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)

Magnesium (Mg) plays an important role in cardiovascular homeostasis. A deficiency may be of importance for the etiology of disorders that have vasospasm in common. Mg administration can reduce the peripheral vascular resistance and thus enhance organ perfusion. We observed that Mg sulfate infusion could have a beneficial effect upon the serum urate concentration in preeclamptic women, presumably by affecting the renal function. A study comprising 10 preeclamptic women with a high serum urate level (413-788 umol/l) was carried out. Glomerular filtration rate (GFR) was measured by determination of iohexol clearance. 30 mmol Addex-Magnesium was then given i.v. during 12 h and a second GFR determination performed the next day. We had expected the GFR to increase, but to our surprise, it decreased (in mean, from 74.2 ml/[min x 1.73 m2] to 71.3; p < 0.05; Wilcoxon signed-ranks test). There were no significant changes of blood pressure, proteinuria, blood thrombocytes, transaminases, serum creatinine or serum urate. We conclude that in preeclamptic women with renal dysfunction, Mg infusion therapy had no favourable effect upon either blood pressure nor GFR in the short-term perspective.
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PMID:Short-term effect of magnesium sulfate infusion on renal function in preeclamptic women. 147 18

In passive Heymann nephritis, a rat model of membranous nephropathy, antibody (anti-Fx1A) activates C on the surface of the glomerular epithelial cell (GEC), leading to GEC injury and proteinuria. In this study, we examined C activation by anti-Fx1A in cultured rat GEC. In addition to anti-Fx1A IgG, anti-Fx1A F(ab')2 and Fab' led to GEC injury in the presence of rat or human sera as sources of C. Cytotoxicity was Mg2+ and factor B dependent, but Ca2+ independent, indicating that anti-Fx1A activated the C alternative pathway (AP). Furthermore, in the presence of Mg2+ and factor B, anti-Fx1A enhanced 125I-C3b deposition on GEC in the absence of classical pathway activation. AP C3 and C5 convertases formed on GEC (GEC-C3bBbP) were inactivated over time, probably due to binding of GEC C regulatory proteins. This inactivation was prevented when GEC-C3bBbP were incubated with anti-Fx1A IgG. An antibody raised against cultured GEC that binds to GEC in vitro and in vivo had no effect on C3 and C5 convertases, suggesting that stabilization of C3bBbP is unique to anti-Fx1A. Anti-Fx1A Fab' also stabilized GEC-C3bBbP, indicating that cross-linking of membrane Ag was not required. C3bBbP on E were not affected by anti-Fx1A, excluding direct stabilization of convertases by anti-Fx1A. Therefore, anti-Fx1A inhibits C regulation on GEC, which can account for its ability to activate the AP. This represents a potentially powerful mechanism of producing disease in vivo.
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PMID:Effect of nephritogenic antibody on complement regulation in cultured rat glomerular epithelial cells. 186 Oct 77

The effect of three cycles of high-dose cisplatin (40 mg/m2 day for 5 days) on renal tubular function was evaluated in 30 patients. A significant impairment of proximal tubular salt and water reabsorption rates was observed, but also distal tubular function seemed to be affected. These changes were also present 6 months after termination of treatment. Sodium and magnesium clearance increased significantly during treatment. Magnesium clearance normalized shortly after treatment but sodium clearance was significantly elevated 6 months after treatment. Proteinuria, albuminuria, and amino aciduria, together with an increase of beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase (NAG) excretion rates, were observed during each treatment cycle. A good correlation was registered between the increase in urinary excretion rates of protein, NAG, and magnesium and the decrease in proximal tubular salt and water reabsorption during cisplatin administration.
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PMID:Renal tubular function in patients treated with high-dose cisplatin. 284 Feb 30

