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[PMID]:28888268
[Au] Autor:Hayer MK; Edwards NC; Slinn G; Moody WE; Steeds RP; Ferro CJ; Price AM; Andujar C; Dutton M; Webster R; Webb DJ; Semple S; MacIntyre I; Melville V; Wilkinson IB; Hiemstra TF; Wheeler DC; Herrey A; Grant M; Mehta S; Ives N; Townend JN
[Ad] Endereço:Birmingham Cardio-Renal Group (University of Birmingham Institute of Cardiovascular Sciences), Queen Elizabeth Hospital, Edgbaston, Birmingham.
[Ti] Título:A randomized, multicenter, open-label, blinded end point trial comparing the effects of spironolactone to chlorthalidone on left ventricular mass in patients with early-stage chronic kidney disease: Rationale and design of the SPIRO-CKD trial.
[So] Source:Am Heart J;191:37-46, 2017 Sep.
[Is] ISSN:1097-6744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chronic kidney disease (CKD) is associated with increased left ventricular (LV) mass and arterial stiffness. In a previous trial, spironolactone improved these end points compared with placebo in subjects with early-stage CKD, but it is not known whether these effects were specific to the drug or secondary to blood pressure lowering. AIM: The aim was to investigate the hypothesis that spironolactone is superior to chlorthalidone in the reduction of LV mass while exerting similar effects on blood pressure. DESIGN: This is a multicenter, prospective, randomized, open-label, blinded end point clinical trial initially designed to compare the effects of 40weeks of treatment with spironolactone 25mg once daily to chlorthalidone 25mg once daily on the co-primary end points of change in pulse wave velocity and change in LV mass in 350 patients with stages 2 and 3 CKD on established treatment with an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Because of slow recruitment rates, it became apparent that it would not be possible to recruit this sample size within the funded time period. The study design was therefore changed to one with a single primary end point of LV mass requiring 150 patients. Recruitment was completed on 31 December 2016, at which time 154 patients had been recruited. Investigations included cardiac magnetic resonance imaging, applanation tonometry, 24-hour ambulatory blood pressure monitoring, and laboratory tests. Subjects are assessed before and after 40weeks of randomly allocated drug therapy and at 46weeks after discontinuation of the study drug.
[Mh] Termos MeSH primário: Clortalidona/administração & dosagem
Ventrículos do Coração/diagnóstico por imagem
Hipertrofia Ventricular Esquerda/etiologia
Falência Renal Crônica/complicações
Espironolactona/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Relação Dose-Resposta a Droga
Quimioterapia Combinada
Feminino
Seguimentos
Ventrículos do Coração/fisiopatologia
Seres Humanos
Hipertrofia Ventricular Esquerda/mortalidade
Hipertrofia Ventricular Esquerda/fisiopatologia
Falência Renal Crônica/mortalidade
Falência Renal Crônica/fisiopatologia
Imagem Cinética por Ressonância Magnética
Masculino
Meia-Idade
Antagonistas de Receptores de Mineralocorticoides/administração & dosagem
Estudos Prospectivos
Análise de Onda de Pulso
Método Simples-Cego
Inibidores de Simportadores de Cloreto de Sódio/administração & dosagem
Taxa de Sobrevida/tendências
Fatores de Tempo
Resultado do Tratamento
Estados Unidos/epidemiologia
Rigidez Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Mineralocorticoid Receptor Antagonists); 0 (Sodium Chloride Symporter Inhibitors); 27O7W4T232 (Spironolactone); Q0MQD1073Q (Chlorthalidone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170911
[St] Status:MEDLINE


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[PMID]:28806048
[Au] Autor:Barstow C
[Ad] Endereço:Womack Army Medical Center, 2817 Reilly Road, Fort Bragg, NC 28310.
[Ti] Título:Electrolytes: Calcium Disorders.
[So] Source:FP Essent;459:29-34, 2017 Aug.
