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)

In 55 children in the acute phase of viral hepatitis with HB Ag antigenemia, and in 24 without antigenemia, total urinary protein excretion and frequency of excretion of the following serum proteins in urine were studied: alpha1-glycoprotein, haptoglobin, transferrin, A, G and M immunoglobulins, light immunoglobulin chains of the phi and gamma types, and Fc and Fab fragments of immunoglobulin G. The control group consisted of 15 healthy children without HB Ag antigenemia and 8 with antigenemia. The type of proteinuria was determined by electrophoresis of serum proteins excreted in the urine on Cellogen-RS. In children suffering from viral hepatitis the urine contained serum proteins significantly more often than in healthy children. HB ag antigenemia had no influence on the degree or type of proteinuria. In children suffering from viral hepatitis with and without HG Ag antigenemia, proteinuria was of the selectively glomerular type, and less often of mixed glomerulo-tubular type with selective glomerular component. It follows that the HB Ag antigen has np distinctly detrimental effect on the renal glomeruli in the acute phase of viral hepatitis, in which the vascular endothelium of renal glomerular blood vessels is probably injured. Less ofter, in children in the acute phase of viral hepatitis function of the proximal segment of the tubules is damaged with appearance in the proteinogram of Berggard's microglobulins.
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PMID:Proteinuria in the acute phase of viral hepatitis in children and the influence of HBAg antigen. 82

We showed previously that proteinuria caused delayed chylomicron (CM) clearance in the rat and postulated the existence of a primary defect in CM hydrolysis. It was possible that reduced CM clearance resulted from increased lipogenesis causing saturation of catabolic sites and not from a primary defect in CM catabolism. To clarify this point we measured kinetically the absolute rate of triglyceride (TG) uptake from CM in rats with Heymann nephritis (HN) and normal Sprague-Dawley rats (SD) and determined TG uptake in individual tissues using [3H]TG- and [14C]cholesterol-labeled CM. Hepatic [14C]cholesterol uptake was reduced in HN (69.3 +/- 6 vs. 7.2 +/- 2% of dose, P less than 0.001). TG uptake was reduced in HN measured kinetically (1.01 +/- 0.09 vs. 0.213 +/- 0.028 mg TG.min-1.100 g body wt-1, P less than 0.001) and reduced in all tissues (heart, skeletal muscle, fat, and liver). CM are catabolized on the vascular endothelium to atherogenic, cholesterol-rich remnant (CM remnant) particles, which are then rapidly taken up by the liver. We measured hepatic CM remnant uptake in SD and in HN using [14C]cholesterol-labeled CM remnant. CM remnant uptake was significantly reduced in HN (58 +/- 1.2 vs. 20 +/- 0.86% uptake, P less than 0.01). CM remnants were increased significantly in plasma of HN. Thus the nephrotic syndrome causes a primary defect in the uptake of TG from CM that is expressed in all tissues and a separate defect in hepatic CM remnant uptake. Although CM remnant generation is impaired because of defective CM hydrolysis, the defect in hepatic CM remnant uptake is so severe that these particles accumulate in blood, posing a potential risk for atherogenesis.
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PMID:Both peripheral chylomicron catabolism and hepatic uptake of remnants are defective in nephrosis. 151 Jan 25

Experiments on 5 test and 16 control Wistar-Kyoto rats have shown that streptozocin diabetes mellitus complicated by proteinuria is characterized by the following changes of the fatty acid spectrum of platelet phospholipids: a decrease in the content of C18:2p6, C18:3p3, C20:4p6, C20:3p9, C20:5p3, in the sum of fatty acids of the linoleic group and the ratio of unsaturated/saturated fatty acids and an increase in the content of C18:0, C20:2p6 and C20:3p6. These changes were accompanied by an increase in the platelet aggregation ability, an increase in their synthesis of thromboxane A2 and a decrease in the synthesis of prostacyclin I2 by vascular endothelium and account for them, to a certain degree. The obtained results are promising with relation to achieving a positive effect of the diets, rich in linoleic acid, for prophylaxis of vascular complications in diabetes mellitus.
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PMID:[Tha fatty acid spectrum of the thrombocyte phospholipids in experimental diabetes mellitus complicated by proteinuria]. 239 42