1. Tamm-Horsfall glycoprotein was determined, by radioimmunoassay, in samples of urine from normal individuals under a variety of physiological conditions. 2. The amount of glycoprotein excreted in 24 h by our population (39 +/- 13 mg, corrected for body surface area) was found not to be influenced by sex, age (19-60 years) or amounts of Ca2+, Mg2+ and Na+ excreted. 3. Urine samples collected at 2 h intervals over 24 h from individuals drinking in response to thirst, contained quantities of the glycoprotein which showed high positive correlations with urine volumes, but not with Ca2+, Mg2+ or Na+ excretion. 4. The amounts of urine and of the glycoprotein were correlated for individuals in antidiuresis, induced by restriction of water intake. Relatively small amounts of glycoprotein were excreted by individuals in states of water-induced diuresis. 5. The amounts of glycoprotein excreted after exercise were positively correlated with the small volumes of urine voided, but they were uninfluenced by the degree of proteinuria or of hyaline cast formation. 6. The half-life for turnover of the glycoprotein in a given individual is highly variable, from a minimum of 3-7 to a maximum of 168 h.
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PMID:Factors affecting excretion of human urinary Tamm-Horsfall glycoprotein. 719 48

Proteinuria may be associated with hypertension and progression of renal insufficiency, which in turn may accompany abnormalities in cell calcium homeostasis. Therefore, urine from rats made proteinuric by puromycin aminoglycoside administration was analyzed, in a search for factors affecting cellular calcium transport. Proteinuric urine was fractionated by thin-layer chromatography and HPLC, and the effects of the fractions on the plasma membrane calcium pump in human red blood cells were assessed. Proteinuric urine contained a powerful specific inhibitor of the calcium pump that had little or no effect on the Na+/K+- or Mg2+-ATPases. The inhibitor was characterized as a neutral lipid, migrating as a single band, that inhibited 45Ca2+ efflux. To confirm the presence of an inhibitor in other proteinuric states, the urine from two patients with proteinuria was examined and subjected to chromatography as in the rat studies. These thin-layer chromatographic fractions contained a very strong inhibitor of the red blood cell calcium pump, suggesting that this substance may have relevance for the pathogenesis of proteinuric renal disease in human patients. Rat proximal tubule cells in tissue culture, when challenged with lipid-replete albumin, secreted an inhibitor of the calcium pump that migrated in the same chromatographic band as the urine factor. Therefore, the processing of fatty acids borne by albumin into endocytosing proximal tubular epithelium results in the synthesis and release of a previously unknown lipid modulator of the calcium pump, an effect that may predispose kidney tissue toward elevations in cytosolic calcium levels in target cells.
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PMID:Neutral lipid from proteinuric rat urine is a novel inhibitor of the red blood cell calcium pump. 1036 54

Preeclampsia is a pregnancy-associated illness affecting multiple organ systems. Symptoms typically occur after the 20th week of gestation and consist of hypertension (>140/90 mmHg) and proteinuria (>300 mg/day). It is one of the leading causes of premature birth worldwide and early diagnosis and treatment are essential for both fetal and maternal health. Therapy is aimed at lowering blood pressure sufficiently to prevent the most severe complications such as intracranial hemorrhages. At the same time attention must be paid to the possible untoward effects of blood pressure medications on uteroplacental perfusion and fetal well being. Magnesium is the cornerstone for both prevention and control of eclamptic cerebrovascular events. In cases of severe preeclampsia and eclampsia prompt delivery is indicated, often carried out by Cesarean section (>34 weeks of gestation). Compared to general anesthesia, regional anesthesia techniques offer certain advantages to both mother and fetus and in the absence of contraindications are the methods of choice.
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PMID:[Anesthetic management of parturients with pre-eclampsia and eclampsia]. 1853 23

