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10.1007/s00424-019-02261-8 http://scihub22266oqcxt.onion/10.1007/s00424-019-02261-8 30726531!ä!30726531 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Pflugers+Arch 2019 ; 471 (4): 619-631 Nephropedia Template TP {{tp|p=30726531|t=2019. Deregulated renal magnesium transport during lipopolysaccharide-induced acute kidney injury in mice |pdf=|usr=}}{{30726531}} gab.com Text Deregulated renal magnesium transport during lipopolysaccharide-induced acute kidney injury in mice JO: Pflugers Arch http://www.kidney.de/pget.php?&tw=1&pmid=30726531 #FOAvip Magnesium (Mg(2+)) abnormalities during sepsis have been reported, but the underlying mechanisms during acute inflammation are poorly understood. We hypothesized that a decrease in GFR and/or changes in transporters or channels for Mg(2+) could be responsible for the observed Mg(2+) abnormalities. Therefore, we studied the metabolism of Mg(2+) in a murine model of endotoxemia. LPS-induced hypermagnesemia was paralleled by a decrease in creatinine clearance and an increase in the fractional excretion of Mg(2+). In agreement with an altered renal Mg(2+) handling, endotoxemia decreased the renal expression of claudin (Cldn) 10b, Cldn16, Cldn19, parvalbumin, and of the solute carrier family (Slc) 41a3. Further, LPS increased the renal expression of Cldn14 and Slc41a1. The renal expression of the transient receptor potential melastin (Trpm) 6, Trpm7, and of cyclin M (Cnnm) 2 was unaltered in response to LPS. In vitro studies support a direct effect on the expression of Cldn10b, Cldn14, Cldn16, and Cldn19. Further, endotoxemia increased the fractional excretion of sodium, which was paralleled by a decrease of important renal sodium transporters. In the large intestine, the expression of Trpm7 was increased in response to LPS, whereas the expression of Trpm6 was decreased. Cnnm4 mRNA levels were unchanged in the large intestine. Further, Cldn12 and Na(+)-H(+) exchanger 3 (Slc9a3) expressions were decreased in the small intestine in response to LPS. Our findings indicate that endotoxemia is associated with hypermagnesemia and a disturbed Mg(2+) handling. It seems likely that LPS-induced hypermagnesemia is due to the decrease in renal function in response to LPS. Twit Text FOAVip Deregulated renal magnesium transport during lipopolysaccharide-induced acute kidney injury in mice ????Pflugers Arch http://www.kidney.de/pget.php?&tw=1&pmid=30726531 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30726531 #FOAvip English Wikipedia <ref>{{Cite pmid|30726531}}</ref> Deregulated renal magnesium transport during lipopolysaccharide-induced acute kidney injury in mice #MMPMID30726531 Meurer M; Hocherl K Pflugers Arch 2019[Apr]; 471 (4): 619-631 PMID30726531show ga Magnesium (Mg(2+)) abnormalities during sepsis have been reported, but the underlying mechanisms during acute inflammation are poorly understood. We hypothesized that a decrease in GFR and/or changes in transporters or channels for Mg(2+) could be responsible for the observed Mg(2+) abnormalities. Therefore, we studied the metabolism of Mg(2+) in a murine model of endotoxemia. LPS-induced hypermagnesemia was paralleled by a decrease in creatinine clearance and an increase in the fractional excretion of Mg(2+). In agreement with an altered renal Mg(2+) handling, endotoxemia decreased the renal expression of claudin (Cldn) 10b, Cldn16, Cldn19, parvalbumin, and of the solute carrier family (Slc) 41a3. Further, LPS increased the renal expression of Cldn14 and Slc41a1. The renal expression of the transient receptor potential melastin (Trpm) 6, Trpm7, and of cyclin M (Cnnm) 2 was unaltered in response to LPS. In vitro studies support a direct effect on the expression of Cldn10b, Cldn14, Cldn16, and Cldn19. Further, endotoxemia increased the fractional excretion of sodium, which was paralleled by a decrease of important renal sodium transporters. In the large intestine, the expression of Trpm7 was increased in response to LPS, whereas the expression of Trpm6 was decreased. Cnnm4 mRNA levels were unchanged in the large intestine. Further, Cldn12 and Na(+)-H(+) exchanger 3 (Slc9a3) expressions were decreased in the small intestine in response to LPS. Our findings indicate that endotoxemia is associated with hypermagnesemia and a disturbed Mg(2+) handling. It seems likely that LPS-induced hypermagnesemia is due to the decrease in renal function in response to LPS. |Acute Kidney Injury/*chemically induced/*metabolism[MESH] |Animals[MESH] |Disease Models, Animal[MESH] |Endotoxemia/drug therapy/metabolism[MESH] |Inflammation/metabolism[MESH] |Kidney/*metabolism[MESH] |Lipopolysaccharides/*pharmacology[MESH] |Magnesium/*metabolism[MESH] |Male[MESH] |Membrane Transport Proteins/metabolism[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |RNA, Messenger/metabolism[MESH] |Sodium-Hydrogen Exchanger 3/metabolism[MESH]Deregulated renal magnesium transport during lipopolysaccharide-induce(epmc).pdf DeepDyve Pubget Overpricing