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)

Three children with cyanotic congenital heart disease who developed transient proteinuria and edema are described. One died of an intercurrent illness but the other two are now well. Renal biopsy findings in all three children demonstrated a mesangial proliferative glomerulonephritis on light microscopy. An unusual ultrastructural appearance of localized electron-dense thickening of the basement membrane of the capillary loops was seen in all three and collagen fibers were present in the mesangium of two. There was slight fusion of foot processes in two specimens and marked fusion in the third. Immunofluorescence in two patients demonstrated IgM staining in both and fibrin in one. The cause of the glomerular lesions is unknown but, among the many possible factors involved, anoxia and increased venous pressure may be important.
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PMID:Nephropathy in cyanotic congenital heart disease. 31 49

Degradation and synthesis of the collagen portion (CLP) of the glomerular basement membrane (GBM) in glomeruli of rats with nephrotoxic nephritis (NTN) were determined in vivo and in vitro. Degradation of CLP in rats with NTN was only increased during the first 24 h after induction of NTN. After 24 h, the half-life of CLP in NTN rats (16.9 days) was not significantly different from that in the controls 15.6 days). The loss of CLP during the first 24 h is accompanied by an increased synthesis, measured in vivo and in vitro. The increased synthesis, however, does not seem to be sufficiently high to result in accumulation of CLP-like material in NTN. Since degradation and synthesis of CLP was not altered during the later phase of NTN, it is unlikely that chronic proteinuria is the result of an ongoing abnormal turnover of CLP.
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PMID:Synthesis and degradation of glomerular basement membrane in rats with nephrotoxic nephritis. 74 Jan 13

The light- and electron microscopic changes in the glomeruli of the rat's kidney have been investigated in the course of ageing and after subtotal nephrectomy, constriction of the renal vein, and intoxication by N-nitrosomorpholine. In spite of the fact that four different experimental models have been used, identical changes were always found in the glomeruli. Morphologically they consisted of a diffuse thickening of the glomerular basement membrane and of an increase in the mesangial matrix without a proliferation of the glomerular cells. Despite this thickening of the glomerular basement membrane, functionally an increased permeability of the glomerular capillaries for macroproteins could be observed, shown by a moderate proteinuria. For these morphological changes the term "glomerulosclerosis" is suggested; they are interpreted as a non-specific, non-inflammatory reaction of the glomerulus to an impairment caused by a number of varied influences. From the study of the formal pathogenesis of the glomerulosclerosis presented here one can conclude that in the individual experimental models the same result has been achieved in different ways. One possibility in the development of glomerulosclerosis is an increased production of the components of the basement membrane and of the mesangial matrix. This is the pathway which appears to be followed after nephrectomy. Another possibility is a slowing down of the breakdown of both the matrix and the membrane. This seems to be the case in the glomerulosclerosis occuring in the course of ageing, and after hypoxic and toxic changes. It could be accounted for by a functional disturbance of, presumably, the mesangial cells responsible for the breakdown of the basement membrane and of the matrix. On the other hand, one may have to consider a primary alteration of the macromolecules of these structures, as is already known from studies of the, chemically closely related, collagen. The light- and electron microscopic studies of the normal and of the altered glomeruli have led to certain conclusions concerning the origin and the fomation of the glomerular basement membrane and the mesangial matrix. In order to widen the scope of the studies, additional autoradiographic investigations with 3H-proline and 3H-leucine have been performed in ultrathin and semithin sections of the rat's glomeruli. The results of the studies presented here suggest that of the three cell types of the glomerulus the visceral epithelial cells (podocytes, "Deckzellen") may participate on the formation of the glomerular basement membrane, whereas the mesangial cells appear to be responsible for the synthesis of the mesangial matrix.
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PMID:[On the pathogenesis of the glomerulosclerosis ultrastructural and autoradiographic investigations on the rat kidney (author's transl)]. 79 Aug 31

