Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-two cancer patients were treated with streptozotocin (SZN) in six weekly intravenous doses of 1.0-1.5 g/m2. The results of the initial courses of therapy include 3 complete and 2 partial responses, 11 patients with no change, 4 with progression, and 2 deaths due to tumor progression. Three additional deaths also due to tumor progression occurred in previously responding patients. All responses were in patients with pancreatic tumor. Toxicity consisted of transient proteinuria in 11/15 patients, transient azotemia in 11/18 patients, marked reduction of creatinine clearance in 1 patient, burning pain at site of injection, nausea, and vomiting in 20/22 patients, change of FBS from pretherapy to post-therapy of at least 10 mg/100 ml in 11/17 patients, significantly decreased platelet count in 1/22 patients, decreased Hgb in 2/22 patients, and duodenal ulcer in 2/22 patients. A reduced dosage schedule and combination with other drugs known to be effective in pancreatic tumors deserves further investigations.
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PMID:Streptozotocin therapy in 22 cancer patients. 12 12

From a review of 17 cases of Fanconi syndrome with Bence Jones proteinuria and myeloma or amyloidosis, including three new cases reported here in detail, there emerges a well defined set of characteristics. In most cases, the diagnosis of Fanconi syndrome preceded the development of myeloma or amyloidosis. Myeloma preceding the development of Fanconi syndrome has not been reported. All the patients had Bence Jones proteinuria, but in some it could be detected only by electrophoresis or immunoelectrophoresis, In the seven cases in which the Bence Jones protein was typed, it was of kappa type. There were no serum protein monoclonal abnormalities. In the bone marrow and renal samples of half of the patients, crystalline cytoplasmic inclusion bodies were present in lymphoplasmacytic elements and renal tubular cells. It is proposed that patients with Fanconi syndrome and Bence Jones proteinuria have a distinct type of plasma cell disorder or variant of the monoclonal gammopathies, characterized by a slow progression of the tumor and by an early phase dominated by the metabolic complications of the renal proximal tubular dysfunction. Adult patients with Fanconi syndrome should be carefully investigated for the presence of Bence Jones protein and a plasmacytic dyscrasia should be excluded.
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PMID:Fanconi syndrome in adults. A manifestation of a latent form of myeloma. 16 83

Big renin, a relatively inactive renin which possesses a molecular weight larger than that of normal plasma or renal renin, has been demonstrated by gel filtration in certain human plasma, tumor extracts, and amniotic fluid. Big renin was not present in normal plasma or kidney extracts. Plasma from 3 hypertensive patients with nephropathy contained chiefly big renin. Varying proportions of both big and normal renin activity were present in plasma of other patients with hypertension and proteinuria. The renin present in amniotic fluid, which increased in activity following exposure to acid pH, was shown to be big renin in two patients. Large amounts of circulating big renin apparently can cause hypertension in patients with Wilms' tumors. Furthermore, the relatively inactive big renin may replace normal plasma renin in some patients, resulting in low plasma renin activity.
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PMID:Occurrence of big renin in human plasma, amniotic fluid and kidney extracts. 16 87

There is considerable circumstantial evidence relating neoplasia to glomerular injury. Recently, more convincing evidence has been derived from the demonstration of tumor-associated antigen or antibody to such antigen, in relation to glomerular basement membranes in four patients with glomerular injury and cancer. The most common form of glomerulopathy reported in patients with carcinoma has been membranous glomerulonephritis. However, increased mesangial cells and matrix have also been found in some patients with hematuria and progressive renal failure. In contrast, most patients with Hodgkin's disease and glomerulopathy have had the minimal lesion-type nephrotic syndrome, which has usually responded to successful treatment of the Hodgkin's disease. Glomerular abnormalities have also been reported with chronic lymphocytic leukemia, lymphosarcoma, Waldenstrom's macroglobulinemia, and benign tumors. When there is no apparent cause, proteinuria with or without hematuria or impaired renal function should suggest the possibility of associated neoplasia, particularly in elderly patients.
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PMID:Glomerular injury in patients with neoplasia. 18 Aug 69

A patient with disseminated malignant melanoma developed mild renal failure with proteinuria four months following the diagnosis of his neoplasm. Renal biopsy showed a membranoproliferative glomerulonephritis. Electron microscopy revealed intramembranous dense deposits in the glomeruli as well as in tubular basement membranes and Bowman's capsule. Immunofluorescence microscopy demonstrated granular staining for C3 in these same locations and granular deposits of immunoglobulins in the glomerular capillary loops. Light and electron microscopy of the autopsy kidney obtained 5 months later revealed progression of the number, size and density of the deposits. Eluates from both autopsy and biopsy kidney contained melanoma antigen and anti-melanoma antibodies. This case illustrates the association between the dense deposits and neoplasia with the dense deposits representing immune complexes with the tumor as antigen.
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PMID:Malignant melanoma with renal dense deposits containing tumor antigens. 39 45

A 22-year-old black male presented with erythrocytosis and proteinuria. The erythrocytosis was characterized by increased red cell mass, normal arterial oxygen saturation, and normal hemoglobin electrophoresis and oxygen affinity. There was no splenomegaly, and the white blood cell count, platelet count, serum uric acid concentration, serum B12 levels and leukocyte alkaline phosphatase activity were normal. Tumors of the liver, lung, kidney and cerebellum, which have been associated with erythrocytosis, were not found. The only associated disease was biopsy proven focal glomerulosclerosis. Renal vein thrombosis was excluded by renal venography and arteriography. This case illustrates the rarely reported association of the nephrotic syndrome and erythrocytosis. Other nephrogenic causes of erythrocytosis are mentioned, including renal cysts, tumors, renal artery stenosis and transplantation. The role of the kidney in erythropoietin production and possible mechanisms of nephrogenic erythrocytosis are discussed.
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PMID:Focal glomerulosclerosis and erythrocytosis. 50 18

