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)

The first case of gamma-heavy chain disease described in Spain is here reported. The patient, a 36-year-old woman, presented fever, enlarged regional lymph nodes, and hepatosplenomegaly, without bone marrow abnormalities but with lymphopenia. Serum electrophoresis did not disclose any M-component. The abnormal gamma-chain protein had a alpha2-globulin mobility and was immunochemically related to the Fc fragment. It belonged to the IgG 4 subclass, its molecular weight was about 60,000. Proteinuria was minimal but the electrophoresis of concentrated urine showed a homogeneous peak of alpha2-globulin mobility constituted by the gamma-chain fragment. Biopsy of an axillary lymph node disclosed features of immunoblastic sarcoma. The course was malignant, resulting in death in 8 months.
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PMID:A new case of gamma-heavy chain disease. 41 49

From 1972 through 1991, 404 patients with renal tumor (Wilms' tumor and clear cell sarcoma) were seen at the Pediatric Oncology Unit of Hacettepe Children's Hospital. The genital abnormalities and renal diseases in these patients were evaluated retrospectively. Eight patients with renal tumor had genital abnormality and/or renal disease of various types and degrees. One of these patients had a clear cell sarcoma while all the others had Wilms' tumor. Two patients had all components of the Drash syndrome. Two patients with Wilms' tumor had genital abnormality and mild proteinuria. Another two patients had only Wilms' tumor and renal disease. Two patients had only renal tumor and genital abnormality of whom one was the patient with clear cell sarcoma.
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PMID:Renal tumors with pseudohermaphroditism and glomerular disease. 133 37

Thirty-seven patients with advanced soft tissue sarcoma were treated with merbarone utilizing a daily intravenous schedule for five days. Only one partial response was observed in the thirty-three evaluable patients. The major toxicities were renal, with elevation of creatinine and/or proteinuria, and gastrointestinal, with mild to moderate nausea and vomiting. Merbarone in this dose and schedule has minimal activity in soft tissue sarcoma.
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PMID:Phase II trial of merbarone in soft tissue sarcoma. A Southwest Oncology Group study. 148 11

We have examined the antibody activity and nephritogenicity of anti-Engelbreth-Holm-Swarm (EHS) sarcoma antiserum in order to analyze the pathogenesis of the EHS nephropathy which has already been reported by us. An increased amount of urine protein was not recognized in rats injected with a large quantity of anti-EHS sarcoma antiserum. In addition, rats immunized with rabbit IgG before anti-EHS sarcoma antiserum injection developed no abnormal proteinuria, despite positive fluorescent staining for rat IgG as well as rabbit IgG in the glomeruli. From these results we concluded that nephritogenic antibodies could not be produced in rabbits by immunization with EHS sarcoma, which could induce the EHS nephropathy in an active model.
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PMID:Nephritogenicity of anti-Engelbreth-Holm-Swarm sarcoma antibody. 332 Jul 77

Antilaminin antibodies have been shown to bind to laminin within the glomerular basement membrane (GBM) and mesangium of experimental animals but have induced little or no glomerular injury. We used a sheep antiserum to murine Englebreth-Holm-Swarm sarcoma laminin (sheep antilaminin) to further study the potential of antilaminin antibodies to cause glomerular injury. Intravenous injections of sheep antilaminin into rats produced intense linear GBM deposits of sheep IgG but consistently failed to induce heterologous phase proteinuria as previously shown. In addition, no autologous phase injury appeared even after preimmunization with sheep IgG (N = 4) or passive administration of rat anti-sheep IgG (N = 3) (mean urine protein less than 4 mg/24 hours up to 16 days). GBM deposits of rat C3 in vivo were absent despite the ability of both sheep antilaminin and rat anti-sheep IgG to fix human and rat C3 in vitro as determined by an indirect immunofluorescent assay. In contrast, when kidneys containing sheep antilaminin were transplanted into naive recipients that were passively immunized with rat anti-sheep IgG, severe proteinuria occurred (range 7 to 109 mg/24 hours on day 2; 49 to 350 mg/24 hours on day 5 posttransplantation) in association with glomerular deposition of C3. Histological evaluation at day 5 showed a severe proliferative glomerulonephritis with infiltrating polymorphonuclear and mononuclear leukocytes. Electron microscopy showed endothelial and epithelial cell detachment from the GBM and inflammatory cell adherence to denuded GBM. Epithelial foot process effacement and cytoplasmic absorption droplets were also noted. Identical kidneys transplanted into nonimmunized recipients or immunized recipients depleted of complement had significantly less (p less than 0.05) proteinuria (nonimmunized: 5 to 18 mg/24 hours on day 2, 4 to 9 mg/24 hours on day 5; complement-depleted: 6 to 13 mg/24 hours on day 2, 4 to 27 mg/24 hours on day 5) and no glomerular complement fixation was seen in these animals. Thus, severe glomerular injury can be induced by a focused, amplified, complement-dependent immune attack on glomerular laminin. In contrast, the widespread distribution of laminin and antilaminin probably dilutes the total glomerular immune reaction and precludes effective complement fixation and glomerular injury during the autologous phase in nontransplanted kidneys. A similar explanation might account for the lack of glomerular injury in previous studies that utilized antisera to known GBM constituents.
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PMID:Nephritogenic potential of sheep antibodies against glomerular basement membrane laminin in the rat. 351 87

