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)

Renal glomerular basement membranes (GBMs) exhibit a charge-selective barrier, consisting of heparan sulfate proteoglycan (HSPG) that restricts the passage of anionic molecules into the urine. Previous efforts to localize the HSPG core protein within various layers of the GBM have been contradictory. Furthermore, attempts to correlate proteinuria in several disease states with a decrease in anionic sites of HSPG core protein have yielded conflicting results. When antibodies to HSPG from the EHS tumor matrix [anti-(EHS) HSPG] and GBMs [anti-(GBM) HSPG] were used together with immunogold to label renal tissues from puromycin aminonucleoside nephrotic (PAN) rats, immunolabeling results indicated that a portion of the protein core recognized by anti-(EHS) HSPG was significantly reduced, while immunolabeling with anti-(GBM) HSPG was only slightly reduced in early PAN. Anionic sites (stained with the cationic probe, polyethyleneimine) within the lamina rara externa of the GBM remained unaltered throughout the course of PAN.
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PMID:Anionic site and immunogold quantitation of heparan sulfate proteoglycans in glomerular basement membranes of puromycin aminonucleoside nephrotic rats. 175 Jul 10

Clinical cure was effected in a patient with biopsy-proven membranous nephropathy associated with spinal schwannoma. The renal manifestation of nephrotic syndrome antedated the clinical presentation of the spinal tumor. The proteinuria and edema subsided 4 mths after the complete resection of the intradural component and partial removal of the extradural component of the schwannoma. Careful workup in patients with membranous nephropathy should include not only malignant but also benign tumors.
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PMID:Membranous nephropathy associated with spinal schwannoma. 178 Jan 92

In order to evaluate the pathogenesis of proteinuria and the charge of immune deposits in lupus nephritis, anionic sites of periodate-lysin-paraformaldehyde (PLP) fixed renal tissue (5 patients with renal pelvic tumor as normal control and 17 patients with lupus nephritis), were stained with the critical electrolyte concentration method. Cuprolinic blue (CB) was used as a cationic probe. Ultra-structural study and semi-quantitative analysis were done. In the normal glomerular basement membrane (GBM), the CB stainable anionic sites appeared as filamentous structure with several short lateral branches. On the basis of electron microscopic observation of isolated proteoglycan, it is suggested that the central filaments are the protein core and the branches are the glycosaminoglycans of proteoglycan molecules. These filamentous anionic sites were located mainly in the laminae larae and lie close to each other forming a mesh-like network pattern. The semi-quantitative analysis of the normal GBM revealed that the number of anionic sites in the lamina rara externa (LRE) was 22.9 +/- 1.9-23.7 +/- 1.4/1000 nm GBM and in the lamina rara interna (LRI) 14.0 +/- 1.6-15.1 +/- 1.5/1000 nm GBM. These findings suggest that the anionic sites composed of heparan sulphate proteoglycan occupy large area of the laminae larae and prevent permeation of anionic molecules. In non-proteinuric 5 patients with class II lupus nephritis, the number of anionic sites of the GBM (LRE; 21.3 +/- 2.0-22.3 +/- 1.8/1000 nm GBM, LRI; 13.5 +/- 2.0-14.2 +/- 2.0/1000 nm GBM) showed no significant difference from that of the normal GBM. In contrast, the GBM of proteinuric patients with class IV (6 patients, LRE; 14.8 +/- 2.7-19.3 +/- 1.8/aooo nm GBM, LRI; 5.8 +/- 1.9-11.3 +/- 2.4/1000 nm GBM) and (V) (6 patients, LRE; 13.0 +/- 2.4-17.9 +/- 2.8/1000 nm GBM, LRI; 12.0 +/- 1.9-13.0 +/- 2.5/1000 nm GBM) exhibited loss of the anionic sites in association with the localization of the immune deposits (ID). From these findings, it is concluded that in severe and active lupus nephritis the failure of charge barrier of the GBM is responsible for the proteinuria. The ID observed in the patients with lupus nephritis were not stained with CB. This finding suggests that net charge of the ID could be cationic and that cationic immune complex and/or antibody could involve in the pathogenesis of lupus nephritis.
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PMID:[Electron microscopic study of the glomerular basement membrane charge barrier and the charge of immune deposits in lupus nephritis]. 178 70