[Is] ISSN:2159-3000
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A normal serum calcium level is 8 to 10 mg/dL. The diagnosis of hypercalcemia (ie, levels 10.5 mg/dL or greater) should be confirmed with an albumin-adjusted or ionized calcium level. The two most common causes of hypercalcemia are hyperparathyroidism and malignancy. Drugs, notably lithium and thiazide diuretics, also can cause hypercalcemia. Patients with severe or symptomatic hypercalcemia should be treated initially with hydration to decrease calcium levels. The evaluation should include a parathyroid hormone (PTH) level. If the PTH level is low, cancer is a likely cause, particularly multiple myeloma, breast cancer, or lymphoma. If the PTH level is normal or elevated, hyperparathyroidism is the likely cause. Symptomatic patients with hyperparathyroidism and patients with certain clinical markers should be considered for surgery. For patients with mild disease, monitoring is an option. Hypocalcemia often is caused by vitamin D deficiency. Symptomatic patients and patients with calcium levels less than 7.6 mg/dL should be treated with intravenous calcium gluconate; concomitant magnesium deficiency should be addressed. There is no evidence that routine calcium and vitamin D supplementation reduces the risk of fractures, but studies have shown that vitamin D supplementation does decrease the number of falls in older adults at risk.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Hipercalcemia/metabolismo
Hipocalcemia/metabolismo
Hormônio Paratireóideo/metabolismo
Vitamina D/metabolismo
[Mh] Termos MeSH secundário: Acidentes por Quedas/prevenção & controle
Antimaníacos/efeitos adversos
Cálcio/uso terapêutico
Gluconato de Cálcio/uso terapêutico
Suplementos Nutricionais
Hidratação
Fraturas Ósseas/prevenção & controle
Seres Humanos
Hipercalcemia/diagnóstico
Hipercalcemia/etiologia
Hipercalcemia/terapia
Hiperparatireoidismo/complicações
Hiperparatireoidismo/cirurgia
Hipocalcemia/diagnóstico
Hipocalcemia/etiologia
Hipocalcemia/terapia
Lítio/efeitos adversos
Neoplasias/complicações
Paratireoidectomia
Inibidores de Simportadores de Cloreto de Sódio/efeitos adversos
Vitamina D/uso terapêutico
Deficiência de Vitamina D/complicações
Deficiência de Vitamina D/tratamento farmacológico
Vitaminas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antimanic Agents); 0 (Parathyroid Hormone); 0 (Sodium Chloride Symporter Inhibitors); 0 (Vitamins); 1406-16-2 (Vitamin D); 9FN79X2M3F (Lithium); SQE6VB453K (Calcium Gluconate); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE


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[PMID]:28783044
[Au] Autor: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
[Ad] Endereço:NIHR Biomedical Research Unit in Cardiovascular Disease at Royal Brompton & Harefield, NHS Foundation Trust and Imperial College London, London, United Kingdom.
[Ti] Título:Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia.
[So] Source:J Clin Invest;127(9):3367-3374, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo: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.
[Mh] Termos MeSH primário: Hiponatremia/induzido quimicamente
Inibidores de Simportadores de Cloreto de Sódio/efeitos adversos
Tiazidas/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Aquaporina 1/genética
Aquaporina 2/genética
Estudos de Coortes
Dinoprostona/metabolismo
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Hiponatremia/genética
Masculino
Meia-Idade
Néfrons/metabolismo
Transportadores de Ânions Orgânicos/genética
Farmacogenética
Fenótipo
Polimorfismo de Nucleotídeo Único
Prostaglandinas/metabolismo
Reino Unido
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AQP1 protein, human); 0 (AQP2 protein, human); 0 (Aquaporin 2); 0 (Organic Anion Transporters); 0 (Prostaglandins); 0 (SLCO2A1 protein, human); 0 (Sodium Chloride Symporter Inhibitors); 0 (Thiazides); 059QF0KO0R (Water); 146410-94-8 (Aquaporin 1); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


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[PMID]:28724547
[Au] Autor:Okada Y; Shibata S; Fujimoto N; Best SA; Levine BD; Fu Q
[Ad] Endereço:Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, Dallas, Texas.