The effect of corticosteroids and cytotoxic chemotherapeutic agents on the excretion of Bence Jones protein was determined for periods of 1 - 62 mo in 29 patients with multiple myeloma and Bence Jones proteinuria. The amount of protein present in 24-h urine specimens collected before treatment and at frequent intervals during monthly treatment cycles was determined. Striking variations occurred in the amount of Bence Jones protein excretion; these changes were especially evident when 75 mg of prednisone were given daily for 7 days as part of a monthly chemotherapeutic regimen. Within the 7-day period seven patients showed essentially no decrease (<25%), whereas 13 and 9 patients had a moderate decrease (25-75%) or a marked decrease (>75%), respectively, in Bence Jones proteinuria as compared to pre-treatment values. The decrease in excretion of Bence Jones protein during this period was attributed mainly to corticosteroid therapy because of the transient nature of the response in most patients and the lack of such response in three patients when the hormone was omitted. Biosynthetic studies were performed to determine in vitro the effect of corticosteroids on Bence Jones protein synthesis. Plasma cells obtained from the bone marrow of 13 patients were incubated in a growth medium containing (14)C-labeled lysine and isoleucine and prednisone in concentrations up to 240 mug/ml, and the amount of Bence Jones protein synthesized was determined immunochemically. No differences in viability were apparent between untreated and prednisone-treated cells. The type of response exhibited by an individual patient in the percent decrease of Bence Jones protein excreted after 7 days of prednisone treatment was comparable to the percent decrease in newly-synthesized Bence Jones protein secreted by tumor cells when cultured in the presence of prednisone at a concentration of 120 mug/ml. The marked differences in the capacity of corticosteroids to affect Bence Jones protein synthesis appear to reflect a biochemical heterogeneity among plasma cell neoplasms.
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PMID:Bence Jones proteins and light chains of immunoglobulins. XV. Effect of corticosteroids on synthesis and excretion of Bence Jones protein. 61 16

Sixty-two of 1242 patients with M components were found to have lymphoma. There were 33 patients with immunoglobulin M(IgM), 20 WITH IgG, 5 with IgA, and one patient with Bence Jones protein M components. Three patients had biclonal gammopathy. The types of lymphoma were: lymphocytic, 31; histiocytic, 12; mixed cell, 4; stem cell, 2; Burkitt's, 1; Hodgkin's disease, 9; and unclassified, 3. All patients were in stages III or IV of lymphoma, and the average duration of disease was 29.3 months when M components were detected. Anemia, abnormal peripheral blood lymphocytes, and lymphomatous involvement of the bone marrow were especially common among patients with IgM M components. Osteolytic lesions were found in 12 patients and osteosclerotic lesions in one. A second malignancy occurred in eight patients. The level of M component was below 1.0 gm/dl in 55 per cent of patients. Significant suppression of normal immunoglobulin levels in the serum was noted in 4 and 16 patients with IgG and IgM components, respectively. Bence Jones proteinuria was found in 19 per cent, cryoglobulinemia in 11 per cent, and cold agglutinins, all of anti-i specificity, in 10 per cent of the patients. Most of the M components decreased during therapy. Only two M components gradually increased. The mean survival of 39 patients who died was 10.4 months. The living patients have been followed for a mean period of 21.2 months. The presence of M components in lymphoma may suggest B cell origin of the tumor but the coexistence of plasma cell dyscrasia cannot be ruled out.
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PMID:M components associated with lymphoma: a review of 62 cases. 82 10

A patient whose nephrotic syndrome was controlled by steroids and cyclophosphamide was found to have gastric cancer. After removal of the tumor and discontinuing the steroid therapy, no recurrence of the clinical signs of nephrotic syndrome appeared, but moderate proteinuria persisted. The literature regarding the association of nephrotic syndrome with malignancies is reviewed.
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PMID:Nephrotic syndrome associated with gastric cancer. 86 28

Sixty-six patients of all ages whose renal biopsy appearances satisfied strict criteria for the histopathological diagnosis of membranous nephropathy were studied and followed for a mean of 5-4 years (range 1 to 20 years). From initial investigation seven patients were found to have associated neoplasia, and in two patients the condition followed treatment with a mercurial diuretic and gold. One patient was Australia antigen positive. Two patients developed renal vein thrombosis, but in both this appeared to follow not precede their nephrotic syndrome. In the remaining 56 patients there was no associated factor. During the follow-up period, approximately one-quarter of the patients (15) died, nine from renal failure; one-quarter (10) had a persistent nephrotic syndrome, another one-quarter (15) proteinuria of lesser degree. The final one-quarter (16) are now in complete remission. The prognosis of the 54 patients with an initial nephrotic syndrome was poorer than the 12 with lesser proteinuria and no oedema at onset; five of 11 children were in complete remission when last seen. All but one of the nine patients who developed terminal chronic renal failure 4 to 18 years from onset had an unremitting nephrotic syndrome, eight of the 10 currently alive with a persistent nephrotic syndrome have reduced renal function. Renal functional deterioration did not occur in the absence of proteinuria. There was only slight correspondence between the stage of biopsy appearance, glomerular filtration rate at time of biopsy, time of the biopsy from apparent onset, or status at last follow-up. Staging is therefore of limited prognostic value. Twenty-two patients were treated with corticosteroids for 2 to 36 months; we detected no short or long-term benefit when compared to patients not so treated.
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PMID:Membranous nephropathy. Long-term follow-up and association with neoplasia. 117 11


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