Thirty six patients with advanced solid tumors (24 lung: 3 oat-cell, 14 squamous, 7 adenocarcinomas, 3 soft tissue sarcomas, 6 breast carcinomas; 1 seminoma; 2 ovarian adenocarcinomas) entered a phase II study of high-dose ifosfamide (IF) administered in combination with the uroprotective agent sodium 2-mercapto-ethane-sulfonate (Mesna). Fourteen patients had prior treatment; most patients with lung cancer (22/24) were previously untreated; all had measurable disease. The patients median age was 59 (range 31-74). IF was given at 1.8 g/m2 days 1-5 q 4 weeks. Mesna was given after each IF injection at 0, 4 and 8 h randomly, either i.v. (0.36 g/m2) or orally (0.72 g/m2). Twenty-four patients had greater than or equal to 3 courses of therapy, 9 had 2 courses, and 3 had only 1 course; 129 courses were evaluated for toxicity. Mesna was given orally (17 patients, 57 courses) or i.v. (19 patients, 72 courses). The following side-effect were observed: no gross hematuria, microhematuria (14 courses), transitory mild proteinuria (34 courses), leukopenia grade I-II ECOG (26 courses), anemia grade I ECOG (31 courses), 1 case of pancytopenia, alopecia (31 patients), nausea (moderate, 33 courses; severe, 6 courses), vomiting (moderate, 17 courses; severe, 1 course). Five patients showed a partial response (1 oat-cell carcinoma, 2 with squamous lung cancer, 1 with ovarian carcinoma, 1 with breast carcinoma), 14 showed a minor response (2 patients with oat-cell carcinoma, 2 with lung adenocarcinoma, 5 with squamous lung cancer, 1 with seminoma, 1 with sarcoma, 1 with ovarian carcinoma), and 14 showed progression of disease (7 patients with squamous cell lung cancer, 4 with lung adenocarcinoma, 1 with sarcoma, 2 with breast carcinoma). Considering partial plus minor responses, ifosfamide produced some degree of tumor reduction (PR + MR) in 12/23 (52.1%) lung cancer patients. The data reported support the conclusions that Mesna can prevent high-dose IF bladder toxicity, that IF is active in advanced solid tumors, including lung cancer, and that the IF + Mesna combination is a generally safe treatment procedure.
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PMID:Phase II study of ifosfamide combined with Mesna uroprotection in advanced non-small-cell lung carcinoma and other solid tumors. 643 51

A 65 year old woman had a minimal changes nephrotic syndrome (MCNS) with steroid-induced remission. An underlying malignancy was discovered at the time of relapse of proteinuria: it was a retroperitoneal chordoid sarcoma. Even though the tumor could not be excised, complete remission was again observed with corticosteroids. There was no second relapse when prednisone was discontinued and during the seven months before the patient died. This is a new unusual case of MCNS associated with carcinoma. The response of nephrotic syndrome steroid therapy is further suggestive evidence that deficiency in T-cell function may be involved.
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PMID:[Nephrotic syndrome with minimal glomerular lesions, sensitive to corticoids, disclosing a chordoid sarcoma]. 647 62