[Ti] Título:Long-term effects of a renin inhibitor versus a thiazide diuretic on arterial stiffness and left ventricular diastolic function in elderly hypertensive patients.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(4):R400-R409, 2017 Oct 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arterial stiffness and cardiac function are important predictors of cardiovascular events in patients with hypertension, even with adequate blood pressure (BP) control. We evaluated whether a direct renin inhibitor, aliskiren, reduces arterial stiffness and modulates left ventricular function compared with a diuretic, hydrochlorothiazide, in elderly hypertensive patients. Twenty-one hypertensive patients [67 ± 14 (SD) yr] were randomly assigned to receive 6-mo aliskiren ( = 11) or hydrochlorothiazide ( = 10)-based therapy. We assessed ß-stiffness of the local arteries, arterial elastance ( ), and echocardiographic variables, including early ( ) and late ( ) mitral inflow velocity, deceleration time of E, early ( ') and late ( ') diastolic mitral annular velocity, and left ventricular end-systolic elastance ( ) before and after treatment. BP decreased similarly ( < 0.001) after both therapies. ß-Stiffness of the carotid artery decreased after aliskiren but increased after hydrochlorothiazide treatment (aliskiren: 6.42 ± 2.34 pre vs. 5.07 ± 1.29 post; hydrochlorothiazide: 5.05 ± 1.78 vs. 7.25 ± 2.68, = 0.001 for interaction). ß-Stiffness of the femoral and radial arteries were not different after either treatment. Different from aliskiren, decreased (73 ± 16 vs. 67 ± 14 cm/s, = 0.026), and the deceleration time was prolonged (218 ± 40 vs. 236 ± 35 ms, = 0.032) after hydrochlorothiazide therapy, whereas the / , and ' remained unchanged after both treatments. and decreased after aliskiren therapy (both < 0.05), whereas the / (ventricular-arterial coupling) was maintained after both treatments. Thus, aliskiren decreased the stiffness of carotid artery and left ventricular end-systolic elastance with maintenance of ventricular-arterial coupling without any effects on diastolic filling, while hydrochlorothiazide increased carotid arterial stiffness and slowed early diastolic filling in elderly hypertensive patients.
[Mh] Termos MeSH primário: Amidas/farmacologia
Diástole/efeitos dos fármacos
Fumaratos/farmacologia
Hidroclorotiazida/farmacologia
Hipertensão/tratamento farmacológico
Renina/antagonistas & inibidores
Inibidores de Simportadores de Cloreto de Sódio/farmacologia
Rigidez Vascular/efeitos dos fármacos
Função Ventricular Esquerda/efeitos dos fármacos
[Mh] Termos MeSH secundário: Idoso
Amidas/uso terapêutico
Anti-Hipertensivos/farmacologia
Anti-Hipertensivos/uso terapêutico
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Diástole/fisiologia
Ecocardiografia
Feminino
Artéria Femoral/efeitos dos fármacos
Artéria Femoral/fisiopatologia
Fumaratos/uso terapêutico
Seres Humanos
Hidroclorotiazida/uso terapêutico
Hipertensão/diagnóstico por imagem
Hipertensão/fisiopatologia
Masculino
Meia-Idade
Artéria Radial/efeitos dos fármacos
Artéria Radial/fisiopatologia
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
Resultado do Tratamento
Rigidez Vascular/fisiologia
Função Ventricular Esquerda/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Amides); 0 (Antihypertensive Agents); 0 (Fumarates); 0 (Sodium Chloride Symporter Inhibitors); 0J48LPH2TH (Hydrochlorothiazide); 502FWN4Q32 (aliskiren); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00125.2017


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[PMID]:28515174
[Au] Autor:Rosenbaek LL; Rizzo F; MacAulay N; Staub O; Fenton RA
[Ad] Endereço:InterPrET Center, Department of Biomedicine, Aarhus University, Aarhus, Denmark.
[Ti] Título:Functional assessment of sodium chloride cotransporter NCC mutants in polarized mammalian epithelial cells.
