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      Jejunal Dopamine and Na +,K +-ATPase Activity in Nephrotic Syndrome

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          Background: The occurrence of complementary functions in sodium transport between the intestine and the kidney was suggested to occur when the renal function is immature or compromised and jejunal dopamine has been implicated in this renal-intestinal cross-talk. The jejunal sodium transport was not previously evaluated in the nephrotic syndrome. Methods: We examined the jejunal Na<sup>+</sup>,K<sup>+</sup>-ATPase activity and the role of dopamine in puromycin aminonucleoside (PAN) and HgCl<sub>2</sub>-induced nephrotic syndrome rat models. Results: In both nephrotic syndrome rat models, the jejunal Na<sup>+</sup>,K<sup>+</sup>-ATPase activity was reduced during greatest sodium retention and ascites accumulation (PAN nephrosis, day 7; HgCl<sub>2</sub> nephrosis, day 14), whereas during enhanced sodium excretion and ascites mobilization the jejunal Na<sup>+</sup>,K<sup>+</sup>-ATPase activity was increased in HgCl<sub>2</sub> nephrosis (day 21) and was similar to controls in PAN nephrosis (day 14). In both PAN- and HgCl<sub>2</sub>-induced nephrosis, the jejunal aromatic L-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of jejunal dopamine, did not differ from controls. In addition, the jejunal Na<sup>+</sup>,K<sup>+</sup>-ATPase activity was not sensitive to inhibition by dopamine (1 µ M) in both experimental groups throughout the study. Conclusions: In the nephrotic syndrome the jejunal Na<sup>+</sup>,K<sup>+</sup>-ATPase activity may respond in a compensatory way to changes in extracellular volume, through dopamine-independent mechanisms.

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          Most cited references 23

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          Jejunal microvilli atrophy and reduced nutrient transport in rats with advanced liver cirrhosis: improvement by Insulin-like Growth Factor I

          Background Previous results have shown that in rats with non-ascitic cirrhosis there is an altered transport of sugars and amino acids associated with elongated microvilli. These alterations returned to normal with the administration of Insulin-Like Growth Factor-I (IGF-I). The aims of this study were to explore the evolution of these alterations and analyse the effect of IGF-I in rats with advanced cirrhosis and ascites. Thus, jejunal structure and nutrient transport (D-galactose, L-leucine, L-proline, L-glutamic acid and L-cystine) were studied in rats with ascitic cirrhosis. Methods Advanced cirrhosis was induced by CCl4 inhalation and Phenobarbital administration for 30 weeks. Cirrhotic animals were divided into two groups which received IGF-I or saline during two weeks. Control group was studied in parallel. Jejunal microvilli were studied by electron microscopy. Nutrient transport was assessed in brush border membrane vesicles using 14C or 35S-labelled subtracts in the three experimental groups. Results Intestinal active Na+-dependent transport was significantly reduced in untreated cirrhotic rats. Kinetic studies showed a decreased Vmax and a reduced affinity for sugar and four amino acids transporters (expressed as an increased Kt) in the brush border membrane vesicles from untreated cirrhotic rats as compared with controls. Both parameters were normalised in the IGF-I-treated cirrhotic group. Electron microscopy showed elongation and fusion of microvilli with degenerative membrane lesions and/or notable atrophy. Conclusions The initial microvilli elongation reported in non ascitic cirrhosis develops into atrophy in rats with advanced cirrhosis and nutrient transports (monosaccharides and amino acids) are progressively reduced. Both morphological and functional alterations improved significantly with low doses of IGF-I.
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            Metals and kidney autoimmunity.

             P Bigazzi (1999)
            The causes of autoimmune responses leading to human kidney pathology remain unknown. However, environmental agents such as microorganisms and/or xenobiotics are good candidates for that role. Metals, either present in the environment or administered for therapeutic reasons, are prototypical xenobiotics that cause decreases or enhancements of immune responses. In particular, exposure to gold and mercury may result in autoimmune responses to various self-antigens as well as autoimmune disease of the kidney and other tissues. Gold compounds, currently used in the treatment of patients with progressive polyarticular rheumatoid arthritis, can cause a nephrotic syndrome. Similarly, an immune-mediated membranous nephropathy frequently occurred when drugs containing mercury were commonly used. Recent epidemiologic studies have shown that occupational exposure to mercury does not usually result in autoimmunity. However, mercury induces antinuclear antibodies, sclerodermalike disease, lichen planus, or membranous nephropathy in some individuals. Laboratory investigations have confirmed that the administration of gold or mercury to experimental animals leads to autoimmune disease quite similar to that observed in human subjects exposed to these metals. In addition, studies of inbred mice and rats have revealed that a few strains are susceptible to the autoimmune effects of gold and mercury, whereas the majority of inbred strains are resistant. These findings have emphasized the importance of genetic (immunogenetic and pharmacogenetic) factors in the induction of metal-associated autoimmunity. (italic)In vitro(/italic) and (italic)in vivo(/italic) research of autoimmune disease caused by mercury and gold has already yielded valuable information and answered a number of important questions. At the same time it has raised new issues about possible immunostimulatory or immunosuppressive mechanisms of xenobiotic activity. Thus it is evident that investigations of metal-induced renal autoimmunity have the potential to produce new knowledge with relevance to autoimmune disease caused by xenobiotics in general as well as to idiopathic autoimmunity.
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              The sodium pump.


                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                August 2005
                18 August 2005
                : 25
                : 4
                : 382-392
                aInstitute of Pharmacology and Therapeutics, and bUnit of Research and Development of Nephrology, Faculty of Medicine, Porto, Portugal
                87210 Am J Nephrol 2005;25:382–392
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 9, References: 51, Pages: 11
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                Original Report: Laboratory Investigation


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