Immunoglobulins IgG, IgM and IgA in the serum of 61 patients suffering from chronic renal failure of various etiology and not being under hemodialysis treatment were measured. Cases of nephropathy, due to collagen or blood disease or uremia with heavy proteinuria were excluded. No statistically significant difference was found between patients and controls in respect to the serum level of the 3 immunoglobulins studied. No correlation was found between the level of serum immunoglobulins and the blood urea or the amount of protein daily excreted in the urine.
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PMID:Quantitative determination of immunoglobulins in chronic renal failure. 80 38

Studies are reviewed of the inhibitory effect of flurbiprofen, given in doses ranging from 50 mg to 200 mg per day for 1 week, on platelet aggregation measured by biological tests (adenosine diphosphate and collagen methods). Flurbiprofen at doses of 50 mg and 100 mg daily had a peak time of action of between 1 and 2 hours, the effects usually disappearing after 24 hours, and 100 mg flurbiprofen caused a similar decrease in platelet aggregation to 1 g aspirin daily. In a clinical study of 72 patients with chronic glomerulonephritis treated with doses of flurbiprofen up to 200 daily there was a significant correlation between the parameters of aggregation measured and treatment, and between proteinuria and adenosine disphosphate aggregation when the flurbiprofen dose did not exceed 100 mg daily.
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PMID:Clinical pharmacology of flurbiprofen: a novel inhibitor of platelet aggregation. 91 17

The association of thrombocytopenia, macrothrombocytopathia, nephritis and deafness is rare. Reported here is a new case of this triple association. The clinical course, the nephropathologic findings and the bilateral neurologic hearing loss were similar to those already reported, with a slowly progressive impairment of renal function accompanied by a persistent proteinuria. The platelet diameters were increased. These macroplatelets contained granules of normal structure but with an irregular distribution in the cytoplasm. In other areas the cytoplasm was rich in surface connected system. The survival of these platelets and their contraction were normal. Their aggregation and excretion in response to collagen, adenosine diphosphate and thrombin, and the values of platelet factor 3 activity were all decreased. The degranulation defect, also present, was observed in the absence of a decrease in intracellular cyclic adenosine 5'-monophosphate (AMP) suggesting a relationship between these two findings.
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PMID:Thrombocytopenia, macrothrombocytopathia, nephritis and deafness. 94 91

Out of 136 placentas with vascular obliterations, 25 cases were placentas of children born alive, in 92 cases the placentas belonged to children born dead. In 19 cases we had no data on the baby. In placentas of babies born alive, the same vascular changes (subtotal and total obliterations, septal partitions of vascular lumina) were found as in those of dead-born children, although considerably less severe. Vascular obliterations should not be considered as post-mortal alterations of the placenta blood vessels, since only quantitative differences could be proved. Septum-like partitions are hardly ever found in placentas of babies born alive, in dead-born babies they are more frequent. They seem to present recanalizations, and are understood as a compensation mechanism for a placental insufficiency caused by vascular obliterations. The accentuated collagenization of the placental periphery, noticed in placentas of babies born alive, is being interpreted as the consequence of an impaired blood circulation, caused by partial and total vascular obliterations. The high collagen rate in the placental periphery in placentas of the dead-born is probably a reaction to the diminished fetal circulation. Endangitis obliterations in 73 placentas out of 4600 pregnancies of cases with late abortions, premature deliveries, perinatal death, underweigh and small for gestational age babies, impaired adaptation in newborns of mothers with proteinuria and hypertension speak strongly for assuming that endangitis obliterans presents a form of placental insufficiency. Endangitis obliterans of the placental blood-vessels has, however, been discovered frequently after Rubella infection in early pregnancy. The etiological factors of the endovascular process can be multiple, the morphological and the pathophysiological reactions are the same.
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PMID:[Obliterative angiopathy of placental stem villi (author's transl)]. 99 57