Hyperaldosteronism is associated with hypertension, cardiovascular fibrosis, and electrolyte disturbances, including hypomagnesemia. Mechanisms underlying aldosterone-mediated Mg(2+) changes are unclear, but the novel Mg(2+) transporters TRPM6 and TRPM7 may be important. We examined whether aldosterone influences renal TRPM6/7 and the TRPM7 downstream target annexin-1 and tested the hypothesis that Mg(2+) administration ameliorates aldosterone-induced cardiovascular and renal injury and prevents aldosterone-associated hypertension. C57B6 mice were studied (12 weeks, n=8 to 9/group); (1) control group (0.2% dietary Mg(2+)), (2) Mg(2+) group (0.75% dietary Mg(2+)), (3) aldosterone group (Aldo, 400 microg/kg/min and 0.9% NaCl drinking water), and (4) Aldo+Mg(2+) group. Blood pressure was unaltered by aldosterone and was similar in all groups throughout the experiment. Serum Na(+) was increased and serum K(+) and Mg(2+) decreased in the Aldo group. Aldo mice had hypomagnesuria and proteinuria, and renal, cardiac, and aortic fibrosis, which were normalized by Mg(2+) supplementation. Renal and cardiovascular expression of interleukin-6, VCAM1 and COX2 was increased in the Aldo group. Magnesium attenuated renal and cardiac interleukin-6 content and decreased renal VCAM1 and cardiac COX2 expression (P<0.05). Aldosterone decreased expression of renal TRPM7 and the downstream target annexin-1 (P<0.05) without effect on TRPM6. Whereas Mg(2+) increased mRNA expression of TRPM6 and TRPM7, it had no effect on TRPM7 and annexin-1 protein content. Our data demonstrate that aldosterone mediates blood pressure-independent renal and cardiovascular fibrosis and inflammation through Mg(2+)-sensitive pathways. We suggest that altered Mg(2+) metabolism in hyperaldosteronism may relate to TRPM7 downregulation and that Mg(2+) protects against cardiovascular and renal damaging actions of aldosterone.
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PMID:Downregulation of renal TRPM7 and increased inflammation and fibrosis in aldosterone-infused mice: effects of magnesium. 1826 39

Preeclampsia is characterized by hypertension, peripheral edema and proteinuria, but very often also includes neurologic complications. Neurologic complications of severe preeclampsia are indentical to those of hypertensive encephalopathy. The most common neurologic symptoms are headache, vomiting, mental disorders, visual disturbances, sensorimotor deficits and seizures. Endothelial cell dysfunction is the main cause of multiorgan failure. It is of utmost importance to recognize these symptoms and initiate apropriate therapy. Systemic blood presure must not exceed the cerebrovascular autoregulatory capacity. Serum magnesium level is significantly decreased in pregnant women with severe preeclampsia and cerebral edema. Magnesium has been shown to be effective in reducing the occurrence of seizures in preeclampsia by decreasing neuronal excitability, protecting the endothelium against free radicals and reducing cerebral perfusion.
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PMID:[Neurological disorders in pregnancy]. 2308 92

High fructose intake is a risk of glomerular podocyte dysfunction. Podocyte apoptosis has emerged as a major cause of podocyte loss, exacerbating proteinuria. Magnesium isoglycyrrhizinate (MgIG) is usually used as a hepatoprotective agent in clinic. Liver and kidney injury often occurs in human diseases. Recent report shows that MgIG improves kidney function. In this study, we found that MgIG significantly alleviated kidney dysfunction, proteinuria and podocyte injury in fructose-fed rats. It also restored fructose-induced podocyte apoptosis in rat glomeruli and cultured differentiated podocytes. Of note, high-expression of miR-193a, downregulation of Wilms' tumor protein (WT1) and RelA, as well as upregulation of C-Maf inducing protein (C-mip) were observed in these animal and cell models. The data from the transfection of miR-193a mimic, miR-193a inhibitor, WT1 siRNA or LV5-WT1 in cultured differentiated podocytes showed that fructose increased miR-193a to down-regulate WT1, and subsequently activated C-mip to suppress RelA, causing podocyte apoptosis. These disturbances were significantly attenuated by MgIG. Taken together, these results provide the first evidence that MgIG restrains fructose-induced podocyte apoptosis at least partly through inhibiting miR-193a to upregulate WT1, supporting the application of MgIG with a novel mechanism-of-action against podocyte apoptosis associated with fructose-induced kidney dysfunction.
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PMID:Magnesium isoglycyrrhizinate ameliorates fructose-induced podocyte apoptosis through downregulation of miR-193a to increase WT1. 3108 61