A 52-year-old female had a nephrotic syndrome without neurological or dermatological manifestations. Renal biopsy revealed that glomeruli were filled with tumor cells which bore leukocyte common antigen and pan B cell marker. These cells occupied the capillary lumen and invaded into the mesangial area. Morphological alteration of endothelial cells and glomerular basement membrane were also noticed. The interstitium was well preserved. After five cycles of a combination chemotherapy, CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone), the second biopsy revealed that tumor cells disappeared from glomeruli showing mild sclerosis. Proteinuria became absent. This is the first report of an angiotropic large cell lymphoma manifesting a nephrotic syndrome and treated successfully by CHOP therapy.
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PMID:A case of angiotropic large cell lymphoma manifesting nephrotic syndrome and treated successfully with combination chemotherapy. 192 16

According to whether they are acute or progressive, complete or partial, uni- or bilateral, renal venous thromboses have quite various clinical expressions and biological consequences. The diagnosis is readily suggested by acute pain in the side with an increase in the size of one or both kidneys, associated with hematuria, proteinuria, or in case of renal failure, which is characteristic of acute bilateral thrombosis. On the other hand, chronic thrombosis of a renal vein is sometimes suggested only when complications such as pulmonary embolism occur. This explain why it is often discovered on autopsy. The diagnosis is confirmed on the basis of radiology, with ultrasound combined with vascular Doppler becoming increasingly important. Renal venous thrombosis may have various causes: disorders in renal blood flow, especially in the acute forms in newborns; hypercoagulability, in particular in nephrotic syndromes and above all in extramembranous glomerulonephritis; extension of vena cava thrombosis; retroperitoneal diseases involving the renal pedicle or extension of a renal tumor. The treatment of renal vein thrombosis is mainly medical and based on anticoagulants. The role of fibrinolytic treatment is controversial. Surgery is exceptional.
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PMID:[Thrombosis of renal veins]. 194 Jun 51

Whether extensive ablation of renal mass in humans leads to progressive glomerulosclerosis, proteinuria, and hypertension, as it does in animal models, is a matter of controversy. We have studied kidney function in six patients who underwent enucleation of a renal cell carcinoma in a solitary kidney. Four patients had previously had a nephrectomy. The two others each had one atrophic, nonfunctioning kidney. Serum creatinine levels before surgery were within the normal range (mean, 99.9 mumol/L [1.13 mg/dL]). Two weeks after tumor enucleation, creatinine levels were significantly higher than the preoperative values (mean, 124.6 mumol/L [1.41 mg/dL]). The follow-up period varied from 10 to 23 months. In all patients, kidney function improved during the following months. Serum creatinine levels nearly reached preoperative values in all patients (mean, 105.2 mumol/L [1.19 mg/dL]). None of the patients showed a progressive deterioration in renal function or proteinuria. We found a modest increase in blood pressure in two patients who had been normotensive before surgery. In conclusion, tumor enucleation in a solitary kidney did not cause significant renal injury to the remnant kidneys in our patients, at least in the short term.
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PMID:Renal function after tumor enucleation in a solitary kidney. 199 67

This analysis of IMG has focused on the long-term natural history and current approaches to therapy of this disorder. It seems clear that IMG is intrinsically a relatively benign disease, particularly in certain populations. Risk factors for an unfavorable course can often be identified at the discovery of disease. For example older age at onset, male sex, very heavy proteinuria (greater than 10 g/d), sustained hypertension, impaired renal function, and significant chronic tubulointerstitial lesions in the initial renal biopsy all portend an unfavorable outcome. Contrariwise, patients lacking these prognostic features usually do quite well with a high likelihood of spontaneous complete or partial remissions and stable renal function. Once a complete remission has occurred, whether spontaneous or therapy induced, the long-term evolution of the disorder is quite favorable. Some patients may present with what appears to be "idiopathic" MGN, only to later demonstrate underlying disease, such as neoplasia, chronic viral infection, or systemic lupus erythematosus. Glucocorticoids alone, particularly when administered orally, do not seem to have significant beneficial effects over the long term; however, high-dose intravenous methylprednisolone may at times reverse declining renal function in patients with severe nephrotic syndrome. A small subset of patients may display a remitting and relapsing course following treatment with oral glucocorticoids, resembling to some extent patients with minimal change disease. Combination of alkylating agents, either cyclophosphamide or chlorambucil with glucocorticoids is very likely beneficial for the group of patients having an intrinsically unfavorable prognosis or for patients who demonstrate progressive renal insufficiency. At the present time it is not known whether regimens that involve long-term therapy with oral cyclophosphamide combined with glucocorticoids are superior to, equivalent to, or inferior to regimens that involve the cyclical use of intravenous methyl-prednisolone oral prednisone, and oral chlorambucil. Very long-term use of cyclophosphamide, in excess of 12 months, is probably associated with unacceptable long-term risks, particularly the emergence of neoplasia. Long-term follow-up, more than 10 years, will be required to establish the magnitude of the oncogenic potential of existing shorter term regimens of cyclophosphamide-glucocorticoid combinations and for cyclical regimens using chlorambucil. Further data is required to establish the role of cyclosporine, nonsteroidal antiinflammatory agents and intravenous immunoglobulins in the treatment of patients with IMG. ACE inhibitors, sometimes combined with nonsteroidal antiinflammatory agents, may have some usefulness in patients with heavy proteinuria and declining but not advanced renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The therapy of idiopathic membranous glomerulonephritis. 203 23