[So] Source:Am J Physiol Renal Physiol;313(2):F495-F504, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The thiazide-sensitive sodium chloride cotransporter NCC is important for maintaining serum sodium (Na ) and, indirectly, serum potassium (K ) levels. Functional studies on NCC have used cell lines with native NCC expression, transiently transfected nonpolarized cell lines, or oocytes. Here, we developed the use of polarized Madin-Darby canine kidney type I (MDCKI) mammalian epithelial cell lines with tetracycline-inducible human NCC expression to study NCC activity and membrane abundance in the same system. In radiotracer assays, induced cells grown on filters had robust thiazide-sensitive and chloride dependent sodium-22 ( Na) uptake from the apical side. To minimize cost and maximize throughput, assays were modified to use cells grown on plastic. On plastic, cells had similar thiazide-sensitive Na uptakes that increased following preincubation of cells in chloride-free solutions. NCC was detected in the plasma membrane, and both membrane abundance and phosphorylation of NCC were increased by incubation in chloride-free solutions. Furthermore, in cells exposed for 15 min to low or high extracellular K , the levels of phosphorylated NCC increased and decreased, respectively. To demonstrate that the system allows rapid and systematic assessment of mutated NCC, three phosphorylation sites in NCC were mutated, and NCC activity was examined. Na fluxes in phosphorylation-deficient mutants were reduced to baseline levels, whereas phosphorylation-mimicking mutants were constitutively active, even without chloride-free stimulation. In conclusion, this system allows the activity, cellular localization, and abundance of wild-type or mutant NCC to be examined in the same polarized mammalian expression system in a rapid, easy, and low-cost fashion.
[Mh] Termos MeSH primário: Polaridade Celular
Cloretos/metabolismo
Células Epiteliais/metabolismo
Mutação
Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Cães
Relação Dose-Resposta a Droga
Células Epiteliais/efeitos dos fármacos
Genótipo
Ensaios de Triagem em Larga Escala
Cinética
Células Madin Darby de Rim Canino
Fenótipo
Fosforilação
Potássio/metabolismo
Processamento de Proteína Pós-Traducional
Inibidores de Simportadores de Cloreto de Sódio/farmacologia
Membro 3 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Membro 3 da Família 12 de Carreador de Soluto/genética
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Transfecção
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (SLC12A3 protein, human); 0 (Sodium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 3); 9NEZ333N27 (Sodium); RWP5GA015D (Potassium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00088.2017


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[PMID]:28480805
[Au] Autor:Sarafidis PA; Alexandrou ME; Ruilope LM
[Ad] Endereço:a Department of Nephrology , Aristotle University of Thessaloniki, Hippokration Hospital , Thessaloniki , Greece.
[Ti] Título:A review of chemical therapies for treating diabetic hypertension.
[So] Source:Expert Opin Pharmacother;18(9):909-923, 2017 Jun.
[Is] ISSN:1744-7666
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Hypertension and diabetes are two of the most important modifiable risk factors for cardiovascular and renal disease. The majority of patients with diabetes also have high blood pressure (BP) and the presence of hypertension in these patients dramatically increases cardiovascular and renal risk. Areas covered: This article will discuss chemical therapies for hypertension in patients with diabetes, based on currently available evidence on the effects of antihypertensive treatment on metabolic profile and renal endpoints that are the factors mostly influencing drug choice. Expert opinion: Several lines of evidence suggest that angiotensin-converting-enzyme-inhibitors (ACEIs), angiotensin-receptor-blockers (ARBs) and calcium-channel-blockers (CCBs) have beneficial or neutral effects on carbohydrate metabolism, whereas old ß-blockers and thiazide diuretics have not. Renal outcome trials clearly suggest that in proteinuric diabetic CKD ACEIs and ARBs reduce the rate of disease progression. Thus, an ACEI or an ARB, if tolerated, should be the first choice in diabetic individuals, followed by CCBs, vasodilating ß-blockers and diuretics, depending on the individual patient characteristics. Recent studies suggest that the novel antidiabetic class of sodium-glucose co-transporter 2 inhibitors may offer a small reduction in BP together with important decrease in incidence of cardiovascular and renal events in patients with type 2 diabetes.
