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)

Diagnosis of multiple myeloma is based on the triad paraproteinemia, osteolytic bone lesions and bone marrow plasma cell infiltration. Clinically, rheumatoid-like pain induced by osteolytic skeletal lesions often prevails. Occasionally, foudroyant bacterial infections - the most frequent cause of death in myelomatosis - or acute/subacute renal failure or rarely, acute hemi- or paraparesis precede diagnosis. Establishment of diagnosis early in the course of the disease and improved cytostatic and symptomatic treatment has led to a decrease in episodes of hyperviscosity-syndromes. Severe renal insufficiency due to Bence-Jones proteinuria prevails in 20% of patients already at time of diagnosis. With increasing duration of the disease, frequency of renal insufficiency further increases. Hypercalcemia with consecutive dehydration and renal insufficiency usually is a complication of long-standing disease. Anemia, leukopenia and thrombo-cytopenia are not only side effects of cytostatic treatment, but also consequences of tumor-induced suppression of hematopoiesis. Polyneuropathies are common in myelomatosis. They probably are the result of specific and/or unspecific binding of paraproteins to myelin sheaths. Effective treatment for this complication is not available at present. Thrombohemorrhagic complications are more frequent in patients with myeloma than in the control group of other hospitalized patients. Non-secretory myeloma, osteoblastic myeloma and Takatsuki syndrome are variants of myelomatosis. Solitary and extramedullary plasmocytoma are different, potentially curable entities. Prognosis is especially poor in patients with plasma cell leukemia and poor in primary amyloidosis.
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PMID:[The clinical picture of multiple myeloma]. 353 47

In a 10-year retrospective study, we evaluated the clinicopathologic features and renal immunofluorescence patterns of glomerulonephritis in 41 dogs. On the basis of results of histologic examinations, the dogs were segregated into 3 groups, including membranous (n = 12), mesangioproliferative (n = 15), or membranoproliferative glomerulonephritis (n = 14). No significant differences existed among groups in regard to age or duration of illness. Most dogs had been ill for one month or longer. The proportion of dogs with azotemia, anemia, and hyperphosphatemia were not different among the disease groups. Proportion of dogs with hypoalbuminemia and the severity of hypoalbuminemia were not different among groups. Highest urine protein losses and 24-hour urine protein/creatinine ratios developed in dogs with membranous glomerulonephritis. Although hypoalbuminemia and hypercholesterolemia were common (49%), the formation of edema or ascites was not (15%) and, therefore, few dogs had all of the classic features of the nephrotic syndrome. Few dogs suffered thromboembolic complications. Antinuclear antibody titers developed in 11 dogs, the highest titers developing in dogs with polyarthritis and systemic lupus erythematosis. Cellulose acetate electrophoresis detected alpha 2 and beta 1 globulin spikes in most dogs (87%). Results of renal immunofluorescence testing were positive in 36 dogs, using polyvalent antisera for immunoglobulins (Ig)G, IgA, IgM, and/or antisera for complement factor C3. When monovalent antisera for IgG, IgA, and IgM, and fibrinogen were used, immunofluorescence was not observed as often. The major fluorescent pattern was discrete multifocal segmental granular glomerular fluorescence, consistent with immune-complex deposition. Two dogs had linear glomerular staining patterns; however, antibodies directed against normal glomerular basement membrane were not found via elution studies. A high prevalence of glucocorticoid excess (treatment with glucocorticoids and spontaneous hyperadrenocorticism) (34%), chronic inflammatory skin disease (27%), neoplasia (17%), polyarthritis (12%), and systemic lupus erythematosis (7%) were observed as clinical problems concurrent with glomerulonephritis. In 5 dogs, treatment of glomerulonephritis with prednisolone (0.5 to 1.1 mg/kg) did not result in beneficial effects and in fact appeared to be detrimental, leading to azotemia and worsening proteinuria and physical condition in some of the dogs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinicopathologic, renal immunofluorescent, and light microscopic features of glomerulonephritis in the dog: 41 cases (1975-1985). 354 34