Although a variety of renal lesions may occur in acquired immune deficiency syndrome (AIDS), a rare but aggressive form of focal and segmental glomerulosclerosis with capillary collapse has been considered a possible component of this disorder. It is manifested by heavy proteinuria and progression to renal failure in a short time. We studied renal biopsies from nine patients with HIV infection and the above clinical features and compared the renal tissues to biopsies from HIV-positive individuals with immune complex glomerulonephritis and to biopsies from patients with heroin abuse nephropathy. The HIV-associated nephropathy was characterized by a combination of lesions: focal and segmental glomerulosclerosis, often in an early stage of evolution and with prominent degenerative changes of visceral epithelium; tubular necrosis without identifiable nephrotoxic or hemodynamic etiology; interstitial edema; large plasma protein-containing tubular casts in all segments of the nephron associated with marked tubular dilatation; and widespread tubuloreticular structures in vascular endothelium. In contrast, neither the sclerosing glomerular changes nor the tubulointerstitial abnormalities were present in HIV-infected patients with immune complex glomerulonephritis. Similarly, the tubular and interstitial changes and widespread tubuloreticular structures were absent in heroin-abuse nephropathy. The lesions of HIV-associated nephropathy occurred in patients with AIDS, AIDS-related complex, and in individuals clinically asymptomatic for HIV infection. Their morphological features in asymptomatic patients are sufficiently specific to allow for accurate diagnosis of HIV infection.
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PMID:HIV-associated nephropathy. A unique combined glomerular, tubular, and interstitial lesion. 307 May 50

Preeclampsia is a disorder of pregnancy characterized clinically by hypertension, proteinuria, and edema and characterized pathologically in its late stages by widespread microvascular thrombi. There is evidence from a number of studies that production of prostacyclin (prostaglandin I2, PGI2), a potent vasodilator and inhibitor of platelet aggregation, is deficient in preeclamptic compared to normal pregnancy. Traditional therapy utilizes infusions of large amounts of MgSO4, but the physiologic basis for this is not clear. We studied the effect of MgSO4 on PGI2 release by cultured human umbilical vein endothelial cells (HUVEC) by several methods. By platelet aggregometry, the known antiaggregatory effect of intact HUVEC was enhanced by MgSO4. By radioimmunoassay for 6-keto-PGF1 alpha, the stable metabolite of PGI2, it was shown that MgSO4 amplifies release of PGI2 by HUVEC in a dose-dependent manner, with a peak occurring between 2 and 3 mM. In separate experiments, MgSO4 overcame the enhanced adherence of platelets to HUVEC exhausted by repeated exposure to thrombin. Finally, PGI2 production was 2- to 5-fold greater by HUVEC incubated with plasma obtained from preeclamptic patients undergoing MgSO4 therapy than by HUVEC incubated with pretherapy plasma. We conclude that MgSO4 mediates enhanced production of PGI2 by vascular endothelium, thereby potentially enhancing its thromboresistant properties.
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PMID:Magnesium sulfate: rationale for its use in preeclampsia. 351 61

The aetiology of the primary systemic vasculitides remains obscure. Recent years have seen significant advances in our understanding of inflammation and in particular the role of and interaction between the vascular endothelium, mediators and immune effector cells. This has helped to further elucidate those specific processes relevant to vasculitis which result in endothelial cell damage. In Wegener's granulomatosis and microscopic polyarteritis the evidence favours an autoimmune inflammatory response characterised by specific mediators in which the endothelium is both target and active participant. Current treatment of these disorders with combinations of corticosteroids and cytotoxics is highly effective in inducing remission. However, long-term use of this therapy is potentially toxic and there remains also a significant risk of relapse. It is hoped that increased understanding of the pathogenesis of systemic vasculitis will enable more specific, less toxic and more effective therapies to be defined. Jayne et al. have suggested a beneficial effect of intravenous pooled normal human immunoglobulin (IVIG) in patients with ANCA-positive vasculitis. In vitro studies have shown that IVIG contains antiidiotypic antibodies to ANCA and AECA, capable of inhibiting the binding of these autoantibodies to their autoantigens. In vivo, IVIG may also provide the immunoregulatory elements needed for the idiotype network and control of the autoimmune repertoire. Mathieson et al. successfully used monoclonal antibodies to T cells (Campath-H directed against CDw52) in a patient with ANCA-negative dermal lymphocytic vasculitis. Monoclonal antibodies to CAMs have been used in human renal transplant rejection and reduced the inflammation and proteinuria in animal models of anti-glomerular basement membrane disease. In vasculitis, the therapeutic use of specific anti-CAM antibodies may result from further definition of the role of CAMs. Increased understanding of the pathogenesis of systemic vasculitis is likely to provide the basis for the use of more specific immunotherapies in the future.
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PMID:Mechanisms of endothelial cell injury in vasculitis. 799 43

