- increased secretion of urine; if not due to increased liquid intake or to the action of a diuretic drug it can be a symptom of diabetes mellitus
- 排尿促進の,利尿の / 利尿剤
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- Detection of mutations in KLHL3 and CUL3 in families with FHHt (familial hyperkalaemic hypertension or Gordon's syndrome).
- Glover M1, Ware JS, Henry A1, Wolley M2, Walsh R3, Wain LV4, Xu S2, Van't Hoff WG5, Tobin MD4, Hall IP1, Cook S, Gordon RD2, Stowasser M2, O'Shaughnessy KM6.Author information 1*Division of Therapeutics and Molecular Medicine, University of Nottingham, Nottingham, U.K.2§Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Brisbane, Australia.3†NIHR Biomedical Research Unit in Cardiovascular Disease at Royal Brompton and Harefield NHS Foundation Trust and Imperial College London, London, U.K.4¶Genetic Epidemiology Group, University of Leicester, Leicester, U.K.5∥Paediatric Nephrology Department, Great Ormond Street Hospital for Children, London, U.K.6‡‡Clinical Pharmacology Unit, University of Cambridge, Cambridge, U.K.AbstractThe study of families with rare inherited forms of hypo- and hyper-tension has been one of the most successful strategies to probe the molecular pathophysiology of blood pressure control and has revealed dysregulation of distal nephron Na+ reabsorption to be a common mechanism. FHHt (familial hyperkalaemic hypertension; also known as Gordon's syndrome) is a salt-dependent form of hypertension caused by mutations in the regulators of the thiazide-sensitive Na+-Cl- co-transporter NCC [also known as SLC12A3 (solute carrier family 12 member 3)] and is effectively treated by thiazide diuretics and/or dietary salt restriction. Variation in at least four genes can cause FHHt, including WNK1 [With No lysine (=K) 1] and WNK4, KLHL3 (kelch-like family member 3), and CUL3 (cullin 3). In the present study we have identified novel disease-causing variants in CUL3 and KLHL3 segregating in 63% of the pedigrees with previously unexplained FHHt, confirming the importance of these recently described FHHt genes. We have demonstrated conclusively, in two unrelated affected individuals, that rare intronic variants in CUL3 cause the skipping of exon 9 as has been proposed previously. KLHL3 variants all occur in kelch-repeat domains and so probably disrupt WNK complex binding. We have found no evidence of any plausible disease-causing variants within SLC4A8 (an alternative thiazide-sensitive sodium transporter) in this population. The results of the present study support the existing evidence that the CUL3 and KLHL3 gene products are physiologically important regulators of thiazide-sensitive distal nephron NaCl reabsorption, and hence potentially interesting novel anti-hypertensive drug targets. As a third of our non-WNK FHHt families do not have plausible CUL3 or KLHL3 variants, there are probably additional, as yet undiscovered, regulators of the thiazide-sensitive pathways.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 May 1;126(10):721-6. doi: 10.1042/CS20130326.
- The study of families with rare inherited forms of hypo- and hyper-tension has been one of the most successful strategies to probe the molecular pathophysiology of blood pressure control and has revealed dysregulation of distal nephron Na+ reabsorption to be a common mechanism. FHHt (familial hyperk
- PMID 24266877
- Impact of anticoagulation on the effectiveness of loop diuretics in heart failure with cardiorenal syndrome and venous thromboembolism.
- Targonski R1, Sadowski J, Cyganski PA.Author information 1aDepartament of Cardiology, City Hospital, Al. Niepodleglości 44, Olsztyn, Poland.AbstractThe limitations of diuretics in the treatment of acute decompensated heart failure (ADCHF) are progressive worsening of renal function and resistance to up-titrated doses. The occurrence of resistance to loop diuretics in patients with ADCHF is associated with worsening prognosis and increased mortality. In this study, we report two patients with ADCHF and resistance to loop diuretics suspected for venous thromboembolism, suggesting that heparin administered to ADCHF patients treated for venous thromboembolism with cardiorenal syndrome decreases right-ventricular overload and improves renal function. To our knowledge, these are the first reported cases describing restored responsiveness to loop diuretics in ADCHF patients after additional heparin administration.
- Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis.Blood Coagul Fibrinolysis.2014 Mar;25(2):180-2. doi: 10.1097/MBC.0000000000000012.
- The limitations of diuretics in the treatment of acute decompensated heart failure (ADCHF) are progressive worsening of renal function and resistance to up-titrated doses. The occurrence of resistance to loop diuretics in patients with ADCHF is associated with worsening prognosis and increased morta
- PMID 24284867
- Novel drugs targeting transthyretin amyloidosis.
- Hanna M.Author information Section of Heart Failure and Cardiac Transplantation, Cleveland Clinic, 9500 Euclid Avenue, Desk J3-4, Cleveland, OH, 44195, USA, email@example.com.AbstractTransthyretin amyloidosis (ATTR) is either a hereditary disease related to a mutation in the transthyretin gene that leads to neuropathy and/or cardiomyopathy or an acquired disease of the elderly that leads to restrictive cardiomyopathy. The prevalence of this disease is higher than once thought and awareness is likely to increase amongst physicians and in particular cardiologists. Until recently there have been no treatment options for this disease except to treat the heart failure with diuretics and the neuropathy symptomatically. However, there are several emerging pharmacologic therapies designed to slow or stop the progression of ATTR. This article reviews novel therapeutic drugs that work at different points in the pathogenesis of this disease attempting to change its natural history and improve outcomes.
- Current heart failure reports.Curr Heart Fail Rep.2014 Mar;11(1):50-7. doi: 10.1007/s11897-013-0182-4.
- Transthyretin amyloidosis (ATTR) is either a hereditary disease related to a mutation in the transthyretin gene that leads to neuropathy and/or cardiomyopathy or an acquired disease of the elderly that leads to restrictive cardiomyopathy. The prevalence of this disease is higher than once thought an
- PMID 24464360
- 江口 和男,荒川 伸人,手塚 康裕,大野 彰二,黒田 一,齋藤 建
- 自治医科大学紀要 34, 75-79, 2012-03-01
- 症例は68歳男性,高熱と呼吸困難感を主訴に入院した。肺炎と心不全の診断で抗生剤と利尿剤で治療を開始した。一時軽快傾向となったが,CRP値6以上が持続していた。心エコーでは,び漫性壁運動低下と心尖部付近の心筋肥大がみられた。第18病日に致死的不整脈を発症し、CPRを行ったが,突然死した。病理解剖の結果,下壁の陳旧性心筋梗塞と前壁の急性心筋梗塞に伴う心尖部の感染性血栓がみつかった。本症例では,左室の壁 …
- NAID 110008922596
- 利尿薬は腎保護的でないという意味 (特集 いつもの薬 : ふとした疑問)
- diureticとは。意味や和訳。[形]排尿促進の, 利尿の. [名]利尿剤. - goo辞書は国語、英和、和英、中国語、百科事典等からまとめて探せる辞書検索サービスです。 ... 音節 di • u • ret • ic 発音 dàiərétik | dàijuər-レベル 社会人必須 ...
- diureticの意味は？goo辞書は無料で使える日本最大級の辞書サービスです。国語辞典、英和辞典、和英辞典、類語辞典、中国語辞典、百科事典などを提供しています。 ... 辞書すべて 国語 類語 英和 和英 中日 日中 ※「説明文に ...
- diuretic, diuretics
- diuretic、diuretic drug
- diuretic、diuretic agent、diuretics
- diuretic、diuretic drug、diuretics
抗利尿ホルモン ADH → バソプレシン