Intensive proteinuria accompanied by marked renal enlargement occurs in rats bearing functioning pituitary tumor MtT SA5. Urinalysis showed that protein excretion was up to 700 mg/day, and that the excreted protein consisted mostly of albumin. However, serum total protein and albumin levels remained almost unchanged. Histological examination revealed glomerular lesions, hyaline casts in the tubules, and proliferation of the tubular epithelium. The glomerular lesions consisted of accumulation of proteinaceous material in the subcapsular space; its organization and formation of fibrous crescents was with or without epithelial crescents. Electron microscopy revealed loss of foot processes and accumulation of absorption droplets in glomerular epithelial cells. Removal of the tumor resulted in a rapid reduction in urinary protein excretion. However, proteinuria persisted for at least 4 weeks after tumor removal with levels of approximately one-fourth of those before tumor removal. Histological changes of the kidneys resolved to some extent but damage still remained in the glomerular epithelial cells 4 weeks after tumor removal. Although proteinuria in animals bearing functioning pituitary tumors has long been implicated in hyperprolactinemia, the present study suggests that proteinuria in tumor-bearing rats is a control mechanism for overproduction of albumin in the liver stimulated by elevated serum growth hormone since hyperalbuminemia and possibly the hyperfibrinogenemia would cause the elevation of blood viscosity, resulting in thrombosis, unless control mechanisms were present. This proteinuria may serve for studies of glomerular permeability disorders as a model for homologous protein-overload proteinuria.
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PMID:Proteinuria induced by transplantable rat pituitary tumor MtT SA5. Model for homologous protein-overload proteinuria. 371 38

The authors provide a clinical example illustrating difficulties in the diagnosis of pheochromocytoma in a patient with infarction-like lesions in the heart, marked proteinuria, and diverse symptomatics due to excess catecholamine secretion by the tumor.
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PMID:[Pheochromocytoma with infarction-like changes in the heart and marked proteinuria]. 371 32

The syndrome of intrahepatic inferior vena cava obstruction has neither been commonly recognized nor adequately described. Symptoms include the abrupt onset of ascites, hepatomegaly, and fluid retention below the diaphragm with edema of the lower extremity. Proteinuria can be associated with these symptoms. When this syndrome has been caused by malignant hepatic enlargement, it has not been well characterized in the literature, and its treatment has been ignored. We have diagnosed the inferior vena cava syndrome due to metastatic liver involvement in 34 patients before death. Thirty-three of these patients were treated using a combination of strip radiotherapy to the hepatic vena cava, with or without hepatic arterial infusion of chemotherapy. Fifty-six percent of the patients completed a full course of radiotherapy, with an 83 percent response rate. A dose of 3,000 to 4,500 rads was found to be safe and provided excellent palliation of ascites and edema. Tumors known to be radiosensitive had the best responses and side effects were few and mild in nature. Recognition and treatment of this condition will assume greater importance as survival is prolonged in more patients with advanced malignancy.
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PMID:Diagnosis and treatment of the inferior vena cava syndrome in advanced malignant disease. 372 21

A 68-year-old man presented with nephrotic syndrome. Renal biopsy revealed minimal-change glomerular disease. The proteinuria did not respond to treatment with prednisone and cyclophosphamide. On further workup, the patient was found to have a malignant mesothelioma of the pleura. The proteinuria then improved during treatment with doxorubicin hydrochloride and dacarbazine, without noticeable improvement in the tumor. This case suggests an association between mesothelioma and minimal-change glomerular disease with nephrotic syndrome, previously unreported to our knowledge. Our review revealed only ten previous cases of minimal-change glomerular disease associated with carcinoma.
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PMID:Minimal-change nephrotic syndrome associated with malignant mesothelioma. 375 25