HgCl2 induces the synthesis of anti-GBM Abs with the development of glomerular and interstitial nephritis, as well as proteinuria, in the Brown Norway rat. The development of this autoimmune disease is a consequence of the appearance of an autoreactive T cell subset-inducing activation of B cells. The administration to mercury-treated rats of the mouse anti-human VLA alpha 4 HP2/1 mAb, which cross-reacts with the rat homologue integrin, completely abrogated the interstitial cell infiltrates. As demonstrated by peripheral blood analysis, this effect is not a result of the depletion of circulating leukocytes or leukocyte subsets. Interestingly, the administration of Abs specific for the alpha 4 integrin also highly reduced anti-GBM Ab synthesis, thus preventing detectable glomerular deposits and proteinuria. Our results confirm that in vivo alpha 4 functions in adhesive interaction of circulating leukocytes and vascular endothelium, and is centrally important in the extravasation and migration of T lymphocytes to sites of tissue injury. We also found a complete absence of interstitial cell infiltrates, together with a positive glomerular IgG lineal deposition pattern, when anti-GBM Abs were passively transferred to rats pretreated with anti-alpha 4 mAb, thus indicating an independent role of alpha 4 integrin in both extravasation of immune cells and production of autoantibodies. Furthermore, these in vivo findings provide preliminary evidence for the participation of the VLA-4 integrin in mediating the intercellular interaction of leukocytes regulating the production of Abs, most likely through the existence of additional yet unknown ligand(s).
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PMID:Prevention of mercuric chloride-induced nephritis in the brown Norway rat by treatment with antibodies against the alpha 4 integrin. 805 27

In adults, 12 to 14 g of albumin are synthesized daily. The same quantity is catabolized, essentially by the vascular endothelium and to a lesser degree in renal tubules. During nephrotic syndrome, contrary to what is observed in malnutrition conditions accompanied by hypoalbuminemia, hepatic synthesis is only moderately increased, whereas fractional catabolism is greater than normal. The increase in alimentary protein-intake, which has been proposed to restore the pool of albumin, raises hepatic albumin synthesis, but also its urinary losses, most likely by stimulation of the renin-angiotensin system. A reduction in protein rations lowers proteinuria and improves the hepatic abnormalities of nephrotic syndrome but its longterm nutritional consequences are poorly understood. The association of a converting enzyme inhibitor with a diet moderately restricted in protein content (1 g/kg/day) might constitute a therapeutic satisfactory solution.
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PMID:[Protein metabolism during nephrotic syndrome. Experimental and clinical influence of dietary protein intake]. 823 11

Endothelin (ET) is the most potent endogenous vasoconstrictory substance known. There are three structurally and pharmacologically separate endothelial isopeptides in humans; Endothelin-1 is exclusively produced in the vascular endothelium. It seems likely that ET acts as a local paracrine signal rather than a circulating hormone. The synthesis and release of ET is stimulated among others by hypoxia, thrombin and endotoxin. Its effects are mediated by specific, membrane-bound receptors, which are detectable in high concentrations in the fetoplacental tissue. ET-1 causes an initial transient fall in blood pressure, followed by a strong, long-lasting increase in peripheral resistance and blood pressure. Plasma ET-1 levels are increased in preeclampsia as compared to those of normal pregnancies, and do not correlate with mean arterial blood pressure and degree of proteinuria. In umbilical cord blood ET-1 concentrations are 2.5-10-fold higher than those of maternal plasma. Determination of plasma ET is unlikely to be of value in the prediction of the disease. ET-1 induces an increased synthesis of vasodilatory prostaglandins (PGI2, PGE2) and an increased production of endothelial-derived relaxing factor (EDRF); thromboxane concentrations in blood are elevated by thrombin-induced activation of platelets. In animal models ET-1 causes an activation of plasmatic coagulation with consecutive hypercoagulability. In preeclampsia ET may play an important role in the regulation of the endothelial balance. Future therapeutic approaches may include the development of effective ET-antibodies or of inhibitors of the endothelin-converting enzyme.
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PMID:[Endothelin--possible significance in pregnancy and hypertensive pregnancy]. 823 57

In search of the basic defect and cell type responsible for the massive treatment-resistant proteinuria of congenital nephrotic syndrome of the Finnish type (CNF), we examined tissue samples of CNF kidneys using established antibody and lectin markers of various glomerular cell types. Markers of vascular endothelium (antibodies to factor VIII and a human homologue of podocalyxin (anti-PHM5) and UEA I lectin) showed no qualitative changes in the endothelial cells of glomeruli or peritubular areas in CNF as compared with controls. Markers of glomerular mesangial cells (antibodies to desmin, smooth muscle actin, RCA I lectin) revealed a secondary increase in mesangial reactivity reflecting the sclerosis and expansion of the mesangial areas in CNF. Markers of visceral epithelial cells (antibodies to a human homologue of podocalyxin, C3b receptor, vimentin, common lymphocytic leukemia antigen, gp44, and the WGA, LFA and, after neuraminidase treatment, PNA lectin) failed to show appreciable qualitative changes in CNF kidney samples. Interestingly, the alpha 2 beta 1 integrins appeared greatly reduced in all CNF samples studied, possibly explaining the mechanisms of CNF-associated proteinuria.
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PMID:Glomerular antigens in severe hereditary nephrosis. 854 48


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