A postulated mechanism of immune glomerular injury is a direct interaction between antibody and glomerular epithelial cell (GEC) surface antigens. To explore this hypothesis, we examined the interaction of the noncomplement-fixing gamma 2-subclass of sheep anti-rat nephrotoxic serum (NTS), which causes immediate complement- and neutrophil-independent proteinuria in vivo, with rat GECs in culture. Reactivity of NTS with GEC surface antigens was determined by positive immunofluorescence of GEC plasma membranes and by the ability of NTS-coated tissue culture wells to provide an adhesive substrate for GECs. NTS immunoprecipitated two proteins (135 and 118 kDa) from surface-labeled GECs. Proteins of similar molecular mass were precipitated by a polyclonal rabbit antibody that identifies the beta 1-integrin chain of the mouse fibronectin receptor (anti-FnR). In addition, NTS identified similarly sized bands on Western blot analysis of cell membranes from isolated rat glomeruli. Similar reactivity was eluted from the glomeruli of proteinuric rats injected with NTS. NTS significantly inhibited GEC adhesion to laminin, types I and IV collagen, and fibronectin and prevented GEC spreading on types I and IV collagen. Anti-FnR similarly inhibited GEC adhesion. Cell viability was not affected. These results show that NTS recognizes a pair of GEC surface proteins that have the characteristics of an alpha- and beta 1-integrin and, at low concentrations, disrupt cell-matrix interactions.
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PMID:Nephrotoxic antiserum identifies a beta 1-integrin on rat glomerular epithelial cells. 137 74

Chronic progressive membranous nephropathy (MN) in humans is characterized by thickening of the glomerular basement membrane (GBM) with formation of spikes which contain laminin and other extracellular matrix (ECM) proteins. We have utilized two models of MN in the rat (active and passive Heymann nephritis, AICN, PHN) to define the sequential changes in composition of GBM as they relate to changes in glomerular gene expression for ECM components, altered permeability and morphological changes. Renal biopsies obtained during the course of AICN and PHN were immunostained for various ECM proteins and total glomerular RNA was hybridized with cDNA probes specific for laminin B2-chain, s-laminin, and types I and IV collagen. In addition, the ability of anti-glomerular epithelial cell (GEC) antibody and complement on rat GEC in culture to induce laminin release or laminin and s-laminin mRNA expression was determined. The results demonstrate that at weeks 12, 16, and 20 of AICN, immunostaining for laminin, s-laminin, fibronectin, entactin, and heparan sulfate proteoglycan increased in the GBM in a spike-like pattern. Concomitantly, glomerular mRNA levels of laminin B2-chain and of s-laminin increased. Type IV collagen protein and gene expression remained unchanged or decreased. No glomerular immunostaining for type I collagen occurred during AICN despite increased expression of mRNA for this collagen type. In contrast to AICN, in PHN no pronounced changes of the glomerular ECM occurred, except for transient expression of type I collagen mRNA in whole glomerular RNA and type I collagen protein the GEC cytoplasm. Stimulation of GEC in culture with anti-GEC antibody and complement also failed to induce transcription of laminin or s-laminin mRNA or the release of laminin protein. These findings suggest that the polyantigenic expansion of GBM which occurs in chronic experimental MN may be stimulated by factors different from the C5b-9 mediated processes that cause the initial proteinuria.
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PMID:Altered glomerular extracellular matrix synthesis in experimental membranous nephropathy. 138 96

Irreversible mesangial changes with persistent proteinuria were induced in rats given two consecutive injections 2 weeks apart of a MoAb 1-22-3 to rat mesangial cell. The characteristics of the resulting lesions were investigated and compared with those of the reversible change induced by a single injection. At 24 h after the second injection, mesangiolytic changes similar to those after a single injection were evident. The accumulation of macrophage-like cells in glomeruli observed at 1 week after the first injection was not evident during the experimental period after the second injection. Hypercellularity with the characteristics of intrinsic mesangial cell and increased mesangial matrix were already present 1 week after the second injection. And mesangial sclerotic change progressed up to 6 months. Deposition of collagen type I and type III and accumulation of collagen fibril at the ultrastructural level were evident in rats 6 months after the second injection. Proteinuria started immediately and continued for more than 6 months after the second injection. The mesangial sclerotic change with persistent proteinuria described here is considered to be a better model for investigating the mechanism of chronic progression of human mesangial proliferative glomerulonephritis.
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PMID:Mesangial sclerotic change with persistent proteinuria in rats after two consecutive injections of monoclonal antibody 1-22-3. 139 93


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