Fifteen patients with advanced malignancy were treated with escalating doses of recombinant beta ser 17 interferon (IFN). Doses ranging from 0.006 to 500 X 10(6) units/m2 were administered according to a dosage escalation scheme by iv push twice weekly (starting 1 week after an initial dose) for a planned minimum of 5 weeks, to be continued as a function of response. Toxic effects were broad in scope but generally low in grade. They included fever, malaise, leukopenia, proteinuria, nausea/vomiting, diarrhea, and mild elevations of serum transaminases and creatinine. In one patient, transient hypotension with bradycardia ensued. Malaise and fever increased somewhat with increasing dose. Doses of up to 500 X 10(6) units/m2 were tolerated without severe toxicity. A maximum tolerated dose was not defined. IFN pharmacokinetics followed a biphasic decay curve, with a distribution phase alpha-half-life of 9 minutes and an elimination phase beta-half-life of 103 minutes. Anti-IFN antibodies by the ELISA technique were present in seven of 15 patients. Presence of antibody did not correlate with toxicity or response. 2',5'-Adenylate synthetase levels were increased 2 and 24 hours after the initial dose, with a trend toward higher increments with higher doses. Minimal anti-tumor responses were seen in two patients with melanoma.
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PMID:Phase I study of recombinant beta ser 17 interferon in the treatment of cancer. 379 Dec 49

Carboplatin has been developed for clinical trials as a less nephrotoxic, less emetogenic analog of cisplatin. In preclinical tumor models it was less potent than the parent compound on a molar basis, but reduced toxicity allowed comparable antitumor doses to be given. In phase I studies its dose-limiting toxicities were reversible myelosuppression, especially thrombocytopenia. Leucopenia and anemia occurred to a lesser degree. Other reported toxicities included nausea, vomiting, malaise, myalgia, arthralgia, ototoxicity, hypomagnesemia, and proteinuria. Nausea and vomiting occurred frequently, but was much less severe than that observed with cisplatin. The incidence of serum creatinine elevations was low. The increase was usually reversible and occurred only in association with administration of aminoglycosides, or abnormal pretreatment renal function. Recommended phase II doses by schedule are: bolus every 4 weeks, 400-500 mg/m2 (560 mg/m2 in children); 24 hour continuous infusion every 4 weeks, 320-400 mg/m2; weekly bolus for 4 consecutive weeks with 2 weeks rest, 100-125 mg/m2 (175 mg/m2 in children); bolus for 5 consecutive days every 4 weeks, 77-95 mg/m2. Objective responses were observed during these phase I studies in adult patients (head and neck, breast, renal carcinomas) and children (osteosarcoma, brain stem lesions). In addition to phase II evaluations in all major tumor types, plans for phase III studies in selected tumors are underway.
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PMID:Results of NCI-sponsored phase I trials with carboplatin. 391 Feb 21

Glomerular lesions have been recognized in nearly all forms of malignant diseases. The incidence within each category of malignancy varies substantially but in most series represents less than 2% of the population. While there is a considerable variety of glomerular lesions, a number of general statements may be made. In Hodgkin's disease and other lymphomas, the most common lesion is minimal lesion nephrotic syndrome, reflecting possibly an anomaly of T cell function. Amyloidosis which used to be the commonest lesion has nearly disappeared. On the other hand, in patients with chronic lymphocytic leukemia a large proportion of glomerular lesions fall into the category of proliferative glomerulonephritis. In carcinoma the vast majority of glomerular lesions with proteinuria or the nephrotic syndrome are due to membranous glomerulonephritis. This suggests either a local alteration of fixed glomerular antigens, or localization of tumor antigens planted in the glomeruli leading to the formation of local immunocomplexes. Amyloid AA is still frequent in carcinoma and complicates as much as 3% of renal adenocarcinomas.
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PMID:Glomerular lesions in malignancies. 391 7

In 6 horses with urinary bladder neoplasms, common clinical findings included a palpable mass in the bladder, anemia, hematuria, and/or proteinuria. Squamous cell carcinoma was found in 4 horses and appears to be the most common bladder tumor in the horse. Single cases of transitional cell carcinoma and fibromatous polyp also were identified. All horses except one were over 10 years of age. In one mare, treatment with 5-fluorouracil intracystically resulted in decreased bleeding from the bladder mass and apparent stabilization of the mass size. The mare ultimately died because of abdominal metastasis. Although rare, neoplasia of the urinary bladder should be considered when evaluating horses with hematuria.
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PMID:Neoplasia of the equine urinary bladder as a cause of hematuria. 401 87


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