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10.1172/JCI89812 http://scihub22266oqcxt.onion/10.1172/JCI89812 28783044!5669583!28783044     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2017 ; 127 (9): 3367-3374 Nephropedia Template TP {{tp|p=28783044|t=2017. Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia |pdf=|usr=}}{{28783044}} gab.com Text Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28783044 #FOAvip Thiazide diuretics are among the most widely used treatments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically significant adverse effect, is poorly understood. Here, we have studied the phenotypic and genetic characteristics of patients hospitalized with TIH. In a cohort of 109 TIH patients, those with severe TIH displayed an extended phenotype of intravascular volume expansion, increased free water reabsorption, urinary prostaglandin E2 excretion, and reduced excretion of serum chloride, magnesium, zinc, and antidiuretic hormone. GWAS in a separate cohort of 48 TIH patients and 2,922 controls from the 1958 British birth cohort identified an additional 14 regions associated with TIH. We identified a suggestive association with a variant in SLCO2A1, which encodes a prostaglandin transporter in the distal nephron. Resequencing of SLCO2A1 revealed a nonsynonymous variant, rs34550074 (p.A396T), and association with this SNP was replicated in a second cohort of TIH cases. TIH patients with the p.A396T variant demonstrated increased urinary excretion of prostaglandin E2 and metabolites. Moreover, the SLCO2A1 phospho-mimic p.A396E showed loss of transporter function in vitro. These findings indicate that the phenotype of TIH involves a more extensive metabolic derangement than previously recognized. We propose one mechanism underlying TIH development in a subgroup of patients in which SLCO2A1 regulation is altered. Twit Text FOAVip Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28783044 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28783044 #FOAvip English Wikipedia <ref>{{Cite pmid|28783044}}</ref> Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia #MMPMID28783044 Ware JS; Wain LV; Channavajjhala SK; Jackson VE; Edwards E; Lu R; Siew K; Jia W; Shrine N; Kinnear S; Jalland M; Henry AP; Clayton J; O'Shaughnessy KM; Tobin MD; Schuster VL; Cook S; Hall IP; Glover M J Clin Invest 2017[Sep]; 127 (9): 3367-3374 PMID28783044show ga Thiazide diuretics are among the most widely used treatments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically significant adverse effect, is poorly understood. Here, we have studied the phenotypic and genetic characteristics of patients hospitalized with TIH. In a cohort of 109 TIH patients, those with severe TIH displayed an extended phenotype of intravascular volume expansion, increased free water reabsorption, urinary prostaglandin E2 excretion, and reduced excretion of serum chloride, magnesium, zinc, and antidiuretic hormone. GWAS in a separate cohort of 48 TIH patients and 2,922 controls from the 1958 British birth cohort identified an additional 14 regions associated with TIH. We identified a suggestive association with a variant in SLCO2A1, which encodes a prostaglandin transporter in the distal nephron. Resequencing of SLCO2A1 revealed a nonsynonymous variant, rs34550074 (p.A396T), and association with this SNP was replicated in a second cohort of TIH cases. TIH patients with the p.A396T variant demonstrated increased urinary excretion of prostaglandin E2 and metabolites. Moreover, the SLCO2A1 phospho-mimic p.A396E showed loss of transporter function in vitro. These findings indicate that the phenotype of TIH involves a more extensive metabolic derangement than previously recognized. We propose one mechanism underlying TIH development in a subgroup of patients in which SLCO2A1 regulation is altered. |Aged[MESH] |Aged, 80 and over[MESH] |Aquaporin 1/genetics[MESH] |Aquaporin 2/genetics[MESH] |Cohort Studies[MESH] |Dinoprostone/metabolism[MESH] |Female[MESH] |Genome-Wide Association Study[MESH] |Humans[MESH] |Hyponatremia/*chemically induced/genetics[MESH] |Male[MESH] |Middle Aged[MESH] |Nephrons/metabolism[MESH] |Organic Anion Transporters/genetics[MESH] |Pharmacogenetics[MESH] |Phenotype[MESH] |Polymorphism, Single Nucleotide[MESH] |Prostaglandins/metabolism[MESH] |Sodium Chloride Symporter Inhibitors/*adverse effects[MESH] |Thiazides/*adverse effects[MESH] |United Kingdom[MESH]Phenotypic and pharmacogenetic evaluation of patients with thiazide-in(epmc).pdf DeepDyve Pubget Overpricing