[Mh] Termos MeSH primário: Antagonistas de Receptores de Angiotensina/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipertensão/tratamento farmacológico
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos beta/administração & dosagem
Antagonistas Adrenérgicos beta/efeitos adversos
Antagonistas Adrenérgicos beta/uso terapêutico
Antagonistas de Receptores de Angiotensina/administração & dosagem
Antagonistas de Receptores de Angiotensina/efeitos adversos
Inibidores da Enzima Conversora de Angiotensina/administração & dosagem
Inibidores da Enzima Conversora de Angiotensina/efeitos adversos
Anti-Hipertensivos/administração & dosagem
Anti-Hipertensivos/efeitos adversos
Bloqueadores dos Canais de Cálcio/administração & dosagem
Bloqueadores dos Canais de Cálcio/efeitos adversos
Bloqueadores dos Canais de Cálcio/uso terapêutico
Diabetes Mellitus Tipo 2/complicações
Seres Humanos
Hipertensão/complicações
Inibidores de Simportadores de Cloreto de Sódio/administração & dosagem
Inibidores de Simportadores de Cloreto de Sódio/efeitos adversos
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Antihypertensive Agents); 0 (Calcium Channel Blockers); 0 (Sodium Chloride Symporter Inhibitors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1080/14656566.2017.1328054


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[PMID]:28442491
[Au] Autor:Grimm PR; Coleman R; Delpire E; Welling PA
[Ad] Endereço:Department of Physiology, Maryland Kidney Discovery Center, University of Maryland Medical School, Baltimore, Maryland; and.
[Ti] Título:Constitutively Active SPAK Causes Hyperkalemia by Activating NCC and Remodeling Distal Tubules.
[So] Source:J Am Soc Nephrol;28(9):2597-2606, 2017 Sep.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aberrant activation of with no lysine (WNK) kinases causes familial hyperkalemic hypertension (FHHt). Thiazide diuretics treat the disease, fostering the view that hyperactivation of the thiazide-sensitive sodium-chloride cotransporter (NCC) in the distal convoluted tubule (DCT) is solely responsible. However, aberrant signaling in the aldosterone-sensitive distal nephron (ASDN) and inhibition of the potassium-excretory renal outer medullary potassium (ROMK) channel have also been implicated. To test these ideas, we introduced kinase-activating mutations after Lox-P sites in the mouse gene, which encodes the terminal kinase in the WNK signaling pathway, Ste20-related proline-alanine-rich kinase (SPAK). Renal expression of the constitutively active (CA)-SPAK mutant was specifically targeted to the early DCT using a DCT-driven Cre recombinase. CA-SPAK mice displayed thiazide-treatable hypertension and hyperkalemia, concurrent with NCC hyperphosphorylation. However, thiazide-mediated inhibition of NCC and consequent restoration of sodium excretion did not immediately restore urinary potassium excretion in CA-SPAK mice. Notably, CA-SPAK mice exhibited ASDN remodeling, involving a reduction in connecting tubule mass and attenuation of epithelial sodium channel (ENaC) and ROMK expression and apical localization. Blocking hyperactive NCC in the DCT gradually restored ASDN structure and ENaC and ROMK expression, concurrent with the restoration of urinary potassium excretion. These findings verify that NCC hyperactivity underlies FHHt but also reveal that NCC-dependent changes in the driving force for potassium secretion are not sufficient to explain hyperkalemia. Instead, a DCT-ASDN coupling process controls potassium balance in health and becomes aberrantly activated in FHHt.