We report a perineurioma of the kidney. A 66-year-old woman had a renal mass discovered as an incidental finding during the evaluation of hypertension and proteinuria. This neoplasm radiographically mimicked renal cell carcinoma, but the diagnosis of perineurioma was confirmed with histologic and ultrastructural studies. Perineurioma is a recently described, rare, benign tumor of the peripheral nervous system composed of perineurial cells. Histologically, the differential diagnosis includes low-grade fibromyxoid sarcoma and other myxoid tumors.
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PMID:Perineurioma of the kidney. Report of a case with histologic, immunohistochemical, and ultrastructural studies. 850 41

Reactive oxygen species (ROS) are produced and released into the extracellular spaces in numerous diseases and contribute to development and progression, for example, of inflammatory diseases, proteinuria, and tumor invasion. However, little is known about ROS-induced chemical changes of interstitial matrix proteins and their consequences for the integrity of the matrix meshwork. As basement membranes and other matrices are highly cross-linked and complex, the relatively simple matrix produced by Engelbreth-Holm-Swarm (EHS) sarcoma, and proteins isolated therefrom, were incubated in vitro with defined concentrations of ROS that were generated by the Fenton or xanthine oxidase/xanthine reactions. This resulted in two counter-current effects. Although up to approximately 15% of the EHS matrix proteins were released into the supernatant in a ROS dose-response relationship, the residual insoluble matrix was partially cross-linked by ROS. Matrix proteins released into the supernatants were examined by rotary shadowing, quantitative sodium dodecyl sulfate polyacrylamide gel electrophoresis, immunoblotting, and fluorospectrometry for loss of tryptophans and formation of bityrosine residues. At relatively low ROS concentrations, selective liberation of morphologically intact laminin/entactin was found that, however, failed to reassociate and showed oxidative damage of its tryptophan residues. At higher ROS concentrations, laminin and entactin were progressively disintegrated, partially fragmented, and eventually completely degraded. At this point oligomers of type IV collagen predominated in the supernatant, and proteoglycans were not encountered at any concentration of ROS. Similar gradual molecular changes were also obtained when fractions of isolated soluble EHS matrix proteins were incubated with graded concentrations of ROS. In these experiments, the formation of covalently linked oligomers and aggregates paralleled the ROS-dependent formation of cross-linking bityrosine groups. ROS scavengers pinpointed to the hydroxyl radical as the most damaging radical species. Protease inhibitor experiments suggested that degradation of matrix proteins was caused primarily by the direct action of ROS and not by proteolysis by potentially contaminating proteases. Collectively, these results provide evidence that EHS matrix proteins show differential sensitivity to ROS-induced damage in a reproducible, sequential pattern, in the order entactin > laminin > type IV collagen, and that ROS cause partial dissociation and cross-linking of the EHS matrix.
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PMID:Reactive oxygen species cause direct damage of Engelbreth-Holm-Swarm matrix. 921 47

Chinese-herb nephropathy (CHN) is a rapidly progressive renal fibrosis associated with the intake of a Chinese herb (Aristolochia fangchi) containing nephrotoxic and carcinogenic aristolochic acids (AA). This study attempted to reproduce the main features of human CHN (renal failure, tubular atrophy, and interstitial fibrosis) in a rat model similar to that of cyclosporin-induced nephropathy. Salt-depleted male Wistar rats received daily subcutaneous injections of either 1 mg/kg body wt AA (low-dose AA group), 10 mg/kg body wt AA (high-dose AA group), or vehicle (control group) for 35 d. On days 10 and 35, assessment of renal function, measurements of urinary excretion of glucose, protein, and leucine aminopeptidase, and histologic analyses were performed (six rats euthanized/group). High-dose AA induced glucosuria, proteinuria, and elevated serum creatinine levels and reduced leucine aminopeptidase enzymuria on days 10 and 35, whereas low-dose AA had no significant effect. Tubular necrosis associated with lymphocytic infiltrates (day 10) and tubular atrophy surrounded by interstitial fibrosis (day 35) were the histologic findings for the high-dose AA-treated rats. In both AA groups, urothelial dysplasia was also observed, as well as fibrohistiocytic sarcoma at the injection site. A short-term model of AA-induced renal fibrosis was established in salt-depleted Wistar rats. These results support the role of AA in human CHN and provide a useful model for examination of the pathophysiologic pathways of renal fibrosis.
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PMID:Aristolochic acids induce chronic renal failure with interstitial fibrosis in salt-depleted rats. 1180 72


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