monoclonal antibody, PHM 5, directed against human glomerular epithelial cells, was prepared after immunisation of a mouse with isolated human glomeruli and fusion of spleen cells with a mouse myeloma. Binding of antibody to isolated glomeruli was detected by radioimmune indirect binding assay, and specificity for glomerular epithelial cells was shown using a four-layer peroxidase-antiperoxidase technique applied to epoxy resin sections of the human kidney cortex. PHM 5 appears to detect a human-specific cell surface carbohydrate antigen not previously described, and can be used to identify epithelial cells in renal biopsy sections and in culture outgrowths of isolated glomeruli.
Nephron 1983
PMID:Monoclonal antibodies to human glomerular cells: a marker for glomerular epithelial cells. 633 71

A 45-year-old male was admitted to the hospital because of polyuria and polydipsia. After admission, proteinuria and hematuria were found. The kidney function deteriorated and necessitated the initiation of chronic hemodialysis. Examination of the bone marrow revealed multiple myeloma and kappa light chains were found in the urine. The kidney biopsy showed membranoproliferative glomerulonephritis with dense deposits in the glomerular basement membrane.
Nephron 1983
PMID:Multiple myeloma presenting as dense deposit disease. Light chain nephropathy. 640 20


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