[Mh] Termos MeSH primário: Hidroclorotiazida/farmacologia
Túbulos Renais Distais/patologia
Proteínas Serina-Treonina Quinases/metabolismo
Pseudo-Hipoaldosteronismo/metabolismo
Inibidores de Simportadores de Cloreto de Sódio/farmacologia
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
[Mh] Termos MeSH secundário: Aldosterona/metabolismo
Animais
Pressão Sanguínea/efeitos dos fármacos
Canais Epiteliais de Sódio/metabolismo
Hidroclorotiazida/uso terapêutico
Túbulos Renais Distais/metabolismo
Camundongos
Natriurese/efeitos dos fármacos
Fosforilação
Potássio/urina
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Proteínas Serina-Treonina Quinases/genética
Pseudo-Hipoaldosteronismo/tratamento farmacológico
Pseudo-Hipoaldosteronismo/genética
Pseudo-Hipoaldosteronismo/urina
Transdução de Sinais
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channels); 0 (Kcnj1 protein, mouse); 0 (Potassium Channels, Inwardly Rectifying); 0 (Sodium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 3); 0J48LPH2TH (Hydrochlorothiazide); 4964P6T9RB (Aldosterone); EC 2.7.1.- (Stk39 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); RWP5GA015D (Potassium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016090948


  8 / 2838 MEDLINE  
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[PMID]:28343298
[Au] Autor:Vasco RFV; Reis ET; Moyses RMA; Elias RM
[Ad] Endereço:Department of Medicine, Renal Division, Hospital das Clinicas, Universidade de São Paulo, São Paulo, Brazil. raquelfvvasco@gmail.com.
[Ti] Título:Thiazide increases serum calcium in anuric patients: the role of parathyroid hormone.
[So] Source:Arch Osteoporos;12(1):31, 2017 Dec.
[Is] ISSN:1862-3514
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We evaluated the effect of hydrochlorothiazide in a sample of anuric patients on hemodialysis and found an increase in serum calcium, which occurred only in those with parathyroid hormone >300 pg/ml. This finding highlights the extra-renal effect of this diuretic and a possible role of parathyroid hormone in the mechanism. PURPOSE: Thiazide diuretics are commonly used in patients with chronic kidney disease to treat hypertension. Their effects on calcium and bone metabolism are not well established, once calciuria may not fully explain levels of calcium and parathyroid hormone (PTH) in this population. A previous study has suggested that thiazides require the presence of PTH as a permissive condition for its renal action. In anuric patients, however, the role of PTH, if any, in the thiazide effect is unknown. METHODS: To assess thiazide extra renal effect on serum calcium and whether such an effect is reliant on PTH, hydrochlorothiazide (HCTZ) 100 mg was given orally once a day to a sample of 19 anuric patients on hemodialysis for 2 weeks. Laboratories' analyses were obtained in three phases: baseline, after diuretic use, and after a 2-week washout phase. RESULTS: We demonstrated that serum calcium (Ca) increased in ten patients (52.6%) after HCTZ use, returning to previous levels after the washout period. Out of the 19 patients, ten presented PTH ≥ 300 pg/ml, and Ca has increased in eight of them, whereas in the other nine patients with PTH < 300 pg/ml, serum Ca has increased only in two individuals (RR risk of increase Ca 3.9; p = 0.012). CONCLUSIONS: HCTZ was capable of increasing serum Ca in a sample of anuric patients on hemodialysis and seems this effect is highly dependent on PTH levels. Caution is required while interpreting this result, as the small sample size might implicate in a finding caused by chance.
[Mh] Termos MeSH primário: Anuria/sangue
Anuria/tratamento farmacológico
Cálcio/sangue
Hidroclorotiazida/farmacologia
Hormônio Paratireóideo/sangue
Inibidores de Simportadores de Cloreto de Sódio/farmacologia
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
Diálise Renal
Resultado do Tratamento
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Parathyroid Hormone); 0 (Sodium Chloride Symporter Inhibitors); 0J48LPH2TH (Hydrochlorothiazide); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170327
[St] Status:MEDLINE
[do] DOI:10.1007/s11657-017-0326-3


  9 / 2838 MEDLINE  
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[PMID]:28274929
[Au] Autor:Pathare G; Tutakhel OAZ; van der Wel MC; Shelton LM; Deinum J; Lenders JWM; Hoenderop JGJ; Bindels RJM
[Ad] Endereço:Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands.