A case of IgA glomerulonephritis associated with renal cell carcinoma is reported. A 61-year-old male was admitted because of a left renal mass and proteinuria. A diagnosis of renal cell carcinoma was made by computed tomography and angiography. Left radical nephrectomy was performed. Microscopically, the tumor tissue revealed renal cell carcinoma of the clear cell type. Light, immunofluorescent and electron microscopic examinations demonstrated characteristic features of IgA glomerulonephritis. The proteinuria and hematuria disappeared 8 months after removal of the tumor. These findings suggest that the IgA glomerulonephritis in our patient may have been attributable to an immune response against the renal cell carcinoma.
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PMID:IgA glomerulonephritis in a patient with renal cell carcinoma. 203 37

Twenty-eight patients with a tumor thrombus 914 in the inferior vena cava and 14 in the renal vein), among a series of 170 renal cell carcinoma patients receiving hospital treatment at the Gunma University during the period from 1961 to 1989, were explored for clinical features, with the results leading to the following conclusions: 1) There were 19 male and 9 female with respective mean ages of 62.1 and 54.4 years. 2) The disease was right-sided in 16 patients and left-sided in the other 12, but there were no striking left-to-right difference in tumor location. 3) The most frequent chief complaint was symptoms arising from the urinary tract. Among symptoms and sings occlusion of the inferior vena cava or renal vein, proteinuria was most frequent, being present in 56% of patients with clinical evidence of occlusion, followed by tortuosity of veins of the abdominal wall and edema in the lower extremities noted in 3 patients. 4) Selective renal arteriography demonstrated tumor hypervascularity in all 22 patients (except for one with a hypovascular tumor mass) and A-V shunt at a high percentage. Profuse striated vascular pattern representing arterialization of an extensive tumor thrombus was also noted, particularly with intra-caval involvement. Venacavography demonstrated neoplastic thrombi in the inferior vena cava as filling defects, thus proving the diagnosis. CT also provided diagnostic evidence of a tumor thrombus in all cases except for one in which it failed to detect a tumor thrombus in the renal vein preoperatively, with an accurate diagnosis rate of 100% for intra-caval tumor thrombi and 83% for tumor thrombi in the renal vein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical study of operative therapy for renal cell carcinoma. 2. Intravenous tumor thrombectomy]. 204 95

Thrombotic thrombocytopenic purpura (TTP) is a syndrome that occurs mainly in adults with multiorgan microvascular thrombosis consisting of thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, renal involvement, and fever. The female to male ratio is 3:2, and peak incidence occurs in the 3rd decade of life. Clinical signs are the consequence of hyaline thrombosis and occlusion of capillaries and arterioles. Renal ailment manifests itself in hematuria and proteinuria with azotemia and even overt renal failure. In severe disease, azotemia is typical of hemolytic uremic syndrome (HUS). TTP was first described in 1925 by Moschcowitz. The clinical picture of TTP consists of a prodromal phase, a viruslike disease occurring in up to 40% of patients. 60% have neurologic disturbances, 90% have purpura initially, and fever occurs in all. Anemia is often severe with hemoglobin values of 7-9 gm/dl, renal involvement in 90%, and renal failure in 40-80% of patients. Clinical variants include the acute and fulminant variety mortality, the chronic form, and the relapsing form. Predisposing factors and triggering agents are autosomal recessive inherited traits in acute idiopathic TTP, systemic diseases, tumor antigens, pregnancy and puerperium, viruses (endotoxins for HUS), and possibly oral contraceptives and hypertension. Therapy includes corticosteroids (prednisone 100-400 mg/day); heparin for postpartum HUS; and antiplatelet agents (Dextran 70, aspirin, and dipyridamole in high doses). The infusion of PGI2 is controversial; splenectomy is also questionable; and vincristine, azathioprine, and cyclophosphamide have unproven efficacy. Fresh-frozen plasma exchange is the method of choice as it produces survival in 90%. Others are iv immunoglobulins, vitamin E, and dialysis and renal transplant. Platelet transfusions are contraindicated because of sudden death and decreased survival.
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PMID:Thrombotic thrombocytopenic purpura and related disorders. 210 74


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