[Ti] Título:Hydrochlorothiazide treatment increases the abundance of the NaCl cotransporter in urinary extracellular vesicles of essential hypertensive patients.
[So] Source:Am J Physiol Renal Physiol;312(6):F1063-F1072, 2017 Jun 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The thiazide-sensitive NaCl cotransporter (NCC), located apically in distal convoluted tubule epithelia, regulates the fine-tuning of renal sodium excretion. Three isoforms of NCC are generated through alternative splicing of the transcript, of which the third isoform has been the most extensively investigated in pathophysiological conditions. The aim of this study was to investigate the effect of different anti-hypertensive treatments on the abundance and phosphorylation of all three NCC isoforms in urinary extracellular vesicles (uEVs) of essential hypertensive patients. In uEVs isolated from patients ( = 23) before and after hydrochlorothiazide or valsartan treatment, the abundance and phosphorylation of the NCC isoforms was determined. Additionally, clinical biochemistry and blood pressure of the patients was assessed. Our results show that NCC detected in human uEVs has a glycosylated and oligomeric structure, comparable to NCC present in human kidney membrane fractions. Despite the inhibitory action of hydrochlorothiazide on NCC activity, immunoblot analysis of uEVs showed significantly increased abundance of NCC isoforms 1 and 2 (NCC ), total NCC (NCC ), and the phosphorylated form of total NCC (pNCC -T55/T60) in essential hypertensive patients treated with hydrochlorothiazide but not with valsartan. This study highlights that NCC , NCC , and pNCC -T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Vesículas Extracelulares/efeitos dos fármacos
Hidroclorotiazida/uso terapêutico
Hipertensão/tratamento farmacológico
Rim/efeitos dos fármacos
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
Valsartana/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Biomarcadores/urina
Pressão Sanguínea/efeitos dos fármacos
Estudos Cross-Over
Vesículas Extracelulares/metabolismo
Feminino
Glicosilação
Seres Humanos
Hipertensão/fisiopatologia
Hipertensão/urina
Rim/metabolismo
Rim/fisiopatologia
Masculino
Meia-Idade
Países Baixos
Fosforilação
Estudos Prospectivos
Isoformas de Proteínas
Membro 3 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Membro 3 da Família 12 de Carreador de Soluto/urina
Resultado do Tratamento
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Antihypertensive Agents); 0 (Biomarkers); 0 (Protein Isoforms); 0 (SLC12A3 protein, human); 0 (Sodium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 3); 0J48LPH2TH (Hydrochlorothiazide); 80M03YXJ7I (Valsartan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00644.2016


  10 / 2838 MEDLINE  
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[PMID]:28253804
[Au] Autor:Muheim L
[Ad] Endereço:1 Institut für Hausarztmedizin, Horten-Zentrum für praxisorientierte Forschung und Wissenstransfer, Universitätsspital Zürich.
[Ti] Título:Thiaziddiuretika verringern das Risiko für Hüft- und Beckenfrakturen im Vergleich zu anderen Antihypertensiva..
[So] Source:Praxis (Bern 1994);106(5):271-272, 2017.
[Is] ISSN:1661-8157
[Cp] País de publicação:Switzerland
[La] Idioma:ger
[Mh] Termos MeSH primário: Anti-Hipertensivos/uso terapêutico
Fraturas Ósseas/prevenção & controle
Fraturas do Quadril/prevenção & controle
Hipertensão/tratamento farmacológico
Ossos Pélvicos/lesões
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Anlodipino/uso terapêutico
Doenças Cardiovasculares/prevenção & controle
Clortalidona/uso terapêutico
Método Duplo-Cego
Substituição de Medicamentos
Feminino
Seguimentos
Seres Humanos
Lisinopril/uso terapêutico
Masculino
Meia-Idade
Risco
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Sodium Chloride Symporter Inhibitors); 1J444QC288 (Amlodipine); E7199S1YWR (Lisinopril); Q0MQD1073Q (Chlorthalidone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1024/1661